Coronary Artery Vasospasm

Introduction
Background
In 1959, Prinzmetal et al described a syndrome of chest pain at rest secondary to myocardial ischemia associated with ST-segment elevation.1 Exercise tolerance was characteristically normal in these individuals, who experienced a cyclical pain pattern with most episodes occurring in the early morning hours. This syndrome, known as Prinzmetal or variant angina, is due to focal coronary artery vasospasm and may be associated with acute myocardial infarction (MI), serious ventricular arrhythmias, and sudden death.

More recently, Maseri et al2 described the clinical, electrocardiographic, and angiographic features of 138 patients with variant angina and concluded that the syndrome is considerably more polymorphic than initially inferred by Prinzmetal et al. Variant angina is defined by the angiographic demonstration of spontaneous or induced coronary spasm in patients with rest pain. Electrocardiographic features may include ST-segment elevation or depression.

Note that coronary vasoconstriction and dynamic coronary obstruction are also components of atherosclerotic coronary artery disease, which can present as stable and unstable angina pectoris. This suggests a spectrum of clinical, electrocardiographic, and angiographic manifestations that share a common pathophysiology.

A Japanese variant of variant angina (termed vasospastic angina) may constitute a more diffuse disorder of large vessel vasomotor reactivity.
Pathophysiology

Prinzmetal angina is caused by focal coronary artery vasospasm, and a generalized abnormality of coronary artery vasomotor reactivity is not present. Focal coronary artery spasm typically occurs at the site of or adjacent to a fixed stenosis. A substantial number of patients have seemingly normal coronary angiogram results, although many within this subgroup have evidence of early atherosclerosis demonstrated by intravascular ultrasonographic examination or at autopsy.

Nitric oxide is a potent endothelium-derived relaxing factor responsible for maintaining the coronary arteries in a state of relative vasodilatation. Nitric oxide is synthesized from the amino acid L- arginine in a biochemical reaction catalyzed by the enzyme nitric oxide synthase. Nitric oxide is also a potent inhibitor of platelet activation, adhesion, and aggregation. Activated platelets are responsible for the release of several potent vasoconstrictors, including thromboxane A2. Abnormalities of nitric oxide synthase and reduced bioavailability of nitric oxide may result in increased basal vascular tone, vasoconstriction, vasospasm, and in activation, adhesion, and aggregation of platelets with release of additional vasoconstrictors.

Elevated serum low-density lipoprotein (LDL) cholesterol, especially the oxidized form of this lipid moiety, is responsible for the decreased production of nitric oxide due to down-regulation of endogenous nitric oxide synthase and the oxidative inactivation of nitric oxide by oxygen free radicals. Since focal coronary artery spasm in Prinzmetal angina typically occurs at or adjacent to endothelium that overlies a fatty streak of early atherosclerosis or a fibrous plaque of advanced atherosclerosis, focal endothelial dysfunction seems likely. The role of endothelial vasodilator function in the genesis of coronary artery vasospasm remains controversial.

Experimental evidence from porcine models of this disorder suggests that spasm is caused primarily by vascular smooth muscle cell hypercontraction and not by local endothelial vasodilatory dysfunction. The molecular mechanism(s) of this smooth muscle cell abnormality remains unclear. Low levels of intracellular magnesium and increased retained magnesium after an intravenous load in patients with this disorder suggest that magnesium metabolism is abnormal in patients with coronary artery vasospasm. This may occur with vitamin E as well. Hyperinsulinemia and insulin resistance are probable risk factors for variant angina, although the pathogenic mechanisms of these apparent associations have not been defined.

The role of the autonomic nervous system in the pathogenesis of variant angina is controversial. Withdrawal of parasympathetic activity before the onset of angina has been suggested, but Japanese investigators actually found an increase in parasympathetic and sympathetic activity. Whether this discrepancy is due to methodological flaws or to racial vasomotor heterogeneity in vasomotor angina is unclear.

Frequency
United States

Estimates are that 2-3% of all patients undergoing diagnostic cardiac catheterization for chest pain in the United States will subsequently be classified as having variant angina. This percentage may vary depending on the criteria applied to make the diagnosis of variant angina and the intensity of electrocardiographic surveillance for transient ST-segment elevation during episodes of chest pain.
International

In Italy, where rigorous inpatient electrocardiographic monitoring is frequently used, the incidence of variant angina in patients admitted with chest pain is approximately 10%. Variant angina is particularly common in Japan with 20-30% of patients who undergo coronary angiography for chest pain assigned a diagnosis of vasospastic angina (see Background). Of these patients, 40-80% have angiographically normal coronary arteries.
Mortality/Morbidity

Overall, the prognosis of patients with variant angina is favorable. Three-year survival rates vary between 84-98%, and MI-free survival at 3 years varies between 63-98%, depending on application of the relevant diagnostic criteria and the study population. Early and late mortality and morbidity are related to the degree of underlying atherosclerotic coronary artery disease. Patients without a stenosis of 70% or more have a 93% 1-year MI-free survival rate, while patients with multivessel atherosclerotic coronary artery disease and variant angina only have a 65% 1-year MI-free survival rate. Patients who develop serious arrhythmias during episodes of pain and/or who have evidence of diminished left ventricular ejection fraction are at increased risk of early mortality.
Race

Racial heterogeneity probably exists in coronary artery vasomotor reactivity. Japanese patients have a higher relative incidence of variant angina. They may exhibit a more diffuse abnormality of vasomotor tone compared to whites, and angiography may show segmental or diffuse coronary artery spasm. The incidence of variant angina in African Americans is not well defined.
Sex

The major prognostic studies of patients with variant angina confirm that 69-91% are male. Variant angina may be relatively more common in white female patients (22%) than in Japanese patients (11%).
Age

The mean age of patients with variant angina is 51-57 years.
Clinical
History

Angina pectoris is the chest pain experienced by patients with variant angina and usually is described as a retrosternal pressure with radiation to the neck, jaw, left shoulder, or arm. Variant angina occurs at rest and exhibits a circadian pattern, with most episodes occurring in the early hours of the morning. The pain commonly is severe and may be associated with palpitations, presyncope, or syncope secondary to arrhythmia.
Distinguishing unstable angina pectoris related to coronary atherosclerosis from variant angina may be difficult and requires special investigations, including coronary angiography. This may be an arbitrary distinction in some patients because it is likely that vasospasm is both a cause and a consequence of plaque rupture and thrombosis in patients with unstable angina pectoris, and many patients with variant angina have obstructive coronary artery disease.
The absence of risk factors for atherosclerotic coronary artery disease suggests variant angina, although cigarette smoking is a common risk factor for both clinical syndromes and is reported in most patients with variant angina.
A minority of patients with variant angina may have a more systemic abnormality of vasomotor tone; this may include symptoms of migraine headache and Raynaud phenomenon. Although in one series, 30% of patients reported a familial incidence of variant angina, there is no convincing evidence for a genetic predisposition to arterial spasm. It has been suggested that an examination of hereditary pathological and polymorphic variations in factors elaborated by endothelial cells, platelets, and leukocytes responsible for maintaining the patency of blood vessels (eg, nitric oxide, prostacyclin, endothelin-1) may prove enlightening.
Physical

The cardiac examination findings in patients with variant angina typically are normal, although a fourth heart sound or mitral regurgitation may be heard during episodes. Tachycardia or bradycardia may accompany episodes of prolonged chest pain, particularly with marked ST-segment elevation. Noninvasive imaging studies may show regional wall motion abnormalities and even segmental dyskinesis during episodes of pain. Finding other evidence of diffuse atherosclerotic disease does not differentiate patients with variant angina from those with unstable angina pectoris, and the physical examination does not reliably discriminate patients with variant angina who have no obstructive coronary artery disease from those with multivessel disease.
Causes

The pathophysiology of this syndrome is most likely related to an abnormality of normal vasodilator function within the coronary arteries and/or a hypersensitivity of the coronary arteries to normal mediators of vasoconstriction. The underlying cause of these abnormalities of vasomotor function is unknown. Subclinical or clinical atherosclerosis is almost ubiquitous in patients with variant angina, although the reason this subgroup of patients should present with focal coronary artery vasospasm remains unclear. Smoking, hyperinsulinemia, and insulin resistance are probable risk factors for variant angina.

http://emedicine.medscape.com/article/153943-overview

Myocardial Infarction

Introduction
Background

Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance of oxygen supply and demand. The appearance of cardiac enzymes in the circulation generally indicates myocardial necrosis. Myocardial infarction is considered, more appropriately, part of a spectrum referred to as acute coronary syndromes (ACSs), which also includes unstable angina and non–ST-elevation MI (NSTEMI). Patients with ischemic discomfort may or may not have ST-segment elevation. Most of those with ST-segment elevation will develop Q waves. Those without ST elevations will ultimately be diagnosed with unstable angina or NSTEMI based on the presence of cardiac enzymes.

Myocardial infarction may lead to impairment of systolic function or diastolic function and to increased predisposition to arrhythmias and other long-term complications.

Pathophysiology

Atherosclerosis is the disease primarily responsible for most acute coronary syndrome cases. Approximately 90% of myocardial infarctions result from an acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture is considered to be the major trigger of coronary thrombosis. Following plaque rupture, platelet activation and aggregation, coagulation pathway activation, and endothelial vasoconstriction occur and lead to coronary thrombosis and occlusion.

Consider nonatherosclerotic causes of acute myocardial infarctions in younger patients or if no evidence of atherosclerosis is noted. Such causes include coronary emboli from sources such as an infected cardiac valve through a patent foramen ovale (PFO), coronary occlusion secondary to vasculitis, primary coronary vasospasm (variant angina), cocaine use, or other factors leading to mismatch of oxygen supply and demand, as may occur with a significant gastrointestinal bleed.

Frequency
United States

Approximately 1.5 million cases of myocardial infarction occur each year.
International

Cardiovascular diseases cause 12 million deaths throughout the world each year, according to the third monitoring report of the World Health Organization, 1991-93. They cause half of all deaths in several developed countries and are one of the main causes of death in many developing countries; they are the major cause of death in adults everywhere.
Mortality/Morbidity
Cardiovascular disease is the leading cause of death in the United States; approximately 500,000-700,000 deaths related to the coronary artery occur each year.
Ischemic heart disease is the leading cause of death worldwide.
Approximately 6.3 million deaths due to heart disease occurred in 1990 worldwide, which represents 29% of all deaths. The prevalence of coronary artery disease (CAD) is increasing rapidly in nonindustrialized countries.
Race

Cardiovascular disease is the leading cause of morbidity and mortality among African American, Hispanic, and white populations in the United States.
Sex
A male predominance in incidence exists up to approximately age 70 years, when the sexes converge to equal incidence.
Premenopausal women appear to be somewhat protected from atherosclerosis, possibly owing to the effects of estrogen.
Age
Incidence increases with age.
Most patients who develop an acute myocardial infarction are older than 60 years. Elderly people also tend to have higher rates of morbidity and mortality from their infarcts.
Clinical
History

Symptoms of myocardial infarction include the following:

Chest pain
This is usually described as a substernal pressure sensation that also may be described as squeezing, aching, burning, or even sharp pain.
Prolonged chest discomfort lasting longer than 30 minutes is most compatible with infarction.
Radiation to the left arm or neck is common.
The sensation is precipitated by exertion and relieved by rest and nitroglycerin.
Chest pain may be associated with nausea, vomiting, diaphoresis, dyspnea, fatigue, or palpitations.
Atypical chest pain is common, especially in patients with diabetes and in elderly patients. However, any patient may present with atypical symptoms. These symptoms are considered the anginal equivalent for that patient.
Shortness of breath
Shortness of breath may be the patient's anginal equivalent or a symptom of heart failure.
It is due to elevated end-diastolic pressures secondary to ischemia, which may then lead to elevated pulmonary pressures.
Atypical presentations
20% of patients are asymptomatic or have atypical symptoms.
Atypical presentations are common and frequently lead to misdiagnoses.
A patient may, for example, present with abdominal discomfort or jaw pain as his or her anginal equivalent.
An elderly patient may present with altered mental status.
Low threshold should be maintained when evaluating high- and moderate-risk patients, as their anginal equivalents may mimic other presentations.
Women tend to present more commonly with atypical symptoms such as sharp pain, fatigue, weakness, and other nonspecific complaints.

Physical

Physical examination findings for myocardial infarction can vary; one patient may be comfortable in bed, with normal examination results, while another may be in severe pain with significant respiratory distress requiring ventilatory support.

