Mechanical Complications of Acute Myocardial Infarction

Common Misconceptions

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The mechanical complications of acute myocardial infarction are more common in large infarctions.
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The mechanical complications of acute myocardial infarction can be treated medically.
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Patients with ventricular septal rupture should be stabilized for several weeks before surgical repair.
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Early and effective reperfusion of acute myocardial infarction (MI) has resulted in a substantial decline in the incidence of mechanical complications, including free wall rupture, ventricular septal rupture, and papillary muscle rupture resulting in acute mitral regurgitation.
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However, mechanical complications remain important causes of morbidity and mortality in the peri-infarct setting.
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Mechanical complications are frequently associated with cardiogenic shock; approximately 12% of patients with cardiogenic shock have these complications.
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Because in many patients the MI may not be large, if patients can be diagnosed early and treated effectively, they can often be discharged with reasonably preserved left ventricular (LV) function and have an acceptable quality of life.
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The mechanical complications of acute MI are described in this chapter and summarized in Table 5.1 .

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Acute rupture of a cardiac free wall is a sudden, usually catastrophic complication of acute MI.
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It is the second most common cause of post-MI death after cardiogenic shock without mechanical defects.
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Free wall rupture accounts for up to 20% of all deaths resulting from an acute MI.
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The overall incidence of free wall rupture is about 1% to 2%.
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Risk factors for free wall rupture include female sex, advanced age, single-vessel disease, hypertension, transmural MI, and late reperfusion therapy.

Table 5.1

The incidence of rupture for patients with successful reperfusion (0.9%) is less than that without reperfusion treatments (2.7%).

Pathophysiology

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The most frequent site of post-MI cardiac rupture is the LV free wall (80% to 90% of cases) ( Fig. 5.1 ).
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Less commonly, the LV posterior wall, right ventricle (RV), or atria may rupture.
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Rupture may rarely occur at more than one site and occur in combination with papillary muscle or septal rupture.
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The path of the rupture through the wall may be direct (through the center of the necrotic area), but is often serpiginous and frequently seen at an eccentric position, near the “hinge point” of mobility between the normally contracting and dyskinetic myocardium.

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Free wall rupture occurs within 24 hours in 25% to 35% of cases and within the first week in 87% of patients following the onset of the acute coronary syndrome.
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There are no specific symptoms or signs of acute or subacute free wall rupture.
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Patients may present with syncope or signs and symptoms of cardiogenic shock.
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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.
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Some patients have premonitory symptoms, such as unexplained chest pains that are not typical of ischemia or pericarditis-related chest pains, repeated emesis, restlessness, and agitation.
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Rapid onset of tamponade owing to hemopericardium, resulting in severe hypotension and electromechanical dissociation, characterizes acute rupture; antemortem diagnosis is almost impossible in these patients.
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In patients with subacute rupture, relatively slower development of tamponade may allow antemortem diagnosis and corrective surgical therapy with salvage of these patients.
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In some patients, a pseudoaneurysm may develop.
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Elevated jugular venous pressure, pulsus paradoxus, muffled heart sounds, and a pericardial friction rub may indicate subacute rupture.
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A new systolic, diastolic, or “to-and-fro” murmur may be present in these patients with or without pseudoaneurysm.

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