Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:

"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".

(HR. Muslim, Ahmad dan Hakim).

Jumat, 08 Januari 2010

Myocardial Rupture


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.

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.
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.
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.
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.
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).
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.
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.
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.
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 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.
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
Primary cardiac tumors may be present.
Patients may have secondary or metastatic tumors of the heart.
Patients may have lymphoma or acute myeloblastic leukemia.


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