Low-grade fever may be present.
Hypotension or hypertension can be observed depending on the extent of the myocardial infarction.
Fourth heart sound (S 4 ) may be heard in patients with ischemia. With ischemia, diastolic dysfunction is the first physiologically measurable effect and this can then cause a stiff ventricle and an audible S 4 .
Dyskinetic cardiac bulge (in anterior wall myocardial infarction) can occasionally be palpated.
Systolic murmur can be heard if mitral regurgitation (MR) or ventricular septal defect (VSD) develops.
Other findings include cool, clammy skin and diaphoresis.
Signs of congestive heart failure (CHF) may be found, including the following:
Third heart sound (S 3 ) gallop
Pulmonary rales
Lower extremity edema
Elevated jugular venous pressure
Causes
Atherosclerosis with occlusive or partially occlusive thrombus formation
Nonmodifiable risk factors for atherosclerosis
Age
Sex
Family history of premature coronary heart disease
Modifiable risk factors for atherosclerosis
Smoking or other tobacco use
Diabetes mellitus
Hypertension
Dyslipidemia
Obesity
New and other risk factors for atherosclerosis
Elevated homocysteine levels
Male pattern baldness
Sedentary lifestyle and/or lack of exercise
Psychosocial stress
Presence of peripheral vascular disease
Poor oral hygiene
Nonatherosclerotic causes
Vasculitis
Coronary emboli
Congenital coronary anomalies
Coronary trauma
Coronary spasm
Drug use (cocaine)
Factors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidism
Factors that decrease oxygen delivery, such as hypoxemia of severe anemia

http://emedicine.medscape.com/article/155919-overview

Myocardial Rupture

Introduction
Background

Myocardial rupture occurs in the setting of acute myocardial infarction (AMI), blunt and penetrating cardiac trauma, primary cardiac infection, primary and secondary cardiac tumors, infiltrative diseases of the heart, and aortic dissection. The clinical presentation of myocardial rupture depends on the mechanism and site of injury and the hemodynamic effects of the rupture. Mortality rates are extremely high unless early diagnosis and surgical intervention are provided rapidly.
Pathophysiology

AMI is the most common etiology of myocardial rupture. Ischemic myocardial rupture may involve the left ventricular (LV) and right ventricular (RV) free walls, ventricular septum, and LV papillary muscle, in decreasing order of frequency. Myocardial rupture rarely involves the left or right atrial walls.

The consequences of myocardial rupture in the setting of AMI can include pericardial tamponade, ventricular septal defect (VSD) with left-to-right shunt, acute mitral regurgitation (MR), or formation of a pseudoaneurysm. In most instances, the catastrophic clinical presentation occurs within 3-5 days of a rather small AMI. Both hemodynamic factors (increased intracavitary pressure) and regional myocardial structural weakness (myocyte necrosis, collagen matrix resolution, intense inflammation) are important contributory factors to myocardial rupture in the setting of AMI.

In rare instances, patients have been reported to simultaneously experience LV free wall rupture and ventricular septal or papillary muscle rupture (double rupture) following AMI. In the case of a papillary muscle rupture, the posteromedial papillary muscle is twice as likely to rupture as is the anterolateral papillary muscle. This likelihood is because the anteromedial papillary muscle is more often supplied by 2 arterial systems (left anterior descending and left circumflex coronary arteries), whereas the posteromedial papillary muscle is frequently supplied by only one coronary artery (usually the right) system. Rupture of both papillary muscles following AMI has been reported.

In some patients who survive LV free wall rupture following AMI, the rupture can be sealed by the epicardium (visceral pericardium) or by a hematoma on the epicardial surface of the heart. This entity has been referred to as LV diverticulum or contained myocardial rupture and represents a subacute pathologic condition between free rupture into the pericardial cavity and formation of a pseudoaneurysm. A pseudoaneurysm is formed if the area of rupture is contained locally by the adjacent parietal pericardium and represents the chronic stage of LV free wall rupture. The most common etiology of LV pseudoaneurysm is AMI. (LV pseudoaneurysm is twice as common with inferior, rather than anterior, AMI.) LV pseudoaneurysms may develop following surgery, especially following mitral valve replacement.

Blunt cardiac trauma, most commonly in the setting of an automobile accident, may cause myocardial rupture as a result of cardiac compression between the sternum and the spine, direct impact (sternal trauma), or from deceleration injury. It may result in rupture of the papillary muscles, cardiac free wall, or the ventricular septum. The cardiac chambers involved are, in decreasing order of frequency, the right ventricle, left ventricle, right atrium, and left atrium.

However, among those who reach the hospital alive, the right atrium is the most commonly involved chamber. In up to 30% of cases, the rupture involves more than one chamber. Delayed myocardial rupture has been reported as a result of cardiac contusion. Acute mitral or tricuspid regurgitation, VSD, or pericardial tamponade may result from myocardial rupture secondary to blunt cardiac trauma.

Penetrating myocardial injury occurs most commonly as a result of stab or gunshot wounds. Unlike blunt trauma, penetrating cardiac injury always involves the pericardium. Consequently, ventricular free-wall rupture in this setting may result in either pericardial tamponade (if the pericardial wound is obliterated) or intrathoracic hemorrhage. While pericardial tamponade is more common with stab wounds, gunshot wounds more frequently are associated with hypovolemic shock. The cardiac chambers involved are, in decreasing order of frequency, the right ventricle, left ventricle, right atrium, and left atrium.

Myocardial abscesses accompanying infective endocarditis may rupture transmurally, resulting in VSD or pericardial tamponade (pyohemopericardium). Such abscesses are observed most commonly in the setting of Staphylococcus aureus endocarditis involving prosthetic valves in the aortic position. Rarely, myocardial necrosis due to acute myocarditis, tuberculosis, or sarcoidosis may result in myocardial rupture.

Myocardial rupture is rarely caused by primary (hemangiopericytoma, angiosarcoma, lymphoma) or secondary (metastatic) cardiac tumors. Lymphomas and acute myeloblastic leukemia also have been associated with myocardial rupture.
Frequency
United States

Myocardial rupture complicates up to 10% of AMIs. Approximately 6-10% of penetrating chest wounds and 15-75% of blunt chest traumas are associated with cardiac injury. Myocardial rupture occurs in 10-15% of fatal motor vehicle accidents. Incidence of cardiac rupture following blunt trauma is 0.5-2% among hospital trauma admissions.
Mortality/Morbidity
Myocardial rupture is responsible for nearly 15% of all in-hospital deaths among patients with AMI. It is the second most common cause, after pump failure, of in-hospital mortality among patients with AMI.
The overall mortality rate from myocardial rupture following blunt trauma is 76-93%. However, among those who reach the hospital alive, the mortality rate is 29-50%. Mortality from myocardial rupture resulting from penetrating trauma ranges from 62-89% in the field to 2-83% after reaching a hospital. The latter largely depends on the type of injury, rapidity of the transfer to a hospital, and patients' vital signs and condition upon arrival.
Following myocardial rupture as a result of penetrating cardiac trauma, hospital mortality is higher in those presenting with hypovolemia rather than pericardial tamponade (22% vs 8%). In-hospital mortality is lowest for patients with RV rupture.
Sex
Myocardial rupture after AMI is reported more commonly in women than in men (1.4:1).
Traumatic myocardial rupture is more common in males (up to 85% in some series) than in females.
Age
Myocardial rupture after AMI is more common in patients aged 60 years or older.
Traumatic myocardial rupture is observed more commonly in those aged 15-63 years (mean, 34 y).
Clinical
History
Myocardial rupture after AMI may occur from 1 day to 3 weeks after infarction. Most ruptures occur 3-5 days after infarction.
In most patients, myocardial rupture manifests as a catastrophic event (acute pulmonary edema, cardiogenic shock, or circulatory collapse) within days of a first, small, uncomplicated AMI.
Older women, especially those with recurrent postinfarction angina, and patients with systemic hypertension more commonly experience myocardial rupture following AMI.
Acute onset of shortness of breath, chest pain, shock, diaphoresis, unexplained emesis, cool and clammy skin, and syncope may herald the onset of ventricular septal rupture following AMI.
Sudden death due to LV free-wall rupture may be the first manifestation of coronary artery disease in a small percentage of patients with AMI.
Immediate, early, or delayed acute pulmonary edema (papillary muscle rupture), congestive heart failure (ventricular septal rupture), and hypotension (free-wall rupture) are the cardinal manifestations of myocardial rupture following blunt chest trauma. Concomitant rupture of the myocardium, pericardium, and diaphragm may result in the accumulation of blood in the abdominal cavity.
In patients with traumatic myocardial rupture, manifestations depend on the site, mode, and extent of cardiac injury.
Sudden death occurs shortly after the injury in most patients with traumatic myocardial rupture and is due to pericardial tamponade or exsanguination.
Cardiogenic or hypovolemic shock is the predominant manifestation of traumatic myocardial rupture in patients who reach a hospital.
Patients with pericardial tamponade may present with dyspnea, chest pain, hypotension, cold peripheries, and mental status changes.
A small percentage of patients with significant penetrating cardiac trauma have few or no symptoms upon presentation to a hospital.
Pseudoaneurysms may manifest as cerebral or systemic embolic events or sudden death (rupture). Hemoptysis may occur due to the formation of ventriculopulmonary fistulas. Approximately 10% of patients with pseudoaneurysm are asymptomatic.
Physical
Of those who sustain cardiac trauma from stab wounds, 18-35% remain without clinical signs of myocardial injury.
Papillary muscle rupture (partial or complete)
Acute pulmonary edema manifests as tachypnea, tachycardia, hypotension, respiratory distress, diffuse pulmonary rales, and signs of MR.
The MR murmur may be absent or atypical (soft and not holosystolic) due to rapid equalization of pressures between the left ventricle and left atrium. This equalization is due to the noncompliance of the acutely volume-overloaded left atrium (ie, the left atrial pressure increases sharply in response to sudden rise in volume).
Sudden unexplained hypotension and/or pulmonary edema in patients experiencing their first inferior AMI should raise the possibility of papillary muscle rupture, even in the absence of a murmur.
Left ventricle free-wall rupture
Post-AMI pericarditis manifested as pleuritic chest pain and friction rub may be present in some patients prior to onset of rupture and generally indicates transmural extension of the infarct. Cardiogenic shock due to pericardial tamponade manifests as sudden onset of bradycardia, clear lung fields, distended neck veins, Kussmaul sign (ie, paradoxical inspiratory increase in jugular venous pressure), muffled heart sounds, and pulsus paradoxus (ie, an inspiratory drop in systolic blood pressure of >10 mm Hg).
Hypovolemic shock may occur due to direct communication with the thoracic or abdominal cavity through a pericardial tear. This manifests as hypotension, tachycardia, cool and clammy extremities, pallor, and diaphoresis.
Ventricular septal rupture
Hypotension may be present.
Patients may have acute pulmonary edema.
A loud holosystolic murmur may be heard at the lower left sternal border or diffusely over the precordium and is often associated with a thrill.
Ventricular arrhythmias may be present.
Pseudoaneurysm
A friction rub may be heard.
Pseudoaneurysms frequently rupture, resulting in cardiogenic or hypovolemic shock.
Some patients may have a systolic murmur due to the turbulent flow across the narrow neck of the pseudoaneurysm.
Systemic embolism that originates from the pseudoaneurysm may result in various cerebrovascular or systemic ischemic symptoms.
Arrhythmia may be present, especially ventricular tachycardia and fibrillation.
Causes
Acute myocardial infarction
Risk factors for myocardial rupture following AMI include a relatively small first AMI, female sex, age older than 60 years, hypertension, use of nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids during the acute phase of AMI (interference with the healing process), late thrombolysis (>11 h), postinfarct angina and elevated peak serum C-reactive protein.
Protective factors include LV hypertrophy, history of previous infarcts, congestive heart failure, history of chronic ischemic heart disease, early use of beta-blockers after AMI, and successful (and timely) primary percutaneous coronary intervention.
Trauma
Trauma may be blunt or penetrating.
Trauma also may be iatrogenic in nature, resulting from (1) diagnostic catheterization, including transseptal puncture and endomyocardial biopsy; (2) balloon valvuloplasty; (3) pericardiocentesis; (4) placement of temporary or permanent pacing catheters; and (5) cardiac surgery, especially mitral valve replacement.
Infection
Rupture of a myocardial abscess or AMI secondary to coronary embolism of the vegetative material may occur in patients with infective endocarditis.
Other infections may include tuberculosis, echinococcal cysts, and myocarditis.
Aortic dissection
Malignancy
Primary cardiac tumors may be present.
Patients may have secondary or metastatic tumors of the heart.
Patients may have lymphoma or acute myeloblastic leukemia.
Sarcoidosis

http://emedicine.medscape.com/article/156455-overview

Right Ventricular Infarction

Introduction
Background

Right ventricular infarction was first recognized in a subgroup of patients with inferior wall myocardial infarctions who demonstrated right ventricular failure and elevated right ventricular filling pressures despite relatively normal left ventricular filling pressures. Increasing recognition of right ventricular infarction, either in association with left ventricular infarction or as an isolated event, emphasizes the clinical significance of the right ventricle to total cardiac function.

Interest in recognizing right ventricular infarction noninvasively has grown because of the therapeutic implications of distinguishing patients with right ventricular dysfunction from those with the more usual clinical presentation of left ventricular dysfunction. Patients with right ventricular infarctions associated with inferior infarctions have much higher rates of significant hypotension, bradycardia requiring pacing support, and in-hospital mortality than isolated inferior infarctions.1

Pathophysiology

The right ventricle is a thin-walled chamber that functions at low oxygen demands and pressure. It is perfused throughout the cardiac cycle in both systole and diastole, and its ability to extract oxygen is increased during hemodynamic stress. All of these factors make the right ventricle less susceptible to infarction than the left ventricle.

