Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm.

Cardiogenic shock (CS) is the leading cause of death for patients with acute myocardial infarction (MI) who reach the hospital alive. Its incidence has remained constant for 20 years.1,2 Rapidly re-establishing infarct-related artery (IRA) blood flow is essential in the management of patients with shock due to right ventricular or left ventricular (LV) failure. A strategy of early revascularization is superior to initial aggressive medical therapy.3–5 Despite the advantages of early percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG), once shock is diagnosed, the mortality rate remains high (≈50%) despite intervention, and half of the deaths occur within the first 48 hours.6–8 This may be caused by irreversible extensive myocardial or vital-organ damage. New evidence suggests, however, that a systemic inflammatory response, complement activation, release of inflammatory cytokines, expression of inducible nitric oxide (NO) synthase (iNOS), and inappropriate vasodilation may play an important role not only in the genesis of shock but also in outcome after shock. New insights and therapies are needed. The underlying pathophysiology of CS is profound depression of myocardial contractility, resulting in a vicious spiral of reduced cardiac output (CO), low blood pressure, further coronary insufficiency, and further reduction in contractility and CO. The classic paradigm predicts that compensatory systemic vasoconstriction with high systemic vascular resistance (SVR) should occur in response to the depression of CO (Figure 1).9 Figure 1. Classic shock paradigm, as illustrated by S. Hollenberg, is shown in black. The influence of the inflammatory response syndrome initiated by a large MI is illustrated in red. LVEDP indicates left ventricular end-diastolic pressure. Reprinted with permission from Harrison’s Principles of Internal Medicine .9 Autopsy studies have shown that the pathological basis of CS is extensive MI. Varying pathological stages of infarction confirm the stuttering and progressive …