Postinfarction Ventricular Septal Rupture

Etiology

VSR is more likely to occur in patients who are older, female, hypertensive, have chronic kidney disease, and have no prior history of smoking. It commonly occurs in the setting of a first myocardial infarction (MI) in the background of delayed or absent reperfusion therapy. Angiography usually reveals an absence of collateral circulation to the infarct zone. Because previous ischemia induces myocardial preconditioning, decreasing the likelihood of transmural myocardial necrosis and septal rupture, patients with evidence of diabetes mellitus, chronic angina, or previous MI are less likely to experience a rupture. VSR may develop within 1 to 14 days post-STEMI; however, its incidence usually shows a bimodal peak, which is within the first 24 hours or 3 to 5 days post-MI.

Epidemiology

Post-myocardial infarction VSR occurs in 1% to 3% of patients with STEMI in the absence of reperfusion therapy and in 0.2% to 0.34% of patients who receive fibrinolytic therapy. Among those who have received reperfusion therapy, it occurs more commonly in those who have received fibrinolytic therapy rather than percutaneous coronary intervention. The incidence of VSR increases to 3.9% in patients with cardiogenic shock as a complication of STEMI.[2][3]

Histopathology

The defect usually occurs at the myocardial infarct border zone, in the apical septum with anterior wall myocardial infarction, and the basal posterior septum with inferior wall myocardial infarction. A VSR almost always occurs in the setting of a transmural infarction. The defect can range in length from one to several centimeters. It can be direct through an opening or more irregular and serpiginous. Multiple fenestrations are especially common with inferior infarctions.[4]

History and Physical

Signs and Symptoms

Patients with post-myocardial infarction ventricular septal rupture may seem comfortable early in the disease. Recurrence of angina, pulmonary edema, hypotension, and shock may later develop abruptly. Alternatively, abrupt onset of hemodynamic compromise, characterized by hypotension, biventricular failure, and a new murmur, may be the initial manifestation.[3]

Physical Findings

The diagnosis should be suspected when a new pan-systolic murmur develops, especially in the setting of worsening hemodynamic profile and biventricular failure. All patients with MI must have a well-documented cardiac examination at presentation and frequent evaluations after that. The murmur of acute post-MI VSR is usually best heard at the lower left sternal border and is usually accompanied by a thrill in 50% of the cases. In patients with a large VSR and severe heart failure or cardiogenic shock, the murmur may be of low intensity or inaudible, but the absence of a murmur does not rule out VSR.

Evaluation

Electrocardiogram

It establishes the diagnosis of STEMI. In cases of post-MI VSR, it may show atrioventricular or infra-nodal conduction abnormalities in approximately 40% of patients.

Transthoracic Echocardiography

It is the test of choice for the diagnosis of VSR. Echocardiography helps in determining the size and site of rupture and the magnitude of the left-to-right shunt. Basal VSR is best visualized in the parasternal long axis with medial angulation, the apical long axis, and the subcostal long axis. Apical VSR is best visualized in the apical 4-chamber view. Echocardiography also provides insight into the feasibility of using percutaneous closure devices in this setting. The assessment of ventricular function is the key to prognostication and management as they remain important determinants of mortality.[3][5]

Right Heart Catheterization

Pulmonary artery catheterization with oximetry measurement can help diagnose VSR by showing an oxygen saturation step-up in the right ventricle and pulmonary artery. This is helpful in differentiation from post-MI acute mitral regurgitation in which this step-up is absent.

Left Heart Catheterization

Ventriculography performed after angiography may reveal VSR if it is highly suspected. Visualization is best in the left anterior oblique projection with cranial angulation.

Cardiac MRI and CT

These are additional imaging modalities that can be utilized. However, these studies are more difficult to perform in hemodynamically unstable patients and do not play a significant role in this setting.

Treatment / Management

Invasive monitoring is generally recommended on the recognition of post-MI VSR. The measurement of right and left ventricular filling pressures is important to guide the fluid administration and the use of diuretics. Additionally, the measurements of cardiac output and mean arterial pressure permit calculation of systemic vascular resistance to direct vasodilator therapy. If systolic blood pressure is above 90 mm Hg, vasodilator therapy involving nitroglycerine or nitroprusside should be started as soon as possible, preferably once hemodynamic monitoring is available. Inotropes may also be needed to support adequate cardiac output. These interventions may be critically important for stabilizing the patient’s condition in preparation for further diagnostic studies and repair. If pharmacological therapy is not tolerated or if it fails to achieve hemodynamic stability, intra-aortic balloon counterpulsation (IABP) should be considered.[6][7]

An urgent surgical closure is the treatment of choice. Some authors believe surgery may be delayed to allow healing of friable tissue and improve surgical mortality. However, the lower surgical mortality was probably a result of selection bias. Among medically treated patients with VSR, the mortality is 24% at 72 hours and increases to 75% at three weeks. Surgical mortality is high among patients with inferior MI (70%) when compared to patients with anterior infarcts (30%). This is because of greater technical difficulty and the need for concomitant mitral valve repair in patients with basal septal rupture since they often have coexisting mitral regurgitation.[2]

Although surgery remains the gold standard treatment for post-MI VSR, percutaneous closure is increasingly attempted, especially in patients with high surgical risk.[8]

Differential Diagnosis

Distinguishing on clinical grounds between acute mitral regurgitation and rupture of the ventricular septum in patients with STEMI in whom a loud systolic murmur suddenly develops may be difficult. Such differentiation can be made most readily by color flow Doppler echocardiography. Also, right heart catheterization with a balloon-tipped catheter can readily distinguish between these 2 complications. Patients with VSR demonstrate a step-up in oxygen saturation in blood samples from the right ventricle and pulmonary artery as compared with those from the right atrium. Patients with acute mitral regurgitation lack this step-up and may demonstrate tall C-V waves in both the pulmonary capillary and pulmonary arterial pressure tracings.[9][10]