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 culturepositive 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 timedependent model, adjusted for age, showed that culturepositive 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.