The posterior descending branch of the right coronary artery usually supplies the inferior and posterior walls of the right ventricle. The marginal branches of the right coronary artery supply the lateral wall of the right ventricle. The anterior wall of the right ventricle has a dual blood supply: the conus branch of the right coronary artery and the moderator branch artery, which courses from the left anterior descending artery.2

Interestingly, right ventricular infarction noted at necropsy usually involves the posterior septum and posterior wall rather than the right free wall. The relative sparing of the right ventricular anterior wall apparently arises from a high degree of collateralization. This collateral blood flow is thought to be derived from the thebesian veins and diffusion of oxygen directly from the ventricular cavity. A direct correlation exists between the anatomic site of right coronary artery occlusion and the extent of right ventricular infarction. Studies have demonstrated that more proximal right coronary artery occlusions result in larger right ventricular infarctions.3 On occasion, the right ventricle can be subjected to infarction from occlusion of the left circumflex coronary artery.4

Because the right ventricle is considered a low-pressure volume pump, its contractility is highly dependent on diastolic pressure. Hence, when contractility and associated diastolic dysfunction are impaired attendant to right ventricular infarction, the right ventricular diastolic pressure increases substantially and systolic pressure decreases. In such a scenario, concomitant left ventricular dysfunction, with increase in right ventricular afterload, is possible. In such a setting, right ventricular output can decrease dramatically, and the only driving force remaining is elevated right atrial pressure. In such a circumstance, the right ventricle serves as a poorly functioning conduit between the right atrium and the pulmonary artery.

Elevation of right atrial pressure secondary to right ventricular infarction has been noted to serve as a stimulus for secretion of atrial natriuretic factor. Increased levels of this polypeptide can be detrimental to normal left ventricular filling pressures. This occurs by virtue of the potent vasodilating, natriuretic, diuretic, and aldosterone-inhibiting properties of atrial natriuretic factor. Inappropriately elevated levels of atrial natriuretic factor may worsen the clinical syndrome of right ventricular infarction.5 The potential hemodynamic derangements associated with right ventricular infarction render the afflicted patient unusually sensitive to diminished preload (ie, volume) and loss of atrioventricular synchrony. These 2 circumstances can result in a severe decrease in right and, secondarily, left, ventricular output.6,7,8

Early thrombolysis or mechanical reperfusion of an occluded coronary artery resulting in right ventricular infarction is associated with prompt reduction in right atrial pressure. This is extremely important because persistently elevated right atrial pressure has been associated with increased in-hospital mortality rate when associated with myocardial infarction. The extent of right ventricular infarction varies greatly and is dependent on the site of occlusion of the right ventricular arterial supply. If occlusion occurs before the right ventricular marginal branches, and collateral blood flow from the left anterior descending coronary artery is absent, then the size of infarction generally is greater. Extent of infarction depends somewhat on flow through the thebesian veins.9 In general, any major reduction in blood supply to the right ventricular free wall portends an adverse prognosis in association with this disorder.

Frequency
United States

Isolated infarction of the right ventricle is extremely rare; right ventricular infarction usually is noted in association with inferior wall myocardial infarction. The incidence of right ventricular infarction in such cases ranges from 10-50%, depending on the series.10

The frequency of right ventricular infarction, which can be detected by right-sided precordial leads, in association with non–ST-segment elevation or non–Q-wave myocardial infarction is not known and currently is being investigated. Although right ventricular infarction is clinically evident in a sizable number of cases, the incidence is considerably less than that found at autopsy.11,12,13,14 A major reason for the discrepancy is the difficulty in establishing the presence of right ventricular infarction in living subjects. Additionally, right ventricular dysfunction and stunning frequently is of a transient nature, such that estimation of its true incidence is even more difficult.

Criteria have been set forth to diagnose right ventricular infarction; even when strictly employed, however, the criteria lead to underestimation of the true incidence of right ventricular infarction.15,16,17
Clinical
History
Although right ventricular infarction occurs in more than 30% of patients with inferior posterior left ventricular myocardial infarction, hemodynamically significant right ventricular infarction occurs in less than 10% of these patients.18,19
A right ventricular infarct should be considered in all patients who present with an acute inferior wall myocardial infarction, especially in the setting of a low cardiac output.
Patients may describe symptoms consistent with hypotension.
A subtle clue to the presence of hemodynamically significant right ventricular infarction is a marked sensitivity to preload-reducing agents such as nitrates, morphine, or diuretics.20
Other presentations include high-grade atrioventricular block, tricuspid regurgitation, cardiogenic shock, right ventricular free wall rupture, and cardiac tamponade.
Should a patient with right ventricular infarction experience unexplained hypoxia despite administration of 100% oxygen, right-to-left shunting at the atrial level in the presence of right ventricular failure and increased right atrial pressure must be considered.21,22 Despite its rarity, this complication of right ventricular infarction must always be considered when a patient with myocardial infarction is thought to have hypoxia secondary to clinically silent pulmonary emboli. The mechanism for right-to-left shunting in the absence of increased pulmonary arterial pressure resides in patency of the foramen ovale in association with poor right ventricular compliance and increased right atrial filling pressures.
Patients with extensive right ventricular necrosis are at risk for right ventricular catheter–related perforation, and passage of a floating balloon catheter or pacemaker must always be performed with great care in such a setting.
Physical
The classic clinical triad of right ventricular infarction includes distended neck veins, clear lung fields, and hypotension.23
Infrequent clinical manifestations include right ventricular third and fourth heart sounds, which are typically audible at the left lower sternal border and increase with inspiration.
On hemodynamic monitoring, disproportionate elevation of right-sided filling pressures compared with left-sided hemodynamics represents the hallmark of right ventricular infarction.

http://emedicine.medscape.com/article/157961-overview

Saphenous Vein Graft Aneurysms

Introduction
Background

Coronary artery revascularization with saphenous vein grafts (SVGs) has become a surgical standard for treatment of coronary artery disease since Favaloro first described it in 1967. Riahi and associates described the rare complication of saphenous vein graft aneurysm (SVGA) in 1975.1

SVGA is defined as a localized dilation of the vessel to 1.5 times the expected normal diameter. These are classified as true and false aneurysms (or pseudoaneurysms): true aneurysms involve all 3 layers of the vessel wall, whereas false aneurysms involve disruption of 1 or more layers of the vessel wall with a well-defined collection of blood or hematoma outside the endothelium. Further classification of SVGAs as large or small is not well defined, although dilation to more than 2 cm has generally led to consideration for surgical therapy. SVGAs reported in literature range from 1-14 cm in diameter.

Pathophysiology

The SVG to left anterior descending is the most common site for aneurysm formation, followed by the right coronary artery, and least commonly, the left circumflex.

True aneurysms, which usually develop in the body of the vein graft and are typically fusiform, are usually the result of a chronic, degenerative process caused by vascular injury that results from hyperlipidemia and progression of atherosclerosis. The initial event in SVGA formation is thought to be atheroma formation followed by plaque rupture, resulting in injury to the vessel wall, which is exacerbated by arterial pressures within the vein graft. Valve insertion points along the vein graft are especially prone to true SVGA formation, where smooth muscle in the media changes from circular to a weaker longitudinal orientation. Other possible contributing factors include varicosities with impaired elastic tissue integrity not detected at the time of harvesting, vascular injury from previous percutaneous intervention (PCI), and surgical trauma.

False aneurysms are saccular and typically located at the proximal SVG anastomosis, although they have been reported in the body and at the distal anastomosis. These are thought to occur because of tension on the anastomosis with suture rupture, or from technical issues in suture placement. Infection, particularly postoperative mediastinal sepsis involving Staphylococcus aureus, is commonly associated with false aneurysm formation because of suture line dehiscence. SVGA formation in the body of the graft has been reported to occur at the site of previous PCI and in the setting of chronic corticosteroid use.
Frequency
International

Mild aneurysmal dilation of SVGs is relatively common, with a frequency of approximately 14% within 5-7 years of surgery.

A literature review from the first reported case in 1975 until 2002 revealed 50 true aneurysms and 26 false aneurysms. In a review of all bypass cases at one institution from 1975-1991, of 1658 patients with 5579 grafts, 4 developed SVGA, giving an incidence of 0.07%. The incidence of significant SVGA is probably underestimated because the initial presentation may be rupture leading to sudden death, the aneurysm may not appear on angiography if it contains significant thrombus, and many patients are asymptomatic.
Mortality/Morbidity
SVGA rupture is associated with high morbidity and mortality rates.
Ischemic symptoms, either angina or infarction, can occur from graft occlusion, embolic phenomena, or compression of the graft by the aneurysm. Many SVGAs cause no symptoms and remain subclinical; thus, morbidity and mortality estimates are likely affected by a selection bias.
In symptomatic patients, the mortality rate is high, with 13 of 46 patients (28%) dying within 90 days of initial symptoms.
Race

Among reported cases in which race was identified, the patients were white. This may reflect a selection bias.
Sex

SVGAs are more common in men than women. In the literature review cited above, 64 of the 76 patients (84%) were men; this may be, in part, because more men than women undergo coronary artery bypass surgery.
Age

The average age of patients at the time of diagnosis is 59 years (range, 23-80 y).
Women tend to be older than men at presentation, probably because they tend to develop coronary artery disease later in life and therefore undergo coronary artery revascularization later.
Patients with SVGA typically present years after surgery, with 10-20 years as the average time to onset; however, both true and false SVGAs have been reported within months of surgery.
Clinical
History

Most patients with true aneurysms (45-55%) are asymptomatic and present incidentally with a hilar or mediastinal mass on chest radiograph or other imaging modality. Several cases of saphenous vein graft aneurysm (SVGA) that mimic a cardiac mass on echocardiography have been described. Symptomatic patients present with acute coronary syndrome with myocardial infarction (20-25%), unstable angina (15-20%), or congestive heart failure (5%). Compression of surrounding structures may occur; recently, cardiac tamponade from right atrial compression and cardiac ischemia from compression of an adjacent left internal mammary artery bypass graft have been reported.

By contrast, most patients with false aneurysm present with symptoms, including unstable angina (45-50%), myocardial infarction (15%), bleeding (10%), hemoptysis (6%), and infection (4%). Only 15% of patients with false SVGA are asymptomatic.
The sudden onset of chest pain in a patient with SVGA may represent abrupt fistula formation with coronary steal.
Hemoptysis may occur because of bleeding from the SVGA into lung parenchyma or from fistula formation between the SVGA and a bronchus.
The triad of chest pain, mediastinal mass, and previous coronary bypass surgery has been suggested to raise suspicion for SVGA.
Physical

The diagnosis of SVGA is typically not suggested by physical examination. However, the following signs may be uncovered:
Cutaneous bleeding or hemoptysis from fistula development to either the skin or bronchial tree
Palpable pulsatile mass
A new murmur (from fistula formation)
Causes

Authorities have identified a number of disorders in individuals with SVGAs. However, whether the following disorders represent random associations, secondary associations, or true causal factors of SVGAs remains unknown:

Atherosclerosis
Previous aneurysms
Postoperative mediastinitis prior to aneurysm development
Hypertension
In one small series, 15% of SVGAs were mycotic and 5% were associated with torn sutures.

http://emedicine.medscape.com/article/161328-overview

Complications of Myocardial Infarction

Background

Myocardial infarction (MI) due to coronary artery disease is a leading cause of death in the United States, where more than 1 million people have acute myocardial infarctions (AMIs) each year.1

The advent of coronary care units and early reperfusion therapy (lytic or percutaneous coronary intervention) has substantially decreased in-hospital mortality rates and has improved the outcome in survivors of the acute phase of MI.

Complications of MI include arrhythmic, mechanical, inflammatory (early pericarditis and post-MI syndrome) sequelae, as well as left ventricular mural thrombus (LVMT). In addition to these broad categories, right ventricular (RV) infarction and cardiogenic shock are other possible complications of acute MI.

Arrhythmic Complications of MI

Introduction

Cardiac arrhythmias are not uncommon during and immediately after an AMI. Of all patients who have an AMI, about 90% develop some form of cardiac arrhythmia. In 25% of patients, such rhythm abnormalities manifest within the first 24 hours. In this group of patients, the risk of serious arrhythmias, such as ventricular fibrillation, is greatest in the first hour and declines thereafter. The incidence increases with an ST-elevation myocardial infarction (STEMI) and decreases with a non–ST-elevation myocardial infarction (NSTEMI).

The clinician must be aware of these arrhythmias, in addition to reperfusion strategies, and he or she must treat those that require intervention to avoid exacerbation of ischemia and subsequent hemodynamic compromise. Most peri-infarct arrhythmias are benign and self-limited. However, those that result in hypotension, increase myocardial oxygen requirements, and/or predispose the patient to develop additional malignant ventricular arrhythmias should be aggressively monitored and treated.

