CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Carolyn S.P. Lam, MBBS and
Margaret M. Redfield, MD*
* Mayo Clinic and Foundation, Cardiovascular Research, 200 First Street SW, Rochester, Minnesota 55905 (Email: redfield.margaret{at}mayo.edu).
We appreciate these insightful comments on our paper (1) and fully agree that mitral regurgitation can importantly contribute to the development of pulmonary hypertension in left-sided heart failure. As demonstrated in heart failure with reduced ejection fraction (2,3), hemodynamically significant mitral regurgitation can cause left atrial volume and pressure overload with resultant increases in pulmonary artery systolic pressure independent of left ventricular filling pressures. As noted in the Methods section (1), in our sample of heart failure with preserved ejection fraction (HFpEF), patients with hemodynamically significant (greater than moderate) mitral regurgitation were excluded in accordance with American College of Cardiology/American Heart Association guidelines for the diagnosis of HFpEF (4). In our hypertensive control group from the general community, clinically significant mitral valve disease was exceedingly rare (n = 2, 0.4%). Thus, we conclude that mitral regurgitation at rest did not contribute to the development of pulmonary hypertension in our sample.
One could speculate that hemodynamic stress during periods of hypertension or exercise could produce intermittent mitral regurgitation and contribute to the development of pulmonary hypertension. However, we excluded patients with intrinsic valve disease (mitral valve prolapse, and so on) who would be susceptible to stress-induced worsening of mitral regurgitation. Further, in contrast to heart failure with reduced ejection fraction, the lack of ventricular dilation in HFpEF would make it unlikely for significant "functional" mitral regurgitation to develop. We did not exclude patients with coronary artery disease, which could cause ischemic mitral regurgitation with stress. Hence, while we agree that mitral regurgitation can contribute to pulmonary hypertension in heart failure patients, it would seem unlikely to be a major contributor in this cohort.
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References
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1. Lam CSP, Roger VL, Rodeheffer RJ, Borlaug BA, Enders FT, Redfield MM. Pulmonary hypertension in heart failure with preserved ejection fraction: a community-based study J Am Coll Cardiol 2009;53:1119-1123.[Abstract/Free Full Text]2. Enriquez-Sarano M, Rossi A, Seward JB, Bailey KR, Tajik AJ. Determinants of pulmonary hypertension in left ventricular dysfunction J Am Coll Cardiol 1997;29:153-159.[Abstract] 3. Tumminello G, Lancellotti P, Lempereur M, D'Orio V, Pierard LA. Determinants of pulmonary artery hypertension at rest and during exercise in patients with heart failure Eur Heart J 2007;28:569-574.[Abstract/Free Full Text] 4. Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines J Am Coll Cardiol 2009;53:e1-e90.[Free Full Text]
Related Article
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Pulmonary Hypertension in Heart Failure With Preserved Ejection Fraction: Any Pathophysiological Role of Mitral Regurgitation
- Marco Guazzi
J. Am. Coll. Cardiol. 2009 54: 1191-1192.
[Full Text]
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