No abstract

No abstract

Our findings indicate that despite its beneficial hemodynamic actions, long-term therapy with oral milrinone increases the morbidity and mortality of patients with severe chronic heart failure. The mechanism by which the drug exerts its deleterious effects is unknown.

ONGESTIVE HEART FAILURE(CHF) is a clinical syndrome defined by characteristic symptoms and physical findings. Echocardiography is often performed in patients with CHF to measure the ejection fraction (EF) and determine if systolic function is reduced, systolic CHF or preserved, diastolic CHF. Comprehensive Doppler echocardiography can now characterize diastolic function directly in addition to measurement of the EF.Cardiovascular diseases (CVDs) such as hypertension, coronary artery disease, and cardiomyopathies often lead to systolic and diastolic ventricular dysfunction. Nearly all patients with systolic dysfunction have some degree of concomitant diastolic dysfunction, specifically, impaired relaxation and variable decreases in ventricular compliance. 1 However, it is now recognized that patients with normal EF can display marked impairment in diastolic function (isolated diastolic dysfunction). 2 Clinically, it has been recognized that some patients with advanced systolic dysfunction remain free of symptoms of CHF. Thus, individuals may have systolic dysfunction without receiv-

Objectives To define the prevalence, severity and significance of pulmonary hypertension (PH) in heart failure with preserved ejection fraction (HFpEF) in the general community. Background While HFpEF is known to cause PH, its development is highly variable. Population-based data are lacking, and the relative contribution of pulmonary venous versus pulmonary arterial hypertension to PH in HFpEF is unknown. We hypothesized that PH would be a marker of symptomatic pulmonary congestion, distinguishing HFpEF from preclinical hypertensive heart disease (HTN). Methods Population-based study of 244 HFpEF patients (76±13y; 45%male) followed from Doppler echocardiography over 3 years. Controls were 719 adults with HTN without HF (66±10y; 44%male). Pulmonary artery systolic pressure (PASP) was derived from the tricuspid regurgitation velocity and PH defined as PASP>35 mmHg. Pulmonary capillary wedge pressure (PCWP) was estimated from E/e’. Results In HFpEF, PH was present in 83% and median (25th, 75th percentile) PASP was 48 (37, 56) mmHg. PASP increased with PCWP (r=0.21; p<0.007). Adjusting for PCWP, PASP was higher in HFpEF than HTN (p<0.001). PASP distinguished HFpEF from HTN with an area under receiver-operating curve of 0.91 (p<0.001) and strongly predicted mortality in HFpEF (hazard ratio=1.3 per 10 mmHg; p<0.001). Conclusions PH is highly prevalent and often severe in HFpEF. While pulmonary venous hypertension contributes to PH, it does not fully account for the severity of PH in HFpEF, suggesting that a component of pulmonary arterial hypertension also contributes. The potent effect of PASP on mortality lends support for therapies aimed at pulmonary arterial hypertension in HFpEF.