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
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.
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.
Premature atrial contractions
Paroxysmal supraventricular tachycardia
Accelerated junctional rhythms
Atrioventricular (AV) blocks
First-degree AV block
Second-degree AV block
Third-degree AV block
Left anterior fascicular block
Right bundle branch block (RBBB)
Left bundle branch block (LBBB)
Premature ventricular contractions (PVCs)
Accelerated idioventricular rhythm
Arrhythmic Complications: Supraventricular Tachyarrhythmias
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 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.
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 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 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
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.
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.
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.
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
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.
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 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 .
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 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.
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.
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 .
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
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 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.
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.
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.
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.
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
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.
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 for MR are advanced age, female sex, large infarct, previous AMI, recurrent ischemia, multivessel coronary artery disease, and CHF.
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.
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.
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.
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
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.
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.
A history of MI and third or fourth heart sounds are common findings from the patient's history and physical examination.
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.
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.
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.
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.
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
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
Diposting oleh FX di 19.43
The Holy Al-Qur'an (English version)
- Surah 1 - Al Fatiha THE OPENING
- Surah 2 - Al Baqarah THE HEIFER
- Surah 3 - Ali 'Imran - THE FAMILY OF 'IMRAN
- Surah 4 - Al-Nisa' THE WOMEN
- Surah 5 - Al Ma'idah THE REPAST
- Surah 6 - Al An'am THE CATTLE
- Surah 7 - Al A'raf THE HEIGHTS
- Surah 8 - Al Anfal THE SPOILS OF WAR
- Surah 9 - Al Tawbah THE REPENTANCE
- Surah 10 - Yunus JONAH
- Surah 11 - Hud THE PROPHET HUD
- Surah 12 - Yusuf JOSEPH
- Surah 13 - Al Ra'd THE THUNDER
- Surah 14 - Ibrahim ABRAHAM
- Surah 15 - Al Hijr THE ROCKY TRACT
- Surah 16 - Al Nahl BEES
- Surah 17 - Al Isra' THE NIGHT JOURNEY
- Surah 18 - Al Kahf THE CAVE
- Surah 19 - Maryam MARY
- Surah 20 - TA HA
- Surah 21 - Al Anbiya THE PROPHETS
- Surah 22 - Al Hajj THE PILGRIMAGE
- Surah 23 - Al Mu'minun THE BELIEVERS
- Surah 24 - Al Nur THE LIGHT
- Surah 25 - Al Furqan THE CRITERION
- Surah 26 - Al Shu'ara' THE POETS
- Surah 27 - Al Naml THE ANTS
- Surah 28 - Al Qasas THE NARRATIONS
- Surah 29 - Al 'Ankabut THE SPIDER
- Surah 30 - Al Rum THE ROMANS
- Surah 31 - Luqman LUQMAN
- Surah 32 - Al Sajdah THE PROSTRATION
- Surah 33 - Al Ahzab THE CONFEDERATES
- Surah 34 - Saba' SHEBA
- Surah 35 - Fatir THE ORIGINATOR OF CREATION
- Surah 36 - Ya Sin YA SIN
- Surah 37 - Al Saffat THOSE RANGED IN RANKS
- Surah 38 - Sad SAD
- Surah 39 - Al Zumar CROWDS
- Surah 40 - Ghafir FORGIVER
- Surah 41 - Fussilat EXPOUNDED
- Surah 42 - Al Shura CONSULTATION
- Surah 43 - Al Zukhruf THE GOLD ADORNMENTS
- Surah 44 - Al Dukhan THE SMOKE
