Prognosis in cardiogenic shock after acute myocardial infarction in the intervencional era

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Abstract

Objectives. The purpose of this study is to describe the outcome in cardiogenic shock treated with aggressive reperfusion therapy and to identify factors predictive of in-hospital and long-term mortality.

Background. Cardiogenic shock is the most common cause of death in patients admitted to the coronary care unit. Although studies have reported lower mortality rates in shock treated with angioplasty, few studies have described a cohort of patients with shock who were not selected because they were most likely to benefit from reperfusion therapy.

Methods. A consecutive series of 200 patients admitted with acute myocardial infarction complicated by cardiogenic shock were studied.

Results. The in-hospital mortality rate was 53%. Variables with significant univariable association with in-hospital death included patency of the intarct-related artery, patient age, lowest cardiac index, highest arteriovenous oxygen difference and left main coronary artery disease. The most important independent predictors of in-hospital death were patency of the Infarct-related artery, cardiac Index and peak creatine kinase, MB fraction. The mortality rate in patients with patent infarct-related arteries was 33% versus 75% in those with closed arteries and 84% in those in whom arterial patency was unknown. Patients who survived to hospital discharge were followed up for a median of 2 years, with a mortality rate of 18% after 1 year. The best descriptors of the relation between these variables and postdischarge mortality included age, peak creatine kinase, ejection fraction and patency of the infarct-related artery.

Conclusions. In a large consecutive series of patients with cardiogenic shock with complete follow-up, patency of the infarclrelated artery was most strongly associated with in-hospital and long-term mortality. This finding supports an aggressive Interventional strategy in patients with cardiogenic shock.

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This study was supported by Research Grants HL-17670 and HL-36587 from the National Heart, Lung, and Blood Institute, National Institute of Health. Bethesda, Maryland; Research Grants HS-05635 and HS-06503 from the Agency for Health Care Policy and Research, Rockville, Maryland, and grams from the Andrew W. Mellon Foundation, New York. New York, the Robert Wood Johnson Foundation. Princeton, New Jersey and the Nalional Library of Medicine, Bethesda (IAIMS Grant LM04613). This work was presented in part at the 40th Annual Scientific Session of the American Collegs of Cardiology, Atlanta, Georgia, March 1991.