ABSTRACT
The development of heart failure or left ventricular (LV) systolic dysfunction following acute coronary syndromes (ACS) remains prevalent despite major advances in the acute management of ACS. Many patients develop transient pulmonary congestion after ACS and have it resolve quickly, only to emerge years later as chronic heart failure. Patients may develop signs and symptoms of heart failure on admission ranging from mild-tomoderate symptoms to cardiogenic shock, or they may develop clinical heart failure later, sometimes years after the index event [1]. Data from several large-scale clinical trials have suggested that up to one-third of patients developed some degree of mild-to-moderate heart failure within 30 days following an acute ST-segment elevation myocardial infarction (STEMI) [2]. In the Second National Registry of Myocardial Infarction (NRMI-2), 19% of patients with acute STEMI had signs and symptoms of heart failure on admission [3]. More recently, the Global Registry of Acute Coronary Events (GRACE) registry extended these findings to the entire spectrum of ACS and demonstrated that new heart failure presentation occurred in 15% of patients with STEMI, 16% of patients with non-STEMI, and 9% of patients with unstable angina [4]. The latest data from the Valsartan in Acute Myocardial Infarction (VALIANT) Registry reported a much higher 24% incidence of postinfarction clinical heart failure and a 42% incidence of heart failure/LV systolic dysfunction in the 5,567 patients presenting with acute myocardial infarction [5]. What is more startling is that 18% patients with postinfarction LV systolic dysfunction had no overt signs and symptoms of heart failure. Recent data from the Cholesterol And Recurrent Events (CARE) trial further points out that postinfarction heart failure may occur in a time-dependent and linear pattern at a rate of 1.3% per year, with a direct consequence of a detectable interim myocardial infarction occurring in less than a quarter of postinfarction patients who subsequently develop heart failure [1]. These observations highlight the importance of a clinically silent reduction in LV function and its potential to associate with late heart failure from progressive LV remodeling at a time quite remote from the infarction. Recognition of such patients at an early point in time, prior to development of heart failure, would be a most attractive strategy to prevent heart failure. This is particularly
important now that we have therapies that reduce the progression from LV systolic dysfunction to chronic heart failure.