- Surah 45 - Al Jathiyah THE KNEELING DOWN
- Surah 46 - Al Ahqaf WINDING SAND-TRACTS
- Surah 47 - Muhammad MUHAMMAD
- Surah 48 - Al Fath THE VICTORY
- Surah 49 - Al Hujurat THE CHAMBERS
- Surah 50 - Qaf QAF
- Surah 51 - Al Dhariyat THE WINDS THAT SCATTER
- Surah 52 - Al Tur THE MOUNT
- Surah 53 - Al Najm THE STAR
- Surah 54 - Al Qamar THE MOON
- Surah 55 - Al Rahman THE MOST GRACIOUS
- Surah 56 - Al Waq'iah THE INEVITABLE
- Surah 57 - Al Hadid IRON
- Surah 58 - Al Mujadilah THE WOMAN WHO PLEADS
- Surah 59 - Al Hashr THE MUSTERING
- Surah 60 - Al Mumtahinah THAT WHICH EXAMINES
- Surah 61 - Al Saff THE BATTLE ARRAY
- Surah 62 - Al Jumu'ah FRIDAY
- Surah 63 - Al Munafiqun THE HYPOCRITES
- Surah 64 - Al Taghabun THE MUTUAL LOSS AND GAIN
- Surah 65 - Al Talaq DIVORCE
- Surah 66 - Al Tahrim PROHIBITION
- Surah 67 - Al Mulk THE DOMINION
- Surah 68 - Al Qalam THE PEN
- Surah 69 - Al Haqqah THE SURE REALITY
- Surah 70 - Al Ma'arij THE WAYS OF ASCENT
- Surah 71 - Nuh NOAH
- Surah 72 - Al Jinn THE SPIRITS
- Surah 73 - Al Muzzammil THE ENFOLDED ONE
- Surah 74 - Al Muddaththir THE ONE WRAPPED UP
- Surah 75 - Al Qiyamah THE RESURRECTION
- Surah 76 - Al Insan MAN
- Surah 77 - Al Mursalat THOSE SENT FORTH
- Surah 78 - Al Naba' THE GREAT NEWS
- Surah 79 - Al Nazi'at THOSE WHO TEAR OUT
- Surah 80 - 'Abasa HE FROWNED
- Surah 81 - Al Takwir THE FOLDING UP
- Surah 82 - Al Infitar THE CLEAVING ASUNDER
- Surah 83 - Al Mutaffifin THE DEALERS IN FRAUD
- Surah 84 - Al Inshiqaq THE RENDING ASUNDER
- Surah 85 - Al Buruj THE CONSTELLATIONS
- Surah 86 - Al Tariq THE NIGHT STAR
- Surah 87 - Al A'la THE MOST HIGH
- Surah 88 - Al Ghashiyah THE OVERWHELMING EVENT
- Surah 89 - Al Fajr THE DAWN
- Surah 90 - Al Balad THE CITY
- Surah 91 - Al Shams THE SUN
- Surah 92 - Al Layl THE NIGHT
- Surah 93 - Al Duha THE GLORIOUS MORNING LIGHT
- Surah 94 - Al Sharh THE EXPANSION OF THE BREAST
- Surah 95 - Al Tin THE FIG
- Surah 96 - Al Alaq THE CLINGING CLOT
- Surah 97 - Al Qadr THE NIGHT OF POWER
- Surah 98 - Al Bayyinah THE CLEAR EVIDENCE
- Surah 99 - Al Zalzalah THE EARTHQUAKE
- Surah 100 - Al 'Adiyat THOSE THAT RUN
- Surah 101 - Al Qari'ah THE GREAT CALAMITY
- Surah 102 - Al Takathur THE PILING UP
- Surah 103 - Al 'Asr TIME THROUGH THE AGES
- Surah 104 - Al Humazah THE SCANDALMONGER
- Surah 105 - Al Fil THE ELEPHANT
- Surah 106 - Quraysh THE TRIBE OF QURAYSH
- Surah 107 - Al Ma'un THE NEIGHBOURLY ASSISTANCE
- Surah 108 - Al Kawthar THE ABUNDANCE
- Surah 109 - Al Kafirun THOSE WHO REJECT FAITH
- Surah 110 - Al Nasr THE HELP
- Surah 111 - Al Masad THE PLAITED ROPE
- Surah 112 - Al Ikhlas THE PURITY OF FAITH
- Surah 113 - Al Falaq THE DAYBREAK
- Surah 114 - Al Nas MANKIND
- Acute Coronary Syndromes
- Angina Pectoris
- Anomalous Left Coronary Artery From the Pulmonary Artery
- Aortic Coarctation
- Aortic Dissection
- Aortic Regurgitation
- Aortic Stenosis
- Aortic Stenosis, Subaortic
- Aortic Stenosis, Supravalvar
- Ashman Phenomenon
- Atrial Fibrillation
- Atrial Flutter
- Atrial Myxoma
- Atrial Septal Defect
- Atrial Tachycardia
- Atrioventricular Block
- Atrioventricular Dissociation
- Atrioventricular Nodal Reentry Tachycardia (AVNRT)
- Benign Cardiac Tumors
- Brugada Syndrome
- Complications of Myocardial Infarction
- Coronary Artery Atherosclerosis
- Coronary Artery Vasospasm
- Digitalis Toxicity
- Dissection, Aortic
- Ebstein Anomaly
- Eisenmenger Syndrome
- First-Degree Atrioventricular Block
- HACEK Group Infections (Infective Endocarditis)
- Heart Failure - Decompensatio Cordis
- Holiday Heart Syndrome
- Hypertensive Heart Disease
- Junctional Rhythm
- Loeffler Endocarditis
- Long QT Syndrome
- Lutembacher Syndrome
- Mitral Regurgitation
- Mitral Stenosis
- Mitral Valve Prolapse
- Myocardial Infarction
- Myocardial Rupture
- Paroxysmal Supraventricular Tachycardia
- Patent Ductus Arteriosus
- Patent Foramen Ovale
- Pericardial Effusion
- Pericarditis Acute
- Pericarditis, Constrictive
- Pericarditis, Constrictive-Effusive
- Pulmonic Regurgitation
- Pulmonic Stenosis
- Right Ventricular Infarction
- Saphenous Vein Graft Aneurysms
- Second-Degree Atrioventricular Block
- Sinus of Valsalva Aneurysm
- Sudden Cardiac Death
- Tetralogy of Fallot
- Third-Degree Atrioventricular Block
- Torsade de Pointes
- Tricuspid Regurgitation
- Tricuspid Stenosis
- Unstable Angina
- Ventricular Fibrillation
- Ventricular Septal Defect
- Ventricular Tachycardia
- Wolff-Parkinson-White Syndrome