Pathophysiology

AMI is characterized by generalized autonomic dysfunction that results in enhanced automaticity of the myocardium and conduction system. Electrolyte imbalances (eg, hypokalemia and hypomagnesemia) and hypoxia further contribute to the development of cardiac arrhythmia. The damaged myocardium acts as substrate for re-entrant circuits, due to changes in tissue refractoriness.

Enhanced efferent sympathetic activity, increased concentrations of circulating catecholamines, and local release of catecholamines from nerve endings in the heart muscle itself have been proposed to play roles in the development of peri-infarction arrhythmias. Furthermore, transmural infarction can interrupt afferent and efferent limbs of the sympathetic nervous system that innervates myocardium distal to the area of infarction. The net result of this autonomic imbalance is the promotion of arrhythmias.

Classification of peri-infarction arrhythmias

Peri-infarction arrhythmias can be broadly classified into the categories listed below. Each category is discussed in subsequent sections.
Supraventricular tachyarrhythmias
Sinus tachycardia
Premature atrial contractions
Paroxysmal supraventricular tachycardia
Atrial flutter
Atrial fibrillation
Accelerated junctional rhythms
Bradyarrhythmias
Sinus bradycardia
Junctional bradycardia
Atrioventricular (AV) blocks
First-degree AV block
Second-degree AV block
Third-degree AV block
Intraventricular blocks
Left anterior fascicular block
Right bundle branch block (RBBB)
Left bundle branch block (LBBB)
Ventricular arrhythmias
Premature ventricular contractions (PVCs)
Accelerated idioventricular rhythm
Ventricular tachycardia
Ventricular fibrillation
Reperfusion arrhythmias

Arrhythmic Complications: Supraventricular Tachyarrhythmias

Sinus tachycardia

Sinus tachycardia is associated with enhanced sympathetic activity and can result in transient hypertension or hypotension. The elevated heart rate increases myocardial oxygen demand, and a decreased length of diastole compromises coronary flow, worsening myocardial ischemia.

Persistent sinus tachycardia may be caused by pain, anxiety, heart failure, hypovolemia, hypoxia, anemia, pericarditis, or pulmonary embolism.

In the setting of an AMI, sinus tachycardia must be identified, and appropriate treatment strategies must be devised. Treatment strategies include adequate pain medication, diuresis to manage heart failure, oxygenation, volume repletion for hypovolemia, administration of anti-inflammatory agents to treat pericarditis, and use of beta-blockers and/or nitroglycerin to relieve ischemia.

Premature atrial contractions

Premature atrial contractions often occur before the development of paroxysmal supraventricular tachycardia, atrial flutter, or atrial fibrillation. The usual cause of these extra impulses is atrial distention due to increased left ventricular (LV) diastolic pressure or inflammation associated with pericarditis.

No specific therapy is indicated. However, attention should be given to identifying the underlying disease process, particularly occult congestive heart failure (CHF).

Paroxysmal supraventricular tachycardia

The incidence of a paroxysmal supraventricular tachycardia in the setting of an AMI is less than 10%. In the absence of definitive data in the patient with AMI, the consensus is that adenosine can be used when hypotension is not present. In patients without clinically significant LV failure, intravenous diltiazem or a beta-blocker can be used instead. In patients who develop severe CHF or hypotension, synchronized electrical cardioversion is required.

Atrial flutter

Atrial flutter occurs in less than 5% of patients with AMI. Atrial flutter is usually transient and results from sympathetic overstimulation of the atria.

Treatment strategies for persistent atrial flutter are similar to those for atrial fibrillation, except that ventricular-rate control with drugs is less easily accomplished with atrial flutter than with atrial fibrillation. Therefore, electrical cardioversion may be needed relatively soon because of a decrease coronary blood flow and/or hemodynamic compromise. For patients whose atrial flutter is refractory to medical therapy, overdrive atrial pacing may be considered.

Atrial fibrillation

The rate of atrial fibrillation is 10-15% among patients who have AMIs. The onset of atrial fibrillation in the first hours of AMI is usually caused by LV failure, ischemic injury to the atria, or RV infarction. Pericarditis and all conditions leading to elevated left atrial pressure can also lead to atrial fibrillation in association with an AMI. The presence of atrial fibrillation during an AMI is associated with an increased risk of mortality and stroke, particularly in patients who have anterior-wall MIs.

Immediate electrical cardioversion is indicated for the patient in unstable condition, such as one with new or worsening ischemic pain and/or hypotension. Synchronized electrical cardioversion begins with 50 J (or the biphasic equivalent) to treat atrial flutter or 200 J (or the biphasic equivalent) to treat atrial fibrillation. Conscious sedation (preferred) or general anesthesia is advisable prior to cardioversion. For patients in stable condition, controlling the ventricular response is the immediate objective. If the AF does not respond to cardioversion, IV Amiodarone2 or IV digoxin (in patients with LV dysfunction or heart failure) can be used to achieve ventricular rate control.

For patients who do not develop hypotension, a beta-blocker can be used. For example, metoprolol may be given in 5-mg intravenous boluses every 5-10 min with a maximum dose of 15 mg. Intravenous diltiazem is an alternative for slowing the ventricular rate, but it should be used with caution in patients with moderate-to-severe CHF. In patients with new onset sustained tachycardia (absent before MI), conversion to sinus rhythm should be considered as an option.

Atrial fibrillation and atrial flutter confer an increased risk of thromboembolism (see Deep Venous Thrombosis and Pulmonary Embolism). Therefore, anticoagulation with either UFH or LMWH should be started if contraindications are absent. It is unclear whether anticoagulation is needed in cases of transient AF and how long after the onset of AF should the anticoagulation be started.

Arrhythmic Complications: Accelerated Junctional Rhythm

An accelerated junctional rhythm results from increased automaticity of the junctional tissue that leads to a heart rate of 70-130 bpm. This type of dysrhythmia is most common in patients who develop inferior MIs. Treatment is directed at correcting the underlying ischemia.
Arrhythmic Complications: Bradyarrhythmias

Sinus bradycardia

Sinus bradycardia is a common arrhythmia in patients with inferior or posterior AMIs. The highest incidence of 40% is observed in the first 1-2 hours after AMI.

The likely mechanism leading to bradycardia and hypotension is stimulation of cardiac vagal afferent receptors that result in efferent cholinergic stimulation of the heart. In the early phases of an AMI, resultant sinus bradycardia may actually be protective, reducing myocardial oxygen demand. Clinically significant bradycardia that decreases cardiac output and hypotension may result in ventricular arrhythmias and should, therefore, be treated aggressively. Isolated sinus bradycardia is not associated with an increase in the acute mortality risk, and therapy is typically unnecessary when the patient has no adverse signs or symptoms.

When emergency therapy is indicated (eg, in a patient with a sinus rate of <40 bpm with hypotension), atropine sulfate 0.5-1 mg may be given every 3-5 minutes to a maximum of 0.03-0.04 mg/kg. The inability to reverse hypotension with atropine in patients who develop sinus bradycardia and inferior MI suggests volume depletion and/or RV infarction.

When atropine is ineffective and the patient is symptomatic or hypotensive, transcutaneous or transvenous pacing is indicated (see External Pacemakers). Denervate, transplanted hearts do not respond to atropine and, therefore, require cardiac pacing.

If these interventions fail, additional pharmacologic intervention may be useful. Examples are dopamine 5-20 mcg/kg/min given intravenously, epinephrine 2-10 mcg/min, and/or dobutamine.

Junctional bradycardia

Junctional bradycardia is a protective AV junctional escape rhythm at a rate of 35-60 bpm in patients who have an inferior MI. This arrhythmia is not usually associated with hemodynamic compromise, and treatment is typically not required.
Arrhythmic Complications: AV and Intraventricular Blocks

AV blocks
First-degree AV block

First-degree AV block is characterized by prolongation of the PR interval to longer than 0.20 seconds. This type of block occurs in approximately 15% of patients who have an AMI, most commonly an inferior infarction. Almost all patients who develop first-degree AV block have conduction disturbances above the His bundle. In these patients, the progression to complete heart block or ventricular asystole is rare. No specific therapy is indicated unless associated hemodynamic compromise is present.

Calcium channel blockers and beta-blockers may cause or exacerbate a first-degree AV block and should be stopped only if hemodynamic impairment or a higher-degree block occurs. For a first-degree AV block associated with sinus bradycardia and hypotension, atropine should be administered. Continued cardiac monitoring is advisable in view of possible progression to higher degrees of block.

Second-degree AV block

Mobitz type I, or Wenckebach AV block, occurs in approximately 10% of patients who have an AMI and accounts for 90% of all patients who have an AMI and a second-degree AV block. A second-degree AV block is associated with a narrow QRS complex and is most commonly associated with an inferior MI. It does not affect the patient's overall prognosis.

A Mobitz type I block does not necessarily require treatment. If the heart rate is inadequate for perfusion, immediate treatment with atropine 0.5-1 mg administered intravenously is indicated. Transcutaneous or temporary transvenous pacing is rarely required.

A Mobitz type II AV block accounts for 10% of all second-degree AV blocks (overall rate of <1% in the setting of AMI). A Mobitz type II block is characterized by a wide QRS complex, and it is almost always associated with anterior infarction. This type of block often progresses suddenly to a complete heart block.

Mobitz type II AV blocks are associated with a poor prognosis, as the mortality rate associated with their progression to a complete heart block is approximately 80%. Therefore, this type of second-degree AV block should be immediately treated with transcutaneous pacing or atropine. Atropine helps in about 50% of cases, but it occasionally worsens the block with an increased heart rate. A temporary transvenous pacemaker, and possibly a permanent demand pacemaker, must ultimately be placed.

Third-degree AV block

A third-degree AV block, or a complete heart block, occurs in 5-15% of patients who have an AMI and may occur in patients with anterior or inferior infarctions. In patients with inferior infarctions, this type of block usually develops gradually, progressing from first-degree or a type I second-degree block. In most patients, the level of the block is supranodal or intranodal, and the escape rhythm is usually stable with a narrow QRS and rates exceeding 40 bpm. In 30% of patients, the block is below the His bundle, where it results in an escape rhythm with a rate slower than 40 bpm and a wide QRS complex.

Complete heart block in patients who develop an inferior MI usually responds to atropine. In most patients, it resolves within a few days without the need for a temporary or permanent pacemaker. The mortality rate for patients with inferior MI who develop complete heart block is approximately 15% unless a coexisting RV infarction is present, in which case the mortality rate is higher than this.

Immediate treatment with atropine is indicated for patients with third-degree AV blocks. As with therapy for a Mobitz type II block, this treatment may not help and may sometimes worsens the block. Temporary transcutaneous or transvenous pacing is indicated for symptomatic patients whose condition is unresponsive to atropine. Permanent pacing should be considered in patients with persistent symptomatic bradycardia that remains unresolved with lysis or percutaneous coronary intervention.

In patients who develop an anterior MI, an intraventricular block or a Mobitz type II AV block usually precedes a third-degree AV block. The third-degree block occurs suddenly and is associated with a high mortality rate. Patients with these blocks typically have unstable escape rhythms with wide QRS complexes and at rates of less than 40 bpm.

Immediate treatment with atropine and/or transcutaneous pacing is indicated. This is followed by temporary transvenous pacing. Patients with an anterior MI who develop a third-degree AV block and who survive to hospitalization often receive a permanent pacemaker.
Intraventricular blocks

Conduction from the His bundle is transmitted through 3 fascicles: the anterior division of the left bundle, the posterior division of the left bundle, and the right bundle. An abnormality of electrical conduction in 1 or more of these fascicles is noted in about 15% of patients with AMI. Isolated left anterior fascicular block (LAFB) occurs in 3-5% of patients with AMI; progression to complete AV block is uncommon. Isolated left posterior fascicular block occurs in only 1-2% of patients who have an AMI. The blood supply of the posterior fascicle is larger than that of the anterior fascicle; therefore, a block here is associated with a relatively large infarct and high mortality rate.

The right bundle branch received its dominant blood supply from the left anterior descending (LAD) artery. Therefore, a new RBBB, which is seen in approximately 2% of patients with AMI, suggests a large infarct territory. However, progression to complete heart block is uncommon. In patients who develop an anterior MI and a new RBBB, the substantial risk for death is mostly caused by cardiogenic shock, which is presumably due to the large size of the myocardial infarct.

The combination of RBBB with a LAFB is known as bifascicular block and commonly occurs with occlusion of the proximal LAD coronary. The risk for developing complete AV block is heightened, but complete block is still uncommon. Mortality is mostly related to the amount of muscle loss. Bifascicular block in the presence of first-degree AV block called a trifascicular block. In 40% of patients, a trifascicular block progresses to a complete heart block.

Arrhythmic Complications: Ventricular Arrhythmias

Premature ventricular contractions

In the past, frequent PVCs were considered to represent warning arrhythmias and indicators of impending malignant ventricular arrhythmias. However, presumed warning arrhythmias are frequently observed in patients who have an AMI and who never develop ventricular fibrillation. On the converse, primary ventricular fibrillation often occurs without antecedent premature ventricular ectopy.

For these reasons, prophylactic suppression of PVCs with antiarrhythmic drugs, such as lidocaine, is no longer recommended. Prophylaxis has been associated with an increased risk for fatal bradycardia or asystole because of the suppression of escape pacemakers.

