Systemic Inflammatory Response Syndrome After Acute Myocardial Infarction Complicated by Cardiogenic Shock

BACKGROUND: 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). METHODS: 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). RESULTS: 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). CONCLUSIONS: 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.