BackgroundLimited information is available on the contemporary and potentially changing trends in the incidence, management, and outcomes of cardiogenic shock complicating ST‐elevation myocardial infarction (STEMI).Methods and ResultsWe queried the 2003–2010 Nationwide Inpatient Sample databases to identify all patients ≥40 years of age with STEMI and cardiogenic shock. Overall and age‐, sex‐, and race/ethnicity‐specific trends in incidence of cardiogenic shock, early mechanical revascularization, and intra‐aortic balloon pump use, and inhospital mortality were analyzed. From 2003 to 2010, among 1 990 486 patients aged ≥40 years with STEMI, 157 892 (7.9%) had cardiogenic shock. The overall incidence rate of cardiogenic shock in patients with STEMI increased from 6.5% in 2003 to 10.1% in 2010 (Ptrend<0.001). There was an increase in early mechanical revascularization (30.4% to 50.7%, Ptrend<0.001) and intra‐aortic balloon pump use (44.8% to 53.7%, Ptrend<0.001) in these patients over the 8‐year period. Inhospital mortality decreased significantly, from 44.6% to 33.8% (Ptrend<0.001; adjusted OR, 0.71; 95% CI, 0.68 to 0.75), whereas the average total hospital cost increased from $35 892 to $45 625 (Ptrend<0.001) during the study period. There was no change in the average length of stay (Ptrend=0.394). These temporal trends were similar in patients <75 and ≥75 years of age, men and women, and across each racial/ethnic group.ConclusionsThe incidence of cardiogenic shock complicating STEMI has increased during the past 8 years together with increased use of early mechanical revascularization and intra‐aortic balloon pumps. There has been a concomitant decrease in risk‐adjusted inhospital mortality, but an increase in total hospital costs during this period.

Chronic diuretic use was associated with increased long-term mortality and hospitalizations in a wide spectrum of ambulatory chronic systolic and diastolic HF patients. The findings of the current study challenge the wisdom of routine chronic use of diuretics in HF patients who are asymptomatic or minimally symptomatic without fluid retention, and are on complete neurohormonal blockade. These findings, based on a non-randomized design, need to be further studied in randomized trials.

Background-About half of the 5 million heart failure patients in the United States have diastolic heart failure (clinical heart failure with normal or near-normal ejection fraction). Except for candesartan, no drugs have been tested in randomized clinical trials in these patients. Although digoxin was tested in an appreciable number of diastolic heart failure patients in the Digitalis Investigation Group ancillary trial, detailed findings from this important study have not previously been published. Methods and Results-Ambulatory chronic heart failure patients (nϭ988) with normal sinus rhythm and ejection fraction Ͼ45% (median, 53%) from the United States and Canada (1991 to 1993) were randomly assigned to digoxin (nϭ492) or placebo (nϭ496). During follow-up with a mean length of 37 months, 102 patients (21%) in the digoxin group and 119 patients (24%) in the placebo group (hazard ratio [HR], 0.82; 95% confidence interval [CI], 0.63 to 1.07; Pϭ0.136) experienced the primary combined outcome of heart failure hospitalization or heart failure mortality. Digoxin had no effect on all-cause or cause-specific mortality or on all-cause or cardiovascular hospitalization. Use of digoxin was associated with a trend toward a reduction in hospitalizations resulting from worsening heart failure (HR, 0.79; 95% CI, 0.59 to 1.04; Pϭ0.094) but also a trend toward an increase in hospitalizations for unstable angina (HR, 1.37; 95% CI, 0.99 to 1.91; Pϭ0.061). Conclusions-In ambulatory patients with chronic mild to moderate diastolic heart failure and normal sinus rhythm receiving angiotensin-converting enzyme inhibitor and diuretics, digoxin had no effect on natural history end points such as mortality and all-cause or cardiovascular hospitalizations.

The burden of heart failure with preserved ejection fraction (HFpEF) is considerable and is projected to worsen. To date, there are no approved therapies available for reducing mortality or hospitalizations for these patients. The pathophysiology of HFpEF is complex and includes alterations in cardiac structure and function, systemic and pulmonary vascular abnormalities, end-organ involvement, and comorbidities. There remain major gaps in our understanding of HFpEF pathophysiology. To facilitate a discussion of how to proceed effectively in future with development of therapies for HFpEF, a meeting was facilitated by the FDA and included representatives from academia, industry and regulatory agencies. This document summarizes the proceedings from this meeting.