Given this evidence, most clinicians pursue a conservative course when PVCs are observed in a patient with an AMI, and they do not routinely administer prophylactic antiarrhythmics. Instead, attention should be directed toward correcting any electrolytic or metabolic abnormalities, plus identifying and treating recurrent ischemia.
Accelerated idioventricular rhythm

An accelerated idioventricular rhythm is seen in as many as 20% of patients who have an AMI. This pattern is defined as a ventricular rhythm characterized by a wide QRS complex with a regular escape rate faster than the atrial rate, but less than 100 bpm. AV dissociation is frequent. Slow, nonconducted P waves are seen; these are unrelated to the fast, wide QRS rhythm.

Most episodes are short, occur with equal frequency in anterior and inferior infarctions, and terminate spontaneously. The mechanism might involve (1) the sinoatrial node or the AV node, which may sustain structural damage and depress nodal automaticity, and/or (2) an abnormal ectopic focus in the ventricle that takes over as the dominant pacemaker.

The presence of accelerated idioventricular rhythm does not affect the patient's prognosis. No definitive evidence has shown that, an untreated occurrence increases the incidence of ventricular fibrillation or death. This rhythm occurs somewhat more frequently in patients who develop early reperfusion than in others; however, it is neither sensitive nor specific as a marker of reperfusion.

Temporary pacing is not indicated unless the rhythm is sustained and results in hypotension or ischemic symptoms. An accelerated idioventricular rhythm represents an appropriate escape rhythm. Suppression of this escape rhythm with an antiarrhythmic can result in clinically significant bradycardia or asystole. Therefore, an accelerated idioventricular rhythm should be left untreated.
Ventricular tachycardia

Nonsustained ventricular tachycardia

Nonsustained ventricular tachycardia is defined as 3 or more consecutive ventricular ectopic beats at a rate of greater than 100 bpm and lasting less than 30 seconds. In patients who experience multiple runs of nonsustained ventricular tachycardia, the risk for sudden hemodynamic collapse may be substantial.

Nonetheless, nonsustained ventricular tachycardia in the immediate peri-infarction period does not appear to be associated with an increased mortality risk, and no evidence suggests that antiarrhythmic treatment offers a morbidity or mortality benefit. However, nonsustained ventricular tachycardia occurring more than 48 hours after infarction in patients with LV systolic dysfunction (LV ejection fraction <0.40) poses an increased risk for sudden cardiac death; electrophysiologic testing and appropriate therapy are indicated in these patients.

Multiple episodes of nonsustained ventricular tachycardia require intensified monitoring and attention to electrolyte imbalances. Serum potassium levels should be maintained above 4.5 mEq/L, and serum magnesium levels should be kept above 2.0 mEq/L. Ongoing ischemia should aggressively be sought and corrected if found.

Sustained ventricular tachycardia

Sustained ventricular tachycardia is defined as 3 or more consecutive ventricular ectopic beats at a rate greater than 100 bpm and lasting longer than 30 seconds or causing hemodynamic compromise that requires intervention. Monomorphic ventricular tachycardia is most likely to be caused by a myocardial scar, whereas polymorphic ventricular tachycardia may be most responsive to measures directed against ischemia. Sustained polymorphic ventricular tachycardia after an AMI is associated with a hospital mortality rate of 20%.

Emergency treatment of sustained ventricular tachycardia is mandatory because of its hemodynamic effects and because it frequently deteriorates into ventricular fibrillation. Rapid polymorphic ventricular tachycardia (rate >150 bpm) associated with hemodynamic instability should be treated with immediate direct-current unsynchronized cardioversion of 200 J (or biphasic energy equivalent). Monomorphic ventricular tachycardia should be treated with a synchronized discharge of 100 J (or biphasic energy equivalent).

If sustained ventricular tachycardia is well tolerated, antiarrhythmic therapy with amiodarone (drug of choice) or procainamide may be attempted before electrical cardioversion. Precipitating causes, such as electrolyte abnormalities, acid-base disturbances, hypoxia, or medication, should be sought and corrected. For persistent or recurrent ventricular tachycardia, overdrive pacing may be effective in electrically converting the patient's rhythm to a sinus rhythm.
Ventricular fibrillation

The incidence of primary ventricular fibrillation (4.5%) is greatest in the first hour after the onset of infarct; thereafter, the incidence rapidly declines. Approximately 60% of episodes occur within 4 hours, and 80% occur within 12 hours.

Secondary or late ventricular fibrillation occurring more than 48 hours after an MI is usually associated with pump failure and cardiogenic shock. Factors associated with an increased risk of secondary ventricular fibrillation are a large infarct, an intraventricular conduction delay, and an anteroseptal AMI. Secondary ventricular fibrillation in conjunction with cardiogenic shock is associated with an in-hospital mortality rate of 40-60%.

Treatment for ventricular fibrillation is unsynchronized electrical countershock with at least 200-300 J (or biphasic energy equivalent) administered as rapidly as possible. Each minute after the onset of uncorrected ventricular fibrillation is associated a 10% decrease in the likelihood of survival. Restoration of synchronous cardiac electrical activity without the return of effective contraction (ie, electromechanical dissociation, or pulseless electrical activity) is generally due to extensive myocardial ischemia and/or necrosis or cardiac rupture.

Antiarrhythmics, such as intravenous amiodarone and lidocaine, facilitate successful electrical defibrillation and help prevent recurrent or refractory episodes. After ventricular fibrillation is successfully converted, antiarrhythmic therapy is generally continued as a constant intravenous infusion for 12-24 hours.

Prophylactic lidocaine reduces the incidence of ventricular fibrillation, but it is not used because it seems to be associated with an excessive mortality risk owing to bradycardic and asystolic events3 . On the other hand, early use of beta-blockers in patients with AMI reduces the incidence of ventricular fibrillation as well as death4 .

Arrhythmic Complications: Reperfusion Arrhythmias

In the past, the sudden onset of rhythm disturbances after thrombolytic therapy in patients with AMI was believed to be a marker of successful coronary reperfusion. However, a high incidence of identical rhythm disturbances is observed in patients with AMI in whom coronary reperfusion is unsuccessful. Therefore, these so-called reperfusion arrhythmias are neither sensitive nor specific for reperfusion and should be treated as discussed under Accelerated Idioventricular Rhythm in the Arrhythmic Complications: Ventricular Arrhythmias section above.
Mechanical Complications of MI

The 3 major mechanical complications of AMI are those listed below. Each of these complications can result in cardiogenic shock. Clinical issues related to these mechanical problems are discussed below. (See also Myocardial Rupture.)
Ventricular free wall rupture (VFWR)
Ventricular septal rupture (VSR)
Papillary muscle rupture with severe mitral regurgitation (MR)

Mechanical Complications: VFWR

Introduction

VFWR is the most serious complication after AMI. VFWR is usually associated with large transmural infarctions and antecedent infarct expansion. It is the most common cause of death, second only to LV failure, and it accounts for 15-30% of the deaths associated with AMI. Incontrovertibly the most catastrophic of mechanical complications, VFWR leads to acute hemopericardium and death from cardiac tamponade.

Incidence

The overall incidence of VFWR ranges from 0.8-6.2%. The incidence of this complication has declined over the years with better 24 hour systolic blood pressure control; increased use of reperfusion therapy, beta blockers, ACE inhibitors; and decreased use of heparin5 .

Data from the National Registry of Myocardial Infarction (NRMI) showed an elevated incidence of in-hospital mortality among patients who received thrombolytic therapy (12.1%) than among patients who did not (6.1%).6

In the Thrombolysis in Myocardial Infarction Phase II (TIMI II) trial, 16% of patients died from cardiac rupture within 18 hours of therapy.7 Patients who underwent percutaneous transluminal coronary angioplasty (PTCA) had an incidence of free wall rupture lower than that of patients receiving thrombolytic therapy.

Risk factors

Risk factors of VFWR include advanced age (>70 y), female sex, no previous MIs, Q waves on ECG, hypertension during the initial phase of STEMI, corticosteroid or NSAID use and fibrinolytic therapy more than 14 hours after STEMI onset. Patients with a history of angina pectoris, previous AMI, multivessel coronary disease, and CHF are less likely than others to develop VFWR of the LV because they develop collaterals and ischemic preconditioning6,8,9 .

Pathophysiology

VFWRs are dramatic, they present acutely or occasionally subacutely as pseudoaneurysms, and they most often involve the anterior or lateral wall of the LV. Most of the VFWRs typically occur within the first week after AMI.

Becker et al classified the following 3 types of VFWRs10 :
Type I is an abrupt slitlike tear that is frequently associated with anterior infarcts and that occurs early (within 24 h).
Type II is an erosion of infarcted myocardium at the border between the infarcted and viable myocardium.
Type III is an early aneurysm formation correlated with older and severely expanded infarcts.

Type III usually occurs later than do type I or type II ruptures. Thrombolytic therapy accelerates the occurrence of cardiac rupture in Becker type I and type II VFWRs. In severely expanded infarctions (type III), thrombolytic therapy decreases the incidence of cardiac rupture.

A pseudoaneurysm is formed when adjacent pericardium and hematoma seals of a myocardial rupture or perforation. The wall of a pseudoaneurysm is most often visualized as an aneurysmal outpouching that communicates with the LV cavity by means of a narrow neck. This wall is composed of pericardium and organized thrombus and/or hematoma. It is devoid of myocardial elements, whereas a true aneurysm has all the elements of the original myocardial wall and a relatively wide base. The pseudoaneurysm may vary in size and is at high risk of rupturing.

Clinical presentation

Clinical presentations of VFWR vary depending on the acuity, location, and size of the rupture. Patients with acute VFWR present with severe chest pain, abrupt electromechanical dissociation or asystole, hemodynamic collapse, and possibly death. In about one third of the patients, the course is subacute, and they present with symptoms such as syncope, hypotension, shock, arrhythmia, and prolonged and recurrent chest pain.

Diagnosis

Early diagnosis of VFWRs and intervention are critical to patient survival. A high index of suspicion is required when patients with AMI present with severe chest pain, shock or arrhythmias, and abrupt development of electromechanical dissociation. ECG signs of impending VFWR have limited specificity but include sinus tachycardia, intraventricular conduction defect, and persistent or recurrent ST-segment elevation.

Echocardiography is the diagnostic tool of choice. The key diagnostic finding is a moderate-to-large pericardial effusion with clinical and echocardiographic signs of impending pericardial tamponade. The absence of pericardial effusion on echocardiography has high negative predictive value. If the ability to obtain transthoracic echocardiograms is limited in patients receiving mechanical ventilation, transesophageal echocardiography can assist in confirming VFWR.

MRI provides superior image quality and permits identification of the site and anatomy of a ventricular pseudoaneurysm (ie, ruptured LV restrained by the pericardium with enclosed clot). However, MRI is of limited use in the acute setting because of the time involved and nonportability of imaging units.

Prevention

The most important prevention strategy is early reperfusion therapy, with PCI being the preferred modality. Fibrinolytic therapy is associated with overall decreased risk of VFWR, however, its use more than 14 hours after STEMI onset can cause increased risk of early rupture11,12 .

Management

The standard treatment for VFWR is emergency surgical repair after hemodynamic stability is achieved. Patients may first need intravenous fluids, inotropic agents, and emergency pericardiocentesis.

Pifarré and associates recommended the deployment of an intra-aortic balloon pump to decrease systolic afterload and improve diastolic myocardial perfusion.13

Several surgical techniques have been applied, including infarctectomy, adhering with biologic glue patches made of polyethylene terephthalate polyester fiber (Dacron; DuPont, Wilmington, DE) or polytetrafluoroethylene fluoropolymer resin (Teflon; DuPont), and use of pledgeted sutures without infarctectomy.

The mortality rate is significantly high and largely depends on the patient's preoperative hemodynamic status. Early diagnosis, rapid institution of the measures described above to achieve hemodynamic stability, and prompt surgical repair can improve survival rates.
Mechanical Complications: VSR

Introduction

VSR is an infrequent but life-threatening complication of AMI. Despite optimal medical and surgical treatment, patients with VSR have a high in-hospital mortality rate. During the prethrombolytic era, VSRs occurred in 1-3% of individuals with MIs. The incidence declined with thrombolytic therapy (0.2-0.34%) because of improvements in reperfusion and myocardial salvage. The bimodal distribution of VSR is characterized by a high incidence in the first 24 hours, with another peak on days 3-5 and rarely more than 2 weeks after AMI.

In patients receiving thrombolytics, the median time from the onset of symptoms of AMI to septal rupture was 1 day in the Global Utilization of Streptokinase and TPA [tissue plasminogen activator] for Occluded Coronary Arteries (GUSTO-I) trial14 and 16 hours in the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock? (SHOCK) trial.15

Risk factors

Risk factors for septal rupture include advanced age (>65 y), female sex, single-vessel disease, extensive MI, and poor septal collateral circulation16,17 . Before the advent of thrombolytics, hypertension and absence of a history of angina were risk factors for VSR. Extensive infarct size and RV involvement are other known risk factors for septal rupture.

