A common cause of CS is secondary to an AMI (Table 20-3). While thrombotic coronary artery occlusion can be well tolerated clinically, approximately 5% to 8% of AMI patients develop clinical manifestations of hemodynamic collapse (6, 11). The most common anatomic distribution of a coronary occlusion associated with CS is the proximal left anterior descending artery. Mean LV ejection fraction (LVEF) in patients with CS following an AMI is approximately 30% (12), and those who develop CS are generally older (age > 65) with a history of hypertension, prior infarction, or multivessel disease (13, 14). Early preclinical studies suggest that approximately 40% of the myocardium must be involved in an AMI to cause CS (15).

The timing of CS onset may influence clinical outcomes. In the Trandolapril Cardiac Evaluation (TRACE) registry, early development of CS within 48 hours of admission was associated with
significantly lower 30-day mortality than patients with late development of CS (16). This may be due to ventricular arrhythmias or mechanical complications such as papillary muscle dysfunction/rupture and acute mitral regurgitation, ventricular septal rupture, or ventricular free wall rupture.

Acute mitral regurgitation is an important mechanical complication of CS after an AMI, and may be due to papillary muscle dysfunction or rupture. In an analysis of 1,190 patients in the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? (SHOCK) registry, severe mitral regurgitation was considered the primary mechanism of shock in 98 (6.9%) (17). Several studies have reported that ischemic papillary muscle rupture occurs most commonly in patients presenting with their first AMI in the inferior territory since the posteromedial papillary muscle receives blood supply from the right coronary artery, while the anterolateral papillary muscle is supplied by both the left anterior descending and circumflex arteries (18, 19).

Ventricular septal rupture and free wall rupture are also important causes of CS after an AMI. Upon rupture of the ventricular septum, a sudden decrease in LV stroke volume occurs as an acute left-to-right shunt develops within the heart. Prior to the reperfusion era, septal rupture occurred in approximately 2% of patients (20, 21). Among 41,021 patients in the Global Utilization of Streptokinase and T-PA for Occluded Coronary Arteries (GUSTO) trial, 84 (0.2%) developed a ventricular septal rupture (22). In the SHOCK registry, 55 (3.9%) developed a ventricular septal rupture (17). Risk factors for development of a ventricular septal rupture include advanced age, female sex, and no prior symptoms of angina or prior myocardial infarction (23). Anterior myocardial infarctions are generally associated with anteroapical septal rupture, while inferior myocardial infarction (IMI) tends to occur in the posterobasal septum (24).

Ventricular free wall rupture can result in acute cardiac tamponade and CS. In these cases, hemopericardium commonly leads to pulseless electrical activity and sudden cardiac death (21). In the prethrombolytic era, free wall rupture was a common cause of death after an AMI. In modern day practice, free wall rupture is rare. In the SHOCK registry, cardiac tamponade from any cause (i.e., pericarditis or free wall rupture) accounted for only 20 (1.4%) of the 1,190 patients enrolled (17). Risk factors for free wall rupture include female sex, the extent of myocardial infarction, and the absence of prior coronary disease (21, 25, 26).

Right ventricular (RV) myocardial infarction (RVMI) is another unique cause of CS after an AMI, and is associated with increased morbidity and mortality, including a higher likelihood of
CS, ventricular fibrillation, and high grade AV-conduction block (27, 28). The diagnosis of RVMI relies on clinical evidence of venous congestion, clear lung fields, and low cardiac output despite relatively preserved LV function. Echocardiographic evidence of RV dilatation or wall motion abnormalities may occur in up to 50% of subjects with acute IMI and may not correlate with clinical findings of RV failure (29). The RV receives blood from acute marginal branches of the right coronary artery and the posterior descending artery. RVMI occurs most commonly after acute proximal right coronary occlusion, but can occur after occlusion of a dominant circumflex artery (30, 31). RV ischemia leads to RV systolic failure and reduced LV preload. As RV pressure and volume overload develop, the interventricular septum shifts toward the LV cavity, further reducing LV stroke volume. Hemodynamic indices of RV failure in AMI include measurements of RV stroke work (RVSW), right atrial to PCWP (RA:PCWP) ratio of >0.8, and pulmonary artery pulse pressure (32). In the SHOCK registry, isolated RV failure accounted for 49 (5.3%) of the 933 patients with myocardial dysfunction as the primary mechanism underlying CS (33).

Primary valvular heart disease is another important cause of CS. Endocarditis, mitral valve prolapse, chordal rupture, or aortic dissection extending to the aortic annulus may cause CS secondary to valve failure (34, 35, 36

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