Sudden decompensation of previously stable patients should always raise concern of the "mechanical" complications of AMI. As a group, these complications usually involve the tearing or rupture of infarcted tissue. Therefore, they are unlikely to occur in patients with non-AMI acute coronary syndromes. The clinical presentation of these entities depends upon the site of rupture (papillary muscles, interventricular septum, or ventricular free wall).
Free wall rupture occurs in 10 percent of AMI fatalities, usually 1 to 5 days after infarction. Rupture of the left ventricular free wall usually leads to pericardial tamponade and death (in more than 90 percent). Patients may complain of tearing pain or sudden onset of severe pain. They will be hypotensive and tachycardic and may have onset of confusion and agitation. Increased neck veins, decreased heart sounds, and pulsus paradoxus may be present. Echocardiography is the diagnostic test of choice, although near equalization of right atrial, right ventricular middiastolic, and right ventricular systolic pressures on pulmonary artery catheterization may also be useful. Treatment is surgical.
Rupture has been attributed to intense necrosis at the distal end of blood supply along with poor collateral blood flow and a thin apical left ventricular wall in conjunction with the shearing effects of muscle contraction. Anti-inflammatory medications, steroids, and late administration of thrombolytic agents have all been linked to an increased likelihood of cardiac rupture. However, studies remain contradictory. The elderly appear to be more prone to cardiac rupture. Left ventricular hypertrophy appears to be protective.
Rupture of the interventricular septum is more often detected clinically than rupture of the ventricular free wall, despite the fact that rupture of the ventricular free wall is more commonly detected in autopsy studies. The size of the defect determines the degree of left-to-right shunt and the ultimate prognosis. Clinically, interventricular septal rupture presents with chest pain, dyspnea, and sudden appearance of a new holosystolic murmur. The murmur is usually accompanied by a palpable thrill and is heard best at the lower left sternal border. Doppler echocardiography is the diagnostic procedure of choice. Demonstration of left-to-right shunt by pulmonary catheter blood sampling may be useful. An oxygen step up of more than 10 percent from right atrial to right ventricular samples is diagnostic. Rupture of the interventricular septum is more common in patients with anterior wall myocardial infarction and patients with extensive (three vessel) coronary artery disease.
Papillary muscle rupture occurs in approximately 1 percent of patients with AMI, is more common with inferior myocardial infarction, and usually occurs 3 to 5 days after AMI. In contrast to rupture of the interventricular septum, papillary muscle rupture often occurs with a small to modest-sized AMI. Patients may have relatively limited coronary artery disease. Patients present with acute onset of dyspnea, increasing degree of congestive heart failure, and a new holosystolic murmur consistent with mitral regurgitation. The posteromedial papillary muscle is most commonly ruptured because it receives blood supply from only a single coronary artery, usually the right coronary artery. Echocardiography can often distinguish rupture of a portion of the papillary muscle from other etiologies of mitral regurgitation. Treatment is surgical.
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