Chapter 21 Marini Acute Coronary Syndromes

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CHAPTER 21 • Acute Coronary Syndromes

Myocardial infarction

Impaired contractility

Tissue necrosis

Electrical instability

Pericardial inflammation

Ventricular thrombosis

Hypotension Coronary perfusion Ischemia

Papillary muscle infarction

Ventricular wall rupture

Arrhythmias Pericarditis

Mitral regurgitation

Stroke (embolism)

Cardiogenic shock

Congestive heart failure

Cardiac tamponade

Acute MI transmural

LV aneurysm

Pericarditis

Ruptured free wall

Ruptured septum

Ruptured papillary muscle

FIGURE 21-7. Complications of acute myocardial infarction. Inset: Structural damage consequent to tissue necrosis from acute transmu­ ral myocardial infarction.

The ECG usually exhibits diffuse ST segment ele- vation not typically seen after occlusion of a major coronary artery. Histologic evidence of pericarditis occurs in almost all transmural MIs but usually is mild and clinically insignificant. Symptoms typical for pericarditis occur in only a small proportion of such cases. In the 10% of patients affected by acute pericarditis, symptoms usually emerge 2 to 4 days after the MI. Nonsteroidal anti-inflammatory drugs (e.g., aspirin and/or indomethacin) are helpful in controlling the inflammation and pain. Although effective as analgesic/anti-inflammatory agents, corticosteroids increase the risk of free ventricu- lar wall rupture. Large pericardial fluid accumula- tions occur in fewer than 10%. Rarely, pericardial fluid may become hemorrhagic and accumulate sufficiently to cause tamponade in anticoagulated patients. Delayed episodes of immunologically mediated febrile pleuropericarditis (Dressler syndrome) may complicate either MI or pericardiotomy any time within the subsequent 3 months. Dressler syn- drome is much less common than acute pericarditis, occurring in only 1% to 3% of patients with MI.

Leukocytosis and an elevated sedimentation rate are associated laboratory features. Pleural effu- sions are common in Dressler syndrome but rare in acute pericarditis. Because there is substantial risk of hemorrhagic pericarditis and tamponade in Dressler syndrome, anticoagulants are contraindi- cated. Indomethacin, with or without colchicines, may be used in the treatment of this condition. Pump Failure with Cardiogenic Shock Most in-hospital deaths from MI occur within 96 hours of admission secondary to shock resulting from LV failure. Assuming normal sinus rhythm, clinical evidence of heart failure develops when more than 20% of the LV sustains damage. (Persistent ST may be a hint of incipient heart failure if present longer than 48 hours after infarction.) Fatal pump failure usually ensues when more than 40% of the LV mass is infarcted or dysfunctional. The extent of lost muscle mass is a much more powerful deter- minant of outcome than the anatomic location of the infarct. Therefore, rapid myocardial reperfusion is the key to an optimal outcome. Contractility of ischemic but salvageable muscle may return after