Contractile dysfunction. In general, MIs affect left ventricular pump function in proportion to the volume of damage. In most cases, there is some degree of left ventricular failure manifested as hypotension, pulmonary congestion, and pulmonary edema. Severe “pump failure” (cardiogenic shock) occurs in roughly 10% of patients with transmural MIs and typically is associated with infarcts that damage 40% or more of the left ventricle.
Papillary muscle dysfunction. Although papillary muscles rupture infrequently after MI, they often are dysfunctional and can be poorly contractile as a result of ischemia, leading to postinfarct mitral regurgitation. Much later, papillary muscle fibrosis and shortening or global ventricular dilation also can cause mitral valve insufficiency.
Right ventricular infarction. Although isolated right ventricular infarction occurs in only 1% to 3% of MIs, the right ventricle is affected by RCA occlusions leading to posterior septal or left ventricular infarction. In either case, right-sided heart failure is a common outcome, leading to pooling of blood in the venous circulation and systemic hypotension.
Myocardial rupture. Rupture complicates only 1% to 5% of MIs but is frequently fatal when it occurs. Left ventricular free wall rupture is most common, usually resulting in rapidly fatal hemopericardium and cardiac tamponade (
Fig. 11.14A ). Ventricular septal rupture creates a VSD with left-to-right shunting (
Fig. 11.14B ), and papillary muscle rupture leads to severe mitral regurgitation (
Fig. 11.14C ). Rupture occurs most commonly within 3 to 7 days after infarction—the time in the healing process when lysis of necrotic myocardium is maximal and when much of the infarct has been converted to soft, friable granulation tissue. Risk factors for free wall rupture include age older than 60 years, anterior or lateral wall infarctions, female gender, lack of left ventricular hypertrophy, and first MI (since scarring associated with prior MIs tends to limit the risk for myocardial tearing).
Arrhythmias. MIs lead to myocardial irritability and conduction disturbances that can cause sudden death. Approximately 90% of patients develop some form of rhythm disturbance, with the incidence being higher in STEMIs versus NSTEMIs. MI-associated arrhythmias include heart block of variable degree (including asystole), bradycardia, supraventricular tachyarrhythmias, ventricular premature contractions or ventricular tachycardia, and ventricular fibrillation. The risk for serious arrhythmias (e.g., ventricular fibrillation) is greatest in the first hour and declines thereafter.
Pericarditis. Transmural MIs can elicit a fibrinohemorrhagic pericarditis; this is an epicardial manifestation of the underlying myocardial inflammation (
Fig. 11.14D ). Heralded by anterior chest pain and a pericardial http://ebooksmedicine.net