Pathophysiology

In patients with AMI without reperfusion, coagulation necrosis develops within 3-5 days after infarction. Neutrophils migrate to the necrotic zone and undergo apoptosis, release lytic enzymes, and hasten the disintegration of necrotic myocardium. Some patients have infarcts with large intramural hematomas, which dissect into the tissue and result in early septal rupture. The size of the septal rupture ranges from a few millimeters to several centimeters.

VSR is categorized as simple or complex depending on its length, course, and location. In simple septal rupture, the perforation is at the same level on both sides of the septum, and a direct through-and-through communication is present across the septum. A complex septal rupture is characterized by extensive hemorrhage with irregular, serpiginous tracts in the necrotic tissue.

Septal ruptures are most common in patients with large anterior MIs due to occlusion of left anterior descending artery causing extensive septal infarcts. These infarcts are associated with ST segment elevations and Q waves in inferior leads (II, III, aVF) and these ECG changes therefore more commonly seen in septal ruptures18 . These ruptures are generally apical and simple.

Septal ruptures in patients with inferior MI occur relatively infrequently. These ruptures involve the basal inferoposterior septum and are often complex.

Clinical presentation

Symptoms of VSR complicating AMI include chest pain, shortness of breath, hypotension, biventricular failure, and shock within hours to days. Patients often present with a new, loud, and harsh holosystolic murmur. This murmur is loudest along the lower left sternal border and is associated with a palpable parasternal systolic thrill. RV and LV S3 gallops are common.

In patients with cardiogenic shock complicating septal rupture, the murmur and thrill may be difficult to identify. In contrast, patients with acute MR often have a soft systolic murmur at the apex without a thrill.

Diagnosis

Echocardiography with color flow Doppler imaging is the diagnostic tool of choice for identifying a VSR. Its sensitivity and specificity have been reported to be as high as 100%. It can also be used to define the site and size of septal rupture, assess the LV and RV function, estimate the RV systolic pressure, and quantify the left-to-right shunt. Cardiac catheterization is usually required to confirm the diagnosis, quantitate the degree of left-to-right shunt, differentiate VSR from other conditions, such as acute MR, plus visualize the coronary arteries.

In patients with VSR, right-heart catheterization shows a step-up in oxygen saturation from the right atrium to the RV, in contrast no step-up in oxygen saturation among patients with MR. The presence of large V waves in the pulmonary-capillary wedge tracing supports the diagnosis of severe acute MR.

Left ventriculography can also be used to identify the site of ventricular rupture (see Cardiac Catheterization [Left Heart]). However, this study is usually unnecessary after a good-quality echocardiographic and Doppler examination is conducted.

Management

The key to management of VSR is prompt diagnosis and an aggressive approach to hemodynamic stabilization, angiography, and surgery. The optimal approach includes hemodynamic stabilization with the administration of oxygen and mechanical support with use of an intra-aortic balloon pump, as well as the administration of vasodilators (to reduce afterload and thus LV pressure and the left-to-right shunt), diuretics, and inotropic agents.

Cardiac catheterization is needed to define the coronary anatomy; this is followed by urgent surgical repair.

Medical therapy is intended only for temporary stabilization before surgery, as most patients' conditions deteriorate rapidly and they die in the absence of surgical intervention.

In the GUSTO-I trial, the 30-day mortality rate was lower in patients with VSR who underwent surgical repair than in patients treated medically (47% vs 94%), as was the 1-year mortality rate (53% vs 97%).14

Lemery et al reported a 30-day survival rate of 24% in patients treated medically compared with 47% in those treated surgically.19

Current guidelines of the American College of Cardiology/American Heart Association for the treatment of patients with septal rupture complicating AMI highlight urgent surgical intervention, regardless of their clinical status. Surgical management of septal rupture includes the following elements:
Prompt establishment of hypothermic cardiopulmonary bypass
An approach to the septal rupture through the infarct area and the excision of all necrotic, friable margins of the septum and ventricular walls to avoid postoperative hemorrhage, residual septal defect, or both
Reconstruction of the septum and ventricular walls by using prosthetic material and preservation of the geometric configuration of the ventricles and heart function

Percutaneous closure of septal rupture is a relatively new approach, one used in select patients as an alternative to surgical repair or for the acute stabilization of critically ill patients. However, percutaneous closure is currently unavailable in many institutions, and with no long-term outcome data are available.

Several studies failed to show a relationship between perioperative mortality and concomitant coronary revascularization (coronary artery bypass grafting). Patients with cardiogenic shock due to septal rupture have the poorest outcome.

In the SHOCK trial, patients with cardiogenic shock due to septal rupture had higher rate of in-hospital mortality (87.3%) than rate of all other causes of cardiogenic shock (59.2% with pure LV failure and 55.1% with acute MR).15

In patients who survive surgical repair, the rate of recurrent or residual septal defect is reported to be about 28%, and the associated mortality rate is high.

Repeat surgical intervention is indicated in patients who have clinical heart failure or a pulmonary-systemic fraction greater than 2.

Mechanical Complications: Acute MR

Introduction

MR is a common complication of AMI that results from local and global LV remodeling and that is an independent predictor of heart failure and death. MR typically occurs 7-10 days after an AMI, though this onset may vary according to the mechanism of MR. Papillary muscle rupture resulting in MR occurs within 1-14 days (median, 1 d).

Mild-to-moderate MR is often clinically silent and detected on Doppler echocardiography performed during the early phase of AMI. In this case, MR rarely causes hemodynamic compromise.

Severe acute MR that results from the rupture of papillary muscles or chordae tendineae results in abrupt hemodynamic deterioration with cardiogenic shock. Rapid diagnosis, hemodynamic stabilization, and prompt surgical intervention are needed because acute severe MR is associated with a high mortality rate.

Incidence

The incidence of MR may vary because of several factors, including the diagnostic methods used, the presence or absence of CHF, the degree of MR reported, the type of therapy rendered, and the time from infarct onset to testing.

During the GUSTO-I trial, incidence of MR in patients receiving thrombolytic therapy was 1.73%.14 The SHOCK trial which included MI patients presenting with cardiogenic shock noted a 39.1% incidence of moderate to severe MR20 . Kinn et al reported that reperfusion with angioplasty resulted in an 82% decrease in the rate of acute MR, as compared with thrombolytic therapy (0.31% vs 1.73%).21

Risk factors

Risk factors for MR are advanced age, female sex, large infarct, previous AMI, recurrent ischemia, multivessel coronary artery disease, and CHF.

Pathophysiology

Several mechanisms can cause MR after AMI. Rupture of the papillary muscle is the most commonly reported mechanism.

Such rupture occurs in 1% of patients with AMI and frequently involves the posteromedial papillary muscle rather than the anterolateral papillary muscle, as the former has a single blood supply versus the dual supply for the latter. Papillary muscle rupture may lead to flailing or prolapse of the leaflets, resulting in severe MR. Papillary muscle dysfunction due to scarring or recurrent ischemia may also lead to MR in the subacute and chronic phases after MI; this condition can resolve spontaneously.

Large posterior infarctions produce acute MR due to asymmetric annular dilation and altered function and geometry of the papillary muscle.

Clinical presentation

Patients with functional mild or moderate MR are often asymptomatic. The severity of symptoms varies depending on ventricular function. Clinical features of acute severe MR include shortness of breath, fatigue, a new apical holosystolic murmur, flash pulmonary edema, and shock.

The new systolic murmur may be only early-to-mid systolic, not holosystolic. It may be soft or even absent because of the abrupt rise in left atrial pressure, which lessens the pressure gradient between the left atrium and the LV, as compared with chronic MR. The murmur is best heard at the apex rather than the lower left sternal border, and it is uncommonly associated with a thrill. S3 and S4 gallops are expected.

Diagnosis

The clinician cannot rely on a new holosystolic murmur to diagnose MR or assess its severity because of the variable hemodynamic status. In a patient with AMI who presents with a new apical systolic murmur, acute pulmonary edema, and cardiogenic shock, a high index of clinical suspicion for severe MR is the key to diagnosis.

Chest radiography may show evidence of pulmonary edema in the acute setting without clinically significant cardiac enlargement.

Echocardiography with color flow Doppler imaging is the standard diagnostic tool for detecting MR. Transthoracic echocardiography is the preferred initial screening tool, but transesophageal echocardiography is invaluable in defining the severity and exact mechanism of acute MR, especially when suspicion for papillary muscle rupture is high.

Cardiac catheterization should be performed in all patients to determine the extent and severity of coronary artery disease.

Management

Determination of hemodynamic stability, elucidation of the exact mechanism of acute MR, and expedient therapy are all necessary for a favorable outcome. Medical management includes afterload reduction with the use of diuretics, sodium nitroprusside, and nitrates in patients who are not hypotensive. In patients have hemodynamic compromise, intra-aortic balloon counterpulsation should be deployed rapidly. This intervention usually substantially reduces afterload and regurgitant volume, improving cardiac output in preparation for surgical repair. Without surgical repair, medical therapy alone in patients with papillary muscle rupture results in inadequate hemodynamic improvement and a poor short-term prognosis.

Emergency surgical intervention is the treatment of choice for papillary muscle rupture. Surgical approaches may include mitral valve repair or replacement. In the absence of papillary muscle necrosis, mitral valve repair improves the survival rate more than mitral valve replacement does. This difference is because the subvalvular apparatus is usually preserved. Mitral valve repair also eliminates complications related to malfunction of the prosthesis.

In patients with extensive necrosis of papillary muscle and/or ventricular free wall, mitral valve replacement is the preferred modality. CABG performed at the time of surgery was shown in one study to improve the short and long term survival22 .

The only situation in which emergency surgery can safely be avoided is in the case of intermittent MR due to recurrent ischemia. In this case, successful myocardial revascularization may be effective. This procedure is accomplished by means of either angioplasty or coronary artery bypass grafting.

Left Ventricular Aneurysm

Introduction

Left ventricular aneurysm (LVA) is defined as a localized area of myocardium with abnormal outward bulging and deformation during both systole and diastole. The rate of LVAs after AMI is approximately 3-15%. Risk factors for LVA after AMI include female sex, total occlusion of the LAD artery, single-vessel disease, and absence of previous angina.

Pathophysiology

More than 80% of LVAs affect the anterolateral wall and are usually associated with total occlusion of the LAD. The posterior and inferior walls are less commonly affected than this. LVAs generally range from 1-8 cm. In terms of histologic composition, LVAs are composed of fibrous scar that is notably thinned. This scar is clearly delineated from the adjacent ventricular muscle on microscopic examination.

Clinical presentation

A history of MI and third or fourth heart sounds are common findings from the patient's history and physical examination.

Diagnosis

The chest radiograph may reveal an enlarged cardiac silhouette.

Electrocardiography is characterized by ST elevation that persists several weeks after AMI and that appears in the same leads as those showing the acute infarct. Echocardiography is 93% sensitive and 94% specific for detection of LVA, but cardiac catheterization remains the standard for establishing the diagnosis.

Management

Patients with small or clinically insignificant aneurysms can be treated conservatively with close follow-up. Medical therapy generally consists of the use of angiotensin-converting enzyme inhibitors, which reduce afterload, infarct extension, and LV remodeling. Anticoagulation is required when patients have severe LV dysfunction and/or thrombus in the LV or aneurysm.

Surgical resection of the LVA is indicated if severe CHF, ventricular tachyarrhythmias are refractory to medical treatment or if recurrent thromboembolism is present.
Miscellaneous Complications

Left ventricular mural thrombus

LVMT is a well-known complication of AMI and frequently develops after anterior infarcts of the LV wall. The incidence of LVMT as a complication of AMI ranges from 20-40% and may reach 60% in patients with large anterior-wall AMIs who are not treated with anticoagulant therapy. LVMT is associated with a high risk of systemic embolization. Anticoagulant therapy may substantially decrease the rate of embolic events by 33% compared with no anticoagulation.

Factors contributing to LVMT formation include LV regional-wall akinesia or dyskinesia with blood stasis, injury to and inflammation of the endocardial tissue that provides a thrombogenic surface, and a hypercoagulable state. The most common clinical presentation of patients with LVMT complicating an MI is stroke. Most episodes occur within the first 10 days after AMI. Physical findings depend on the site of embolism.

Transthoracic echocardiography remains the imaging modality of choice and is 92% sensitive and 88% specific for detecting LVMT. Management of LVMT includes heparin treatment followed by oral warfarin therapy for 3-6 months. In patients with LVAs, lifelong anticoagulation may be appropriate if a mural clot persists.

Pericarditis

The incidence of early pericarditis after MI is approximately 10%, and this complication usually develops within 24-96. Pericarditis is caused by inflammation of pericardial tissue overlying infarcted myocardium. The clinical presentation may include severe chest pain, usually pleuritic, and pericardial friction rub.

The key ECG change is diffuse ST-segment elevation in all or nearly all of leads. Echocardiography may reveal a small pericardial effusion. The mainstay of therapy usually includes aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs). Colchicine may be beneficial in patients with recurrent pericarditis.

