CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Micha T. Maeder, MD and
David M. Kaye, MD, PhD*
* Baker IDI Heart and Diabetes Institute, Alfred Hospital, P.O. Box 6492, St Kilda Road Central, Melbourne 8008 Victoria, Australia (Email: David.kaye{at}bakeridi.edu.au).
In an attempt to further reconcile the paradoxical finding of a normal left ventricular ejection fraction (LVEF) in patients with heart failure with normal ejection fraction (HFNEF), Dr. MacIver proposes that left ventricular (LV) hypertrophy per se augments wall thickening and thereby maintains LVEF in the presence of impaired contractility. While conceptually this may be plausible, the evidence for such a mechanism appears limited. Contrary to this proposition, previous studies have demonstrated that in the presence of lower longitudinal systolic myocardial velocity and variable changes in radial strain, patients with HFNEF or subclinical LV diastolic dysfunction have preserved LVEF in the absence of a significant rise in LV mass (1,2). The mechanism by which this apparent compensation occurs is not clear; however, it has been proposed that preserved circumferential strain and LV twist may contribute (2). These changes may be the result of the relative hypertrophy of mid-wall myocytes, realignment of myocytes, or alterations in the pattern of mechanical activation of fibers of varying spatial orientation resulting in changes in their afterload according to the time of contraction.
Whereas the presence of LV hypertrophy, for example in hypertrophic cardiomyopathy, may be associated with a normal or even high LVEF, studies suggest that wall thickening is reduced and that the preserved LVEF is a function of a smaller LV end diastolic volume (3).
Currently, the key clinical challenge in each patient with a diagnosis of HFNEF is to develop a comprehensive understanding of the pathophysiologic basis of their symptoms on an individual basis. In many cases, it may be difficult to resolve whether symptoms are due to intrinsic LV dysfunction, or whether additional factors such as impaired vasodilatory response, impaired chronotropic competence, fluid overload, ventriculo-vascular mismatch (4), or as suggested very recently, abnormal pulmonary vascular reactivity (5) might play a role. The adoption of other assessment modalities may also be required, including a formal evaluation of the hemodynamic response to exercise to shed light on the pathophysiology of this poorly understood and difficult to manage disease.
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1. Wang J, Khoury DS, Yeh Y, Torre-Amione G, Nagueh SF. Preserved left ventricular twist and circumferential deformation, but depressed longitudinal and radial deformation in patients with diastolic heart failure Eur Heart J 2008;29:1283-1289.[Abstract/Free Full Text]2. Fang ZY, Leano R, Marwick TH. Relationship between longitudinal and radial contractility in subclinical diabetic heart disease Clin Sci (Lond) 2004;106:53-60.[Medline] 3. Yamazaki T, Suzuki J, Shimamoto R, et al. Focalized contractile impairment in hypertrophied myocardium proven in consideration of wall stress in patients with hypertrophic cardiomyopathy Int Heart J 2006;47:247-258.[CrossRef][Web of Science][Medline] 4. Maeder MT, Kaye DM. Heart failure with normal left ventricular ejection fraction J Am Coll Cardiol 2009;53:905-918.[Abstract/Free Full Text] 5. 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;53:1119-1126.[Abstract/Free Full Text]
Related Article
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Heart Failure With Normal Left Ventricular Ejection Fraction May Be Due to Systolic Dysfunction
- David H. MacIver
J. Am. Coll. Cardiol. 2009 54: 488.
[Full Text]
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