Free Wall Rupture

Acute rupture of a free wall is a sudden, usually catastrophic complication of acute MI. It is the second most common cause of post-MI death after cardiogenic shock without mechanical defects.³ More recent studies have reported that free wall rupture accounts for 3% to 20% of all deaths resulting from acute MI.⁴ The overall incidence of free wall rupture is about 2% to 7%, and it accounts for in-hospital mortality of about 15% of all deaths owing to acute MI.⁵ Risk factors for free wall rupture include female gender, advanced age, single vessel disease, hypertension, transmural MI, and late administration of thrombolytic therapy.⁴^–⁸ The incidence of rupture for patients with successful reperfusion (0.9%) is less than that without reperfusion treatments (2.7%). The incidence seems to be similar whether reperfusion is achieved by thrombolytic therapy or by angioplasty.

Pathophysiology

The most frequent site of post-MI cardiac rupture is the left ventricular free wall (80% to 90%).^2,⁹ Less commonly, the left ventricular posterior wall, right ventricle, or atria may rupture.^10,¹¹ Rupture may rarely occur at more than one site,¹² and it may be associated with papillary muscle¹² or septal rupture.¹³

Expansion of the infarct area seems to predispose to rupture.¹⁴ When ruptures occur within 24 hours of onset of infarction, however, infarct expansion or infiltration by neutrophils does not seem to contribute to the pathogenesis.¹⁵ The path of the rupture through the wall may be direct (through the center of the necrotic area), but is often serpiginous and often seen at an eccentric position, near the “hinge point” of mobility between the normally contracting and dyskinetic myocardium. These observations suggest that local shear forces contribute to the disruption of tissue.¹⁶ It has been suggested that apoptosis of cardiomyocytes in the region of maximum wall strain contributes to rupture of the ventricular free wall.¹⁷

Infarct expansion and adverse ventricular remodeling has been suggested to contribute to subacute ventricular rupture.¹⁸ Inappropriate changes in the extracellular matrix, in particular, collagen disruption and its inhibition by dysregulation of matrix metalloproteinase metabolism, have been suggested to be important mechanisms in the pathogenesis of ventricular rupture after MI.¹⁹ In experimental animal models, deficiency of local angiotensin type II receptor has been shown to cause decreased collagen deposition and increased incidence of cardiac rupture after MI.²⁰ Angiotensin II induces transforming growth factor-β1, which promotes fibrogenesis.²¹

Clinical Features

Free wall rupture occurs within 24 hours in 25% to 35% and within the first week in 87% of patients after the onset of acute coronary syndrome.^22,²³ Frequently, rupture occurs in patients with uncomplicated MI. There are no specific symptoms or signs of acute or subacute free wall rupture. Patients may present with syncope or signs and symptoms of cardiogenic shock.^6,¹⁰ Sudden onset of severe chest pain during or after some types of physical stress, such as coughing or straining at stool, may suggest the onset of free wall rupture. Some patients have premonitory symptoms, such as unexplained chest pains that are not typical of ischemia or pericarditis-related chest pains,²³ repeated emesis, restlessness, and agitation.²⁴

Rapid onset of tamponade owing to hemopericardium, resulting in severe hypotension and electromechanical dissociation, characterizes acute rupture, and antemortem diagnosis is almost impossible in these patients. In patients with subacute rupture, relatively slower development of tamponade may allow antemortem diagnosis and corrective surgical therapy with salvage of these patients. Elevated jugular venous pressure, pulsus paradoxus, muffled heart sounds, and a pericardial friction rub may indicate subacute rupture. A new systolic, diastolic, or “to-and-fro” murmur may be present in these patients with or without pseudoaneurysm.²⁵

Diagnosis

In acute free wall rupture, the electrocardiogram (ECG) reveals electromechanical dissociation and terminal bradycardia.^8,²⁶ In subacute rupture, several ECG findings have been described, including presence of Q waves, recurrent ST segment elevation or depression, pseudonormalization of inverted T waves particularly in the precordial leads, persistent ST segment elevation, and new Q waves in two or more leads.^5,^22,^24,^26,²⁷ None of the ECG findings are specific or sensitive enough, however, to be of value for early diagnosis of impending rupture.