Post-MI syndrome (Dressler syndrome)

Before the era of reperfusion, the incidence of post-MI syndrome ranged from 1-5% after AMI, but this rate has dramatically declined with the advent of thrombolysis and coronary angioplasty.

Although the exact mechanism has yet to be elucidated, post-MI syndrome is considered to be an autoimmune process. Clinical features include fever, chest pain, and other signs and symptoms of pericarditis occurring 2-3 weeks after AMI. Management involves hospitalization and observation for any evidence of cardiac tamponade. Treatment comprises rest, use of NSAIDs, and/or steroids in patients with recurrent post-MI syndrome with disabling symptoms.

Abbreviations
AMI = Acute myocardial infarction
AV = Atrioventricular
CHF = Congestive heart failure
GUSTO-I = Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries trial
LAD = Left anterior descending (artery)
LAFB = Left anterior fascicular block
LBBB = Left bundle branch block
LV = Left ventricle, left ventricular
LVA = Left ventricular aneurysm
LVMT = Left ventricular mural thrombus
MI = Myocardial infarction
MR = Mitral regurgitation
NRMI = National Registry of Myocardial Infarction
NSAID = Nonsteroidal anti-inflammatory drug
NSTEMI = Non–ST-elevation myocardial infarction
PVC = Premature ventricular contraction
RBBB = Right bundle branch block
RV = Right ventricle, right ventricular
SHOCK = Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock? trial
STEMI = ST-elevation myocardial infarction
TIMI II = Thrombolysis in Myocardial Infarction Phase II
VFWR = Ventricular free wall rupture
VSR = Ventricular septal rupture

http://emedicine.medscape.com/article/164924-overview

Unstable Angina

Introduction
Background

The traditional term of unstable angina was first used 3 decades ago and was meant to signify the intermediate state between myocardial infarction (MI) and the more chronic state of stable angina. The old term, preinfarction angina, conveys the clinical intent of intervening to attenuate the risk of myocardial infarction or death. Patients with this condition have also been categorized according to their presentation, diagnostic test results, or course over time; these categories include new-onset angina, accelerating angina, rest angina, early postinfarct angina, and early postrevascularization angina.

For the pragmatic purposes of this article, the term unstable angina includes non–Q-wave myocardial infarction (NQMI) because this cannot be confirmed or excluded during the initial contact with the patient. Acute coronary syndromes cover an even wider spectrum, and by some definitions include Q-wave or transmural myocardial infarction.

Pathophysiology

Chest pain is a nonspecific symptom that can have cardiac or noncardiac causes (see Differentials). The term angina is typically reserved for pain syndromes arising from presumed myocardial ischemia.

Unstable angina belongs to the continuum of the acute coronary syndromes because of the shared pathophysiology, evaluation, and treatments with NQMI and Q-wave myocardial infarction. Although the etiology and definition of unstable angina can be broad, an interplay between disrupted atherosclerotic plaque and overlaid thrombi is present in many cases of unstable angina, with consequent hemodynamic deficit or microembolization. This is distinct from stable angina, in which the typical underlying cause is a fixed coronary stenosis with compromised blood flow and slow, progressive plaque growth that allows for the occasional development of collateral flow.

Other causes of angina, such as hypertrophic obstructive cardiomyopathy (HOCM) or microvascular disease (syndrome X), cause ischemia by means of different mechanisms and are considered separate entities.

Factors involved in the pathophysiology of unstable angina include supply-demand mismatch, plaque disruption or rupture, thrombosis, vasoconstriction, and cyclical flow.
Supply-demand mismatch

The myocardial ischemia of unstable angina, like all tissue ischemia, results from excessive demand or inadequate supply of oxygen, glucose, and free fatty acids.

Secondary disorders cause ischemia by increasing myocardial oxygen demand (eg, thyrotoxicosis, cocaine, severe illness, physiologic stress) or by decreasing oxygen supply (eg, hypoxemia, anemia, hypotension). Such causes must be investigated because most of these conditions are reversible. For instance, anemia from chronic gastrointestinal bleeding is not uncommon in elderly patients. This can coexist with coronary artery disease (CAD). However, patients may not benefit or may be harmed by treatments such as anticoagulants and antiplatelet drugs. Avoidance or treatment of the underlying condition is paramount.

Excess demand from increased myocardial workload (heart rate–systolic pressure product) or wall stress is responsible for nearly all cases of stable angina and perhaps one third of all episodes of unstable angina.

Plaque disruption

Accumulation of lipid-laden macrophages and smooth muscle cells, so-called foam cells, occurs within atherosclerotic plaques. The oxidized low-density lipoprotein cholesterol (LDL-C) in foam cells is cytotoxic, procoagulant, and chemotactic. As the atherosclerotic plaque grows, production of macrophage proteases and neutrophil elastases within the plaque can cause thinning of the fibromuscular cap that covers the lipid core. Increasing plaque instability coupled with blood-flow shear and circumferential wall stress lead to plaque fissuring or rupture, especially at the junction of the cap and the vessel wall.

The pathogenesis of acute coronary syndrome is shown in the image below.


Pathogenesis of acute coronary syndromes.


The degree and consequence of plaque disruption covers a wide spectrum. Minor fissuring is typically nonocclusive and hence clinically silent, and repeat occult episodes of plaque ulceration and healing with a gradual growth of plaque volume have been histologically documented. Moderate-to-large plaque disruptions commonly result in unstable angina or acute infarction.

Thrombosis

Exposure of subendothelial components provokes platelet adhesion and activation. Platelets then aggregate in response to exposed vessel wall collagen or local aggregates (eg, thromboxane, adenosine diphosphate). Platelets also release substances that promote vasoconstriction and production of thrombin. In a reciprocating fashion, thrombin is a potent agonist for further platelet activation, and it stabilizes thrombi by converting fibrinogen to fibrin.

The nonocclusive thrombus of unstable angina can become transiently or persistently occlusive. Depending on the duration of occlusion, the presence of collateral vessels, and the area of myocardium perfused, recurrent unstable angina, NQMI, or Q-wave infarction can result.

Vasoconstriction, vasospasm, and cyclic flow variation

Most patients with acute coronary syndrome have recurrent transient reduction in coronary blood supply because of vasoconstriction and thrombus formation at the site of atherosclerotic plaque rupture. These events occur because of episodic platelet aggregation and complex interactions among the vascular wall, leukocytes, platelets, and atherogenic lipoproteins.


Vasospasm, provoked by either ergonovine or acetylcholine, is a common finding in patients with acute coronary syndrome, particularly in Taiwanese and Japanese patients. Although correlated with chest pain, whether this coronary hyperreactivity causes acute coronary syndrome or is simply an associated finding is not known.1

Frequency
United States

The incidence of unstable angina is increasing, and nearly 1 million hospitalized patients each year have a primary diagnosis of unstable angina.

A similar number of unstable angina episodes likely occur outside the hospital and are unrecognized or managed in the outpatient setting. With heightened public awareness, improved survival after myocardial infarction, and aging of the population, this number should continue to rise despite primary and secondary prevention measures.
Reasonably representative statistical estimates for unstable angina can be obtained from 2 registries, the Global Unstable Angina Registry and Treatment Evaluation (GUARANTEE) registry2,3 or the Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the ACC/AHA (CRUSADE) registry.4 GUARANTEE involved 3000 consecutive hospital admissions for unstable angina in 35 hospitals in 6 geographic regions (Northeast, Mideast, Midwest, Southeast, Southwest, Northwest) from September 1995 to August 1996. CRUSADE registered more than 180,000 patients with non–ST-segment elevation myocardial infarction (NSTEMI) in the US from 2001-2006, targeting high-risk patients with unstable angina or NSTEMI using the following inclusion criteria: (1) chest pain or anginal equivalent at rest, more than 10 minutes in duration; (2) ischemic ECG changes (ST-segment depression >0.5 mm, transient ST-segment elevation 0.5–1.0 mm lasting for<10min);and/or (3) elevated markers of myocardial necrosis (CK-MB and/or troponin I or T > the upper limit of normal for the local laboratory assay used at each institution).

The demographics and characteristics of patients in the GUARANTEE registry compared with the CRUSADE registry are shown in Table 1.

Table 1. Patient Characteristics, GUARANTEE Versus CRUSADE

Open table in new window GUARANTEE, 1995-96 CRUSADE, 2001-06
Mean age 62 y 69 y
Patients older than 65 y 44%
Female 39% 40%
Hypertension 60% 73%
Diabetes mellitus 26% 33%
Current smoker 25%
Hypercholesterolemia 43% 50%
Previous stroke 9%
Previous myocardial infarction 36% 30%
Previous angina 66%
Congestive heart failure 14% 18%
Previous coronary intervention 23% 21%
Previous coronary bypass surgery 25% 19%




International

The best demographic data available are from the Organization to Assess Strategies for Ischemic Syndromes (OASIS-2) registry. It included 7987 patients with acute myocardial ischemia without ST elevation from 95 hospitals across 6 countries. Table 2 lists the patients' characteristics.

Table 2. Demographic Characteristics of Patients in the International OASIS-2 Registry

Open table in new windowCharacteristics Australia Brazil Canada Hungary Poland United States
General Number of patients 1899 1478 1626 931 1135 918
Mean age (y) 65 62 66 65 63 66
Women (%) 37 42 37 45 40 37
Clinical NQMI presentation (%) 7 7 14 22 17 16
Abnormal ECG (%) 74 91 82 95 97 87
Select treatments Beta-blocker (%) 67 53 73 67 59 57
Calcium blocker (%) 59 51 53 52 43 59
Invasive procedures (index hospitalization) Cardiac catheterization (%) 24 69 43 20 7 58
Percutaneous coronary intervention (PCI) (%) 7 19 16 5 0.4 24
Coronary artery bypass graft (CABG) (%) 4 20 10 7 0.4 17


Because unstable angina is intimately linked to the incidence of coronary events, an approximation of international trends might be found in the Monitoring Trends and Determinants in Cardiovascular Diseases (MONICA) Registry sponsored by the World Health Organization (WHO). This large project monitored more than 7 million people aged 35-64 years from 30 populations in 21 countries from the mid 1980s. The highest average rates of heart disease were found in Glasgow and Belfast, United Kingdom; North Karelia and Kuopio, Finland; Newcastle, Australia; and Warsaw, Poland. The lowest average myocardial infarction rates, and presumably unstable angina rates, were observed in Beijing, China; Toulouse, France; Catalonia, Spain; Vaud-Fribourg, Switzerland; and Brianza, Italy.5

The GRACE registry is prospectively tracking contemporary ACS treatment and outcome across 30 countries, now accumulating more than 100,000 patients.6
Mortality/Morbidity

The risk of death, myocardial infarction, and complications is variable because of the broad clinical spectrum that is covered by the term unstable angina. The average risk for these patients is discussed here. More specific risk stratification is detailed in Treatment. The aggressiveness of the therapeutic approach should be commensurate to the individualized estimated risk.

Older studies show that the incidence of death in the early weeks after hospitalization is approximately 4%, and the incidence of myocardial infarction is approximately 10%.

Thirty-day event rates are the current standard for cross-comparing studies. The aggregate data for the more than 40,000 patients with acute coronary syndromes in studies using contemporary treatments (albeit in varying degrees) indicate improving outcomes (see Table 3). The 30-day death and myocardial infarction rates are currently around 3.5% and 8.5%, respectively, in spite of increased disease complexity and an aging cohort.

Table 3. Thirty-Day Clinical Outcome in Patients With Acute Coronary Syndromes in Clinical Trials

Open table in new windowStudy Year Number of Patients Death (%) MI (%) Major Bleed (%)
TIMI-3* 1994 1,473 2.5 9.0 0.3
GUSTO-IIb† 1997 8,011 3.8 6.0 1.0
ESSENCE‡ 1998 3,171 3.3 4.5 1.1
PARAGON-A§ 1998 2,282 3.2 10.3 4.0
PRISM|| 1998 3,232 3.0 4.2 0.4
PRISM-PLUS¶ 1998 1,915 4.4 8.1 1.1
PURSUIT# 1998 10,948 3.6 12.9 2.1
TIMI-11B** 1999 3,910 3.9 6.0 1.3
PARAGON-B†† 2000 5,225 3.1 9.3 1.1
Pooled 40,167 3.5 8.5 1.5


* TIMI-3: Thrombolysis in Myocardial Infarction Clinical Trial 3 † GUSTO-IIb: Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries
‡ ESSENCE: Efficacy and Safety of Subcutaneous Enoxaparin in Non–Q-wave Coronary Events
§ PARAGON-A: Platelet IIb/IIIa Antagonism (lamifiban) for the Reduction of Acute Coronary Syndrome Events in a Global Organization Network
|| PRISM: Platelet Receptor Inhibition in Ischemic Syndrome Management
¶ PRISM-PLUS: Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Angina Signs and Symptoms
# PURSUIT: Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy
** TIMI-11B: Thrombolysis in Myocardial Infarction Clinical Trial 11B
†† PARAGON-B: Platelet IIb/IIIa Antagonism (lamifiban) for the Reduction of Acute Coronary Syndrome Events in a Global Organization Network

The Recursos Empleados en el Sindrome Coronario Agudo y Tiempos de Espera (RESCATE) investigators from Spain report a 1.8% mortality rate and a 5.1% myocardial infarction rate at 28 days (n = 791, consecutive series between 1992 and 1994, early revascularization rate about 6%).7 By comparison with the therapeutically aggressive and predominantly North American studies listed in Table 2, these adverse event rates seem lower, probably because of the healthier case-mix (patients with unstable angina without previous myocardial infarction), which illustrates the difficulties of direct outcome comparisons between institutions and countries and across different trials.

