Myocardial rupture more frequently involves the left ventricle than the right ventricle and seldom involves the atria.3 The infarct commonly affects the anterior and lateral walls of the left ventricle near the junction of the infarct and normal myocardium. Ventricular free wall rupture is defined as an acute, traumatic perforation of the ventricles, which may include pericardial rupture.6 With unsuccessful or no reperfusion, coagulation necrosis develops within the first 3 to 5 days.5 As the necrosis progresses, neutrophils infiltrate the myocardial space and release lytic enzymes that disintegrate the necrotic myocardium leading to perforation. The rupture thus is a result of transmural infarction, and the actual perforation can range in size from millimeters to centimeters depending on infarct size.5 Early phase rupture is defined as within 72 hours post-MI and late rupture is >4 days.

The hallmark of rapid deterioration is primarily because of the extravasation of blood into the pericardial space with resultant instantaneous, acute pericardial tamponade. Because these events occur so quickly, patients usually deteriorate before any therapeutic intervention. Less commonly, subacute rupture can provide a longer therapeutic window as the acute rupture may be temporarily contained by pericardial adhesions or by thrombosis at the rupture site. It is in these patients that immediate, lifesaving, cardiovascular surgery is possible (Figure 10.1).11

The clinical course of myocardial rupture is variable and challenging to diagnose, as patients may rapidly decompensate. Their clinical course parallels that of any patient suffering from pericardial tamponade. Thus, rupture can present as sudden death in an undetected or silent MI or as incomplete/subacute rupture in those with known MI.12

Complete rupture of the left ventricular free wall usually leads to hemopericardium and death from cardiac tamponade. Patients may complain of transient chest pain or dyspnea. Acute tamponade can cause tachypnea, tachycardia, muffled heart sounds, elevated jugular venous pressure, and pulsus paradoxus. The presence of rupture is first suggested by the development of sudden profound right heart failure and shock, often progressing rapidly to pulseless electrical activity and death. Emergent transthoracic echocardiography (TTE) will confirm the diagnosis and emergent pericardiocentesis can transiently relieve the tamponade.12

Incomplete/subacute rupture of the left ventricular free wall can occur when organized thrombus and the pericardium seal the ventricular perforation. Patients may present with persistent or recurrent chest pain (particularly pericardial pain), nausea, restlessness, agitation, abrupt hypotension, and/or electrocardiographic features of localized or regional pericarditis.4,5 The diagnosis of incomplete/subacute rupture is again confirmed by TTE.12

The pathophysiology of interventricular septal rupture is similar to that of free wall rupture. Without reperfusion, coagulation necrosis develops within the first 3 to 5 days. The septum that becomes necrotic is infiltrated by neutrophils, which release lytic enzymes and thus disintegrate the necrotic myocardium.16 A transmural septal infarction underlies rupture of the interventricular septum, with the tear ranging in size from millimeters to centimeters.14

The ventricular septum is very vascular. The rarity of septal rupture and the variable infarct location relate to the fact that the interventricular septum has a dual blood supply. The anterior two-thirds is supplied by the left anterior descending (LAD)
coronary artery and its branches. The posterior one-third is supplied by branches of the posterior descending artery, which come from the right coronary or the left circumflex artery, depending on the dominance of the circulation.17 Studies have conflicted in determining the artery that is predominantly responsible for septal rupture, but anterior MI is most frequently followed by inferior infarction. Similar to free wall rupture, interventricular septal rupture occurs most frequently with a first MI when there is less likely to be collateral blood flow. In this setting, with an abrupt cessation of flow in the infarct-related artery, no collateral flow exists to support the infracted zone, thereby making the septum prone to rupture (Figure 10.2).

Whether in the pre-reperfusion era or post-, it is generally agreed upon that the clinical presentation and examination of a patient with a ventricular septal rupture has remained constant. Symptoms of rupture include shortness of breath, chest pain, and signs of low cardiac output and shock.16 In 1934, Sager proposed a set of clinical criteria for suspecting a ruptured septum. The sudden onset of a systolic murmur, often accompanied by a thrill, in a patient with rapid hemodynamic decompensation is highly suggestive of a ruptured interventricular septum.18 The rupture produces a harsh, loud, holosystolic murmur along the left sternal border, radiating toward the base, apex, and right parasternal area with a palpable thrill present in half of patients. Compared with acute mitral regurgitation (MR), initially there is often right ventricular failure and absence of severe pulmonary edema before left ventricular failure ensues. As the disease progresses complete biventricular failure invariably occurs.16

In the setting of cardiogenic shock, the thrill and murmur may be difficult to appreciate because turbulent flow across the defect is reduced. Pulmonary hypertension may cause the pulmonic component of the second heart sound to be accentuated. Right and left ventricular S3 gallops are often heard. Tricuspid regurgitation may be present and biventricular failure generally occurs within hours to days.16