Management and Outcomes of Type I and Type II Myocardial Infarction in Cardiogenic Shock

Abstract

BackgroundType I myocardial infarction (T1MI) or type II myocardial infarction (T2MI) have different underlying mechanisms; however, in the setting of cardiogenic shock (CS), it is not understood if patients experience resultantly different outcomes. The objective of this study was to determine clinical features, biomarker patterns, and outcomes in these subgroups. MethodsPatients from the CAPITAL-DOREMI trial presenting with acute myocardial infarction-associated CS (n = 103) were classified as T1MI (n = 61) or T2MI (n = 42). The primary endpoint was a composite of all-cause in-hospital mortality, cardiac arrest, the need for mechanical circulatory support, or initiation of renal replacement therapy at 30 days. Secondary endpoints were evaluated as individual components of the primary endpoint. ResultsPatients with T1MI CS did not have a higher incidence of the primary composite endpoint compared with T2MI CS (adjusted hazard ratio [HR], 1.63; 95% confidence interval [CI], 0.96-2.77; P = 0.07). Cardiac biomarkers including troponin I (P < 0.001), and creatine kinase levels (P = 0.001) were elevated in patients with T1MI CS compared with T2MI. Furthermore, patients with T1MI CS presented with decreased urine output (P = 0.01) compared with T2MI. Predictors of T2MI CS included nonischemic ventricular dysfunction (P = 0.002), atrial fibrillation (P = 0.02), and chronic obstructive pulmonary disease (P = 0.002). ConclusionsThere were no differences in adverse clinical outcomes between patients with T1MI and T2MI CS, although the events were numerically increased, and the sample size was small. Overall, this study provides a hypothesis-generating analysis regarding the clinical and biochemical outcomes in T1MI vs T2MI CS.