The outcome in patients with abnormal electrocardiographic findings, and in particular ST-segment depression, approximates that of patients with acute myocardial infarction. Other predictors of worse long-term outcome in unstable angina include advanced age, underlying left ventricular systolic dysfunction, and more widespread extent of coronary artery disease.

Race

Disparities in outcomes and the prevalence of risk factors among different ethnic groups have been widely reported. For instance, as a group, blacks exhibit a higher prevalence of atherosclerotic risk factors (eg, hypertension, diabetes mellitus, smoking), greater left ventricular mass, and decreased peripheral vasodilatory response. Relative to whites, myocardial infarction more frequently results in death in blacks at young ages.

Fewer myocardial events but more cerebral complications have been observed in black patients with unstable angina in randomized clinical trials of heparin versus hirudin (GUSTO II) or eptifibatide versus placebo (PURSUIT). This may be due to the enhanced fibrinolytic activity and higher prevalence of hypertension in this population.
Differences also exist in the delivery and response to medical care. Whites have a higher rate of catheterization, angioplasty, and bypass surgery than other racial groups. An analysis of Medicare beneficiaries also showed underuse of catheterization, particularly for managed-care enrollees as opposed to fee-for-service beneficiaries. The coronary angiography rates even for those with American College of Cardiology/American Heart Association (ACC/AHA) class I indications (angiography deemed useful or effective) in this post-myocardial infarction study were 46% versus 37%, respectively (P < .001).
Studies have shown equivalent short-term (30-day) mortality rates from unstable angina (including NQMI) for blacks, but over the long term, persistent worse outcomes have been demonstrated.

Sex

Women with unstable angina are older and have a higher prevalence of hypertension, diabetes mellitus, congestive heart failure, and family history of coronary artery disease than men. Men tend to have a higher previous incidence of myocardial infarction and revascularization, a higher proportion of positive cardiac enzymes on admission, and higher rates of catheterization and revascularization. However, outcome is related more to the severity of the illness than to sex.
Age

The mean age of presentation with unstable angina is 62 years, with an age range of 23-100 years. To put this in perspective, the mean age is 60 years for patients in clinical trials for myocardial infarction, about 67 years for carotid artery stenosis, and 63 years for congestive heart failure. On average, women with unstable angina are 5 years older than men on presentation, with approximately half of women older than 65 years, as opposed to only about a third of men. Blacks tend to present at a slightly younger age (mean ± standard deviation, 59 ± 13 y) than people of other races.
Clinical
History

Patients with unstable angina represent a heterogeneous population. Therefore, the clinician must obtain a focused history of the patient's symptoms and coronary risk factors and immediately review the ECG to develop an early risk stratification.
Initially obtain history to determine whether any evidence of angina is present, and then aim to identify whether it is stable or unstable.
Unstable angina differs from stable angina in that the discomfort is usually more intense and easily provoked, and ST-segment depression or elevation on ECG may occur. Otherwise, the manifestations of unstable angina are similar to those of other conditions of myocardial ischemia such as chronic stable angina and myocardial infarction.
Angina can take many forms, and inquiry should be directed at eliciting not only chest pain but also any discomfort and its frequency, location, radiation pattern, and precipitating and alleviating factors. Ischemic pain can manifest as heaviness, tightness, aching, fullness, or burning of the chest, epigastrium, and/or arm or forearm (usually the left). These sensations less typically involve the lower jaw, neck, or shoulder. Important associated symptoms may be dyspnea, generalized fatigue, diaphoresis, nausea and vomiting, flu-like symptoms, and, less commonly, lightheadedness or abdominal pain.
Elderly and female patients are more likely to present with atypical signs and symptoms.

Risk assessment (Diagnosis)

Clinical tip: Simply put, the 2 fundamental questions in the approach to the patient with possible angina are the following: (1) Is this coronary artery disease? (That is, what is the diagnosis, or what does the patient have?) (2) How dangerous is this? (That is, what is the prognosis, or what is the risk of something bad happening next?) Therefore, a brief history and physical examination, resting 12-lead ECG, and blood draw for evaluation of cardiac enzymes should be accomplished expeditiously.

Estimation of likelihood of acute coronary syndrome is a complex multivariable problem that cannot be fully specified in a list such as this. The following is meant to illustrate major relationships rather than offer rigid algorithms. The likelihood of significant coronary artery disease in patients presenting with chest pain syndrome is as follows:
High likelihood (includes any of the following features):
History of prior myocardial infarction, sudden death, or other known history of coronary artery disease
Chest or left arm pain consistent with prior documented angina
Transient hemodynamic or ECG changes during pain
ST-segment elevation or depression 1 mm or more
Marked symmetrical T-wave inversion in multiple precordial leads
Intermediate likelihood (includes absence of high likelihood features, but one of these risk characteristics is present):
Age older than 70 years
Male sex
Diabetes mellitus
Extracardiac vascular disease (peripheral, brachiocephalic, or renal artery atherosclerosis)
ST depression 0.05-1 mm
T-wave inversion 1 mm or greater in leads with dominant R waves
Low likelihood (includes absence of high or intermediate likelihood features and any of the following):
Chest pain classified as probably not angina
Chest discomfort reproduced by palpation
T-wave flattening or inversion less than 1 mm in leads with dominant R waves
Normal ECG findings

Risk stratification (Prognosis)

After the likelihood for coronary artery disease is determined to be significant, the next step is to stratify the patient's risk for an event. The estimation of likelihood of significant coronary artery disease is critical for identifying high-risk patients who may benefit from more aggressive treatment strategy (ie, cardiac catheterization).

The TIMI Risk Score for unstable angina/NSTEMI is currently the best-validated prognostic instrument that is simple enough to use in an emergency department setting. The gradient of death, myocardial infarction, or severe recurrent ischemia is somewhat proportionate to the TIMI Risk Score.


Thrombolysis in Myocardial Infarction (TIMI) Risk Score correlates with major adverse outcome and the effect of therapy with low molecular weight heparin.



The presence of any of the following variables constitutes 1 point, with the sum constituting the patient risk score on a scale of 0-7:
Aged 65 years or older
Use of aspirin in the last 7 days
Known coronary stenosis of 50% or greater
Elevated serum cardiac markers
At least 3 risk factors for coronary artery disease (including diabetes mellitus, active smoker, family history of coronary artery disease, hypertension, hypercholesterolemia)
Severe anginal symptoms (2 or more anginal events in the last 24 h)
ST deviation on ECG

Of note, studies have shown that ongoing congestive heart failure, presence/history of poor left ventricular ejection fraction (LVEF), hemodynamic instability, recurrent angina despite intensive anti-ischemic therapy, new or worsening mitral regurgitation, or sustained ventricular tachycardia are significant prognosticators for poor outcome. However, these factors were not evaluated in the TIMI Risk Score model and should be taken into consideration when the level of care is decided.

Factors that were specifically examined but were not found to have prognostic value in the multivariate model include prior myocardial infarction, previous percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft, or history of congestive heart failure.

The inflection point for death or myocardial infarction starts at a TIMI Risk Score of 3. Therefore, patients with a score of 3-7 should be considered for use of intravenous glycoprotein IIb/IIIa agents, heparin (low molecular weight or unfractionated), and early cardiac catheterization (see Treatment).

Classification of unstable angina

The number and diversity of clinical conditions that cause the transient myocardial ischemia of unstable angina along with its varying intensity and frequency of pain have made classification within this disorder difficult.

The Braunwald classification is conceptually useful because it factors in the clinical presentation (new or progressive vs rest angina), context (primary, secondary, or post–myocardial infarction), and intensity of antianginal therapy.

[#targetD]Table 4. Braunwald Classification of Unstable Angina


Open table in new windowCharacteristic Class/Category Details
Severity I Symptoms with exertion
II Subacute symptoms at rest (2-30 d prior)
III Acute symptoms at rest (within prior 48 h)
Clinical precipitating factor A Secondary
B Primary
C Postinfarction
Therapy during symptoms 1 No treatment
2 Usual angina therapy
3 Maximal therapy



Patients in class I have new or accelerated exertional angina, whereas those in class II have subacute (>48 h since last pain) or class III acute (<48 h since last pain) rest angina. The clinical circumstances associated with unstable angina are categorized as (A) secondary (anemia, fever, hypoxia), (B) primary, or (C) postinfarction (<2 wk after infarction). Intensity of antianginal therapy is subclassified as (1) no treatment, (2) usual oral therapy, and (3) intense therapy, such as intravenous nitroglycerin.

The Canadian Cardiovascular Society Grading System for effort-related angina is widely used since it is a simple and practical classification that is often used to describe symptom severity. It is as follows:
Grade I: Angina with strenuous, rapid, or prolonged exertion. (Ordinary physical activity such as climbing stairs does not provoke angina.)
Grade II: Slight limitation of ordinary activity. (Angina occurs with postprandial, uphill, or rapid walking; when walking more than 2 blocks of level ground or climbing more than one flight of stairs; during emotional stress; or in the early hours after awakening.)
Grade III: Marked limitation of ordinary activity. (Angina occurs with walking 1-2 blocks or climbing a flight of stairs at a normal pace.)
Grade IV: Inability to carry on any physical activity without discomfort. (Rest pain occurs.)

ECG evaluation
The first line of assessment in any patient with suspected unstable angina is the 12-lead ECG, which should be obtained within 10 minutes of the patient's arrival to the emergency department. The diagnostic accuracy of an ECG is enhanced if a prior tracing is available for comparison.
The highest-risk ECG findings (ST-segment elevation or new left bundle-branch block) necessitate immediate triage for revascularization therapy. Peaked T waves may also indicate early myocardial infarction.
The next level of high-risk patients includes those with ST depression greater than 1 mm on ECG. Approximately 50% of patients with this finding have subendocardial myocardial necrosis. The presence of ST-segment depression portends relatively high in-hospital, 30-day, and 1-year mortality rates irrespective of cardiac biomarker level.
New or reversible ST-segment deviation of 0.5 mm or more from baseline has been associated with a higher incidence (15.8% vs 8.2%) of 1-year death or myocardial infarction in the TIMI-III Registry ECG Ancillary study.
Primary T wave changes are neither sensitive nor specific for ischemia, but they become an important clue in the context of symptoms or if the QRS to T-wave angle is greater than 60°. Isolated symmetric T-wave inversion does not appear to carry additional adverse prognosis.
Clinical tip: The presence of ST-segment elevation or depression on ECG indicates high risk and must therefore be detected and acted on as soon as possible.

Physical

The physical examination is usually not as sensitive or specific for unstable angina as history or diagnostic tests. An unremarkable physical examination is not uncommon. Perform a quick assessment of patients' vital signs, and perform a cardiac examination. Specific diagnoses that must be explicitly considered are aortic dissection, leaking or ruptured thoracic aneurysm, pericarditis with tamponade, pulmonary embolism, and pneumothorax. Ideally, a 12-lead ECG should be performed within 10 minutes of presentation.

Increased autonomic activity may manifest as diaphoresis or tachycardia, and bradycardia may result from vagal stimulation from inferior wall myocardial ischemia.
A large area of myocardial jeopardy may manifest as signs of transient myocardial dysfunction and typically signifies a higher-risk situation.
Systolic blood pressure less than 100 mm Hg or overt hypotension
Elevated jugular venous pressure
Dyskinetic apex
Reverse splitting of the second heart sound
Presence of a third or fourth heart sound
New or worsening apical systolic murmur due to papillary muscle dysfunction
Rales or crackles
Findings indicative of peripheral arterial occlusive disease or prior stroke increases the likelihood of associated coronary artery disease.
Carotid bruit
Supraclavicular or femoral bruits
Diminished peripheral pulses or blood pressure
Clinical tip: Any sign of congestive heart failure, including isolated tachycardia, particularly in physiologically vulnerable populations (eg, very elderly patients), should trigger expeditious work-up, treatment, or consultation with a cardiologist. Such patients can deteriorate rapidly.
Causes

Many different conditions can provoke myocardial ischemia (Braunwald class A), including the following:
Increased myocardial oxygen demand (See Supply-demand mismatch in Pathophysiology.)
Fever
Tachyarrhythmias (eg, atrial fibrillation or flutter)
Malignant hypertension
Thyrotoxicosis
Pheochromocytoma
Cocaine use
Amphetamine use
Aortic stenosis
Supravalvular aortic stenosis
Obstructive cardiomyopathy
Aortovenous shunts
High output states
Congestive failure
Decreased oxygen supply
Anemia
Hypoxemia
Polycythemia

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