Systemic inflammatory response syndrome after acute myocardial infarction complicated by cardiogenic shock

The role of inflammation in patients with coronary artery disease is emerging. We sought to assess the profile and outcomes of patients with a clinical syndrome of severe systemic inflammation that led to a diagnosis of suspected sepsis in the setting of acute myocardial infarction complicated by cardiogenic shock (CS).

Patients enrolled in the randomized SHOCK (SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK) trial (n = 302) were divided into those with clinical signs of severe systemic inflammation (eg, fever [94%] or leukocytosis [72%]) that led to a diagnosis of suspected sepsis (n = 54 [18%]) and those without suspected sepsis (controls; n = 243 [80%]). The patients with suspected sepsis were then further subdivided into those who were considered to be potentially infectious (positive culture result ["culture-positive"]; n = 40) and those who were not (negative culture result ["culture-negative"]; n = 14).

Severe systemic inflammation was diagnosed 4 and 2 days after the onset of CS in culture-positive and culture-negative patients, respectively. Patients who developed systemic inflammation tended to be younger (P = .05) and to have lower systemic vascular resistance (SVR) near the onset of CS (P = .006). Many culture-positive patients (40%) had undergone coronary artery bypass graft surgery. However, the lower the initial SVR, the higher the risk of developing culture-positive systemic inflammation (P = .01), even after controlling for age and coronary artery bypass graft surgery. A time-dependent model, adjusted for age, showed that culture-positive patients were at significantly higher risk for death than were controls (hazard ratio, 2.22; 95% confidence interval, 1.32-3.76; P = .008).

Almost one fifth of patients with acute myocardial infarction complicated by CS showed clinical signs of severe systemic inflammation, and those who were culture-positive for sepsis had twice the risk of death. The observation of lower SVR at the onset of shock in patients who subsequently had culture-positive systemic inflammation suggests that inappropriate vasodilation may play an important role in the pathogenesis and persistence of shock and in the risk of infection.