doi: 10.1161/CIRCULATIONAHA.107.714394
(Circulation. 2007;116:e562.)
© 2007 American Heart Association, Inc.
Correspondence |
Letter by Tartière et al Regarding Article, "Cardiac Structure and Ventricular–Vascular Function in Persons With Heart Failure and Preserved Ejection Fraction From Olmsted County, Minnesota"
Department of Physiology, Lariboisière Hospital, Assistance Publique–Hôpitaux de Paris, Paris, France
Department of Cardiovascular Surgery, Bichat Hospital, Assistance Publique–Hôpitaux de Paris, Paris, France
Department of Cardiology, Lariboisière Hospital, Assistance Publique–Hôpitaux de Paris, Paris, France
We read with great interest the article by Lam et al1 comparing cardiac structure and ventricular–vascular function in subjects with heart failure and normal ejection fraction, hypertensive subjects, and controls. The main result of this noninvasive study is that end-systolic elastance, effective arterial elastance,2 and total arterial compliance do not differ between heart failure subjects and hypertensive subjects, but that heart failure subjects show lower end-diastolic volume, cardiac index, and relaxation capacity and greater diastolic stiffness than do hypertensive subjects. This study highlights major issues in the comprehension of heart failure. Nevertheless, we think that the noninvasive study contains some limitations that could modify the interpretation of the results.
First, 2 of the major determinants of effective arterial elastance and total arterial compliance used by Lam et al1 are brachial systolic pressure and pulse pressure, respectively. Their estimation of the end-systolic pressure is based on the product of brachial systolic blood pressure x0.9, whatever the group, and to assess arterial compliance, brachial pulse pressure is used as an estimate of aortic pulse pressure. These estimations assume that pulse amplification is equivalent among groups and that pulse pressure and systolic blood pressure are the same from the aorta to the brachial artery, which is probably inaccurate, according to previously published results that showed pulse pressure amplification ranges from 1.09 to 1.67.3
Second, end-systolic elastance is estimated using the noninvasive single-beat method.2 Two of the determinants of this parameter are brachial diastolic and end-systolic pressure.2 If brachial diastolic blood pressure is an acceptable surrogate for central diastolic pressure, end-systolic pressure is probably overestimated in both non–heart failure groups because of a different pulse amplification.
Third, Lam et al do not discuss pressure reflection as a source of increased vascular load. This part of the load has been related to cardiovascular damage and prognosis and is not assessed by effective arterial elastance and total arterial compliance.4
Because effective arterial elastance, total arterial compliance, and end-systolic elastance were probably overestimated differently among groups in this study, we think that this study cannot support the absence of a stiffer ventricular–vascular phenotype in heart failure with normal ejection fraction.
In summary, the authors are to be congratulated for having made such a comprehensive study in such a large population; given these methodologic limitations, however, we think that their conclusions are to be taken with caution, and it is likely, as they suggest, that other studies using the carotid pressure5 or the estimated aortic pressure, or made during exercise5 are warranted to confirm these results.
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Acknowledgments |
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Disclosures
None.
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References |
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 Top References |
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1. Lam CS, Roger VL, Rodeheffer RJ, Bursi F, Borlaug BA, Ommen SR, Kass DA, Redfield MM. Cardiac structure and ventricular–vascular function in persons with heart failure and preserved ejection fraction from Olmsted County, Minnesota. Circulation. 2007; 115: 1982–1990.
2. Chen CH, Fetics B, Nevo E, Rochitte CE, Chiou KR, Ding PA, Kawaguchi M, Kass DA. Noninvasive single-beat determination of left ventricular end-systolic elastance in humans. J Am Coll Cardiol. 2001; 38: 2028–2034.
3. Wilkinson IB, Franklin SS, Hall IR, Tyrrell S, Cockcroft JR. Pressure amplification explains why pulse pressure is unrelated to risk in young subjects. Hypertension. 2001; 38: 1461–1466.
4. O’Rourke MF. From theory into practice: arterial haemodynamics in clinical hypertension. J Hypertens. 2002; 20: 1901–1915.[CrossRef][Medline] [Order article via Infotrieve]
5. Tartière JM, Tartière-Kesri L, Logeart D, Beauvais F, Cohen-Solal A. Moderate exercise results in a major increase of proximal arterial stiffness in diastolic heart failure. Circulation. 2006; 114 (Suppl II): II-815. Abstract.
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