Author + information
- Received August 20, 2008
- Revision received November 17, 2008
- Accepted November 30, 2008
- Published online March 31, 2009.
- Carolyn S.P. Lam, MBBS*,†,
- Véronique L. Roger, MD, MPH*,
- Richard J. Rodeheffer, MD*,
- Barry A. Borlaug, MD*,
- Felicity T. Enders, PhD‡ and
- Margaret M. Redfield, MD*,* ()
- ↵*Reprint requests and correspondence:
Dr. Margaret M. Redfield, 200 First Street SW, Rochester, Minnesota 55905
Objectives This study sought to define the prevalence, severity, and significance of pulmonary hypertension (PH) in heart failure with preserved ejection fraction (HFpEF) in the general community.
Background Although HFpEF is known to cause PH, its development is highly variable. Community-based data are lacking, and the relative contribution of pulmonary venous versus pulmonary arterial hypertension (HTN) to PH in HFpEF is unknown. We hypothesized that PH would be a marker of symptomatic pulmonary congestion, distinguishing HFpEF from pre-clinical hypertensive heart disease.
Methods This community-based study of 244 HFpEF patients (age 76 ± 13 years; 45% male) was followed up using Doppler echocardiography over 3 years. Control subjects were 719 adults with HTN without HF (age 66 ± 10 years; 44% male). Pulmonary artery systolic pressure (PASP) was derived from the tricuspid regurgitation velocity and PH defined as PASP >35 mm Hg. Pulmonary capillary wedge pressure (PCWP) was estimated from the ratio of early transmitral flow velocity to early mitral annular diastolic velocity.
Results In HFpEF, PH was present in 83% and the median (25th, 75th percentile) PASP was 48 (37, 56) mm Hg. PASP increased with PCWP (r = 0.21; p < 0.007). Adjusting for PCWP, PASP was higher in HFpEF than HTN (p < 0.001). The PASP distinguished HFpEF from HTN with an area under the receiver-operating characteristic curve of 0.91 (p < 0.001) and strongly predicted mortality in HFpEF (hazard ratio: 1.3 per 10 mm Hg; p < 0.001).
Conclusions PH is highly prevalent and often severe in HFpEF. Although pulmonary venous HTN contributes to PH, it does not fully account for the severity of PH in HFpEF, suggesting that a component of pulmonary arterial HTN also contributes. The potent effect of PASP on mortality lends support for therapies aimed at pulmonary arterial HTN in HFpEF.
Supported by National Institutes of Health grants HL63281-4, HL72435-2, and HL55502-7.
- Received August 20, 2008.
- Revision received November 17, 2008.
- Accepted November 30, 2008.
- American College of Cardiology Foundation