Transthoracic echocardiography should be performed as soon as the subacute rupture is suspected.⁵^–⁷ ²⁶ Color flow Doppler may be useful for the diagnosis of the rupture site.²⁸ The most frequent finding is pericardial effusion. The presence of echogenic masses in the fluid and detection of wall defects enhance diagnostic accuracy. Although transesophageal echocardiography may provide a better delineation of these findings, it should not be performed because of the stress of the procedure until absolutely necessary. Contrast echocardiography may show extravasation of the contrast material into the pericardial space, confirming the diagnosis of free wall rupture.^28,²⁹

Determination of hemodynamics and contrast ventriculography are unnecessary for diagnosis and should be avoided. If a balloon flotation catheter is already in place, determination of right heart hemodynamics reveals elevated right atrial and pulmonary capillary wedge pressures and equalization of the diastolic pressures.^5,²⁶

Management

Surgical repair is the definitive treatment, and for subacute rupture, salvage rates may be considerable. The operative mortality has been reported to be 24% to 35%, and the total in-hospital mortality is 50% to 60%.^5,^7,²⁶ Currently, conservative surgical techniques using simple sutures supported with felt or application of a patch to the epicardial surface with biologic glue are employed.^24,³⁰ Temporizing measures include pericardiocentesis, volume loading, inotropic support, and intra-aortic balloon support. In very high-risk elderly patients, nonsurgical conservative treatment with adequate control of blood pressure with angiotensin inhibition and the use of β-blocking agents has been suggested.³¹ The treatment approach of pseudoaneurysm is similar to that of subacute rupture without pseudoaneurysm.

Mitral Regurgitation

Although mild mitral regurgitation is common in patients with acute coronary syndromes, severe mitral regurgitation owing to papillary muscle and left ventricular wall dysfunction with or without rupture of the papillary muscle is much less frequent. The overall incidence of acute mitral regurgitation in patients receiving thrombolytic therapy was 1.73% in the GUSTO-I trial.³² It has been reported that the incidence is significantly lower (0.31%) in patients undergoing primary angioplasty.³³ The reported incidence of mild to moderate mitral regurgitation is variable and is approximately 29% (mild) and 6% (moderate). The incidence of severe mitral regurgitation complicating MI is approximately 10%,³⁴ and the incidence of mitral regurgitation resulting from papillary muscle rupture is 1%.¹

The risk factors for mitral regurgitation with and without papillary muscle rupture seem to be different, although advanced age and female gender are risk factors for both types.³⁵ In patients without papillary muscle rupture, prior MI, relatively large infarct size, multivessel coronary artery disease, recurrent myocardial ischemia, and heart failure on admission are more prevalent. In contrast, in patients with papillary muscle rupture, absence of previous angina, inferoposterior MI, absence of diabetes, and single vessel disease are more common.

Pathophysiology

Several anatomic and functional derangements may cause mitral regurgitation in patients with acute coronary syndromes. Acute transient papillary muscle ischemia is associated with impaired shortening of the muscle, which usually causes only mild mitral regurgitation. Ischemic dysfunction of anterior and posterior papillary muscles may be associated with more severe mitral regurgitation.³⁶ Ischemia of only papillary muscles without involvement of the adjacent left ventricular walls seldom results in severe mitral regurgitation.³⁷ The subendocardial position of the papillary muscles and their characteristic vascular anatomy (supplied by coronary end arteries) predispose them to ischemia.³⁸ The posteromedial papillary muscle receives its blood supply only via the posterior descending coronary artery, whereas the anterolateral papillary muscle receives its blood supply from the left anterior descending and left circumflex coronary arteries.³⁹ Ischemia of posteromedial papillary muscle is more common than ischemia of anterolateral papillary muscle.

A large posterior MI, including the anchoring area of the posteromedial papillary muscle, may be associated with severe mitral regurgitation. The mechanism seems to be asymmetric annular dilation and misalignment of the papillary muscle and the leaflets during systole causing severe leaflet prolapse.⁴⁰ A small inferior or inferoposterior MI with involvement of the posteromedial papillary muscle can also produce severe mitral regurgitation, however, because of severe leaflet prolapse.

Rupture of the posteromedial papillary muscle is 6 to 12 times more frequent than rupture of the anterolateral papillary muscle, explaining the higher incidence of severe mitral regurgitation in patients with inferior MI.³⁴ In approximately 50% of patients with papillary muscle rupture, the infarct size is small.⁴¹

Mild to moderate mitral regurgitation usually does not induce any additional hemodynamic burden. Neither ejection fraction nor hemodynamics, such as pulmonary capillary wedge and pulmonary artery pressures and cardiac output, is substantially influenced. In contrast, severe mitral regurgitation imposes sudden additional hemodynamic burden on the left ventricular dynamics and function. Sudden large volume overload, resulting from regurgitation to a left atrium with normal compliance and size, causes a marked increase in left atrial and pulmonary capillary wedge pressure, causing severe pulmonary edema. Because of postcapillary pulmonary hypertension, which increases right ventricular afterload, the right ventricle also fails. Left ventricular forward stroke volume decreases, resulting in a reduction in cardiac output and systemic hypotension. All the hemodynamic features of cardiogenic shock develop rapidly and usually abruptly. Left ventricular ejection fraction may increase because of sudden unloading of the ventricle by the mitral regurgitation. The ejection fraction is still less than normal, however, because of presence of dysfunctional ischemic or infarcted myocardium.