Response to Letter Regarding Article, “Cardiac Structure and Ventricular–Vascular Function in Persons With Heart Failure and Preserved Ejection Fraction From Olmsted County, Minnesota”
We appreciate the comments of Tartière et al on our study1 and agree that these are valid concerns about the noninvasive estimation of systolic vascular and ventricular stiffness. As acknowledged in our paper, “Although total vascular load and indirect measures of vascular stiffness were obtained here, further study is needed to evaluate more direct and perhaps regional measures of vascular stiffening and other assessments of arterial impedance and its impact such as characteristic impedance, wave reflections, and pulse-wave velocity.” Whereas effective arterial elastance, derived from the ratio of end-systolic pressure to stroke volume, is a useful index of total vascular load which, importantly, can be linked to measures of ventricular elastance in the assessment of vascular–ventricular coupling, there remains concern that arterial systems with very marked systolic wave reflections and wave transmission effects may be inadequately represented by this parameter. In the human validation study by Kelly et al,2 however, this noninvasive parameter demonstrated near-equivalency to the invasive parameter derived from arterial pressure–flow data over a wide range of systolic pressures and resistances, in normotensive and hypertensive subjects, young and old. The noninvasive determination of end-systolic elastance was similarly validated by Chen et al3 against the invasive gold standard in a spectrum of patients and disease conditions that ranged from noncardiac disease to heart failure and transplantation. On the basis of these previous data in wide spectra of patients, the noninvasive estimates were assumed to be similarly accurate in all 3 of our study groups. Any systematic deviation from true measurements based on central pressure was also equal among groups, because the measurements were made in a uniform manner regardless of group. Hence, the between-group comparisons are meaningful. Further, restricting the analysis to older patients, in whom one would expect to find the stiffest arterial systems, yielded consistent results (Table 3). Importantly, our data do in fact demonstrate systolic ventricular–vascular stiffening in patients with heart failure and normal ejection fraction compared with healthy controls. “Superimposed” worsening diastolic dysfunction was observed in patients with heart failure and normal ejection fraction, compared with hypertensive controls without heart failure, but that does not imply that the “underlying” systolic vascular–ventricular stiffening does not contribute to the pathophysiology of this syndrome.
In conclusion, we reiterate that our data do not exclude a role for increased vascular and ventricular systolic stiffening in patients with heart failure and normal ejection fraction. Recent4 and future work will help to define this role, particularly during exercise or other stressors in which systolic vascular–ventricular stiffening may lead to exaggerated hypertensive responses and further load-dependent diastolic dysfunction.
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.
Kelly RP, Ting C-T, Yang T-M, Liu C-P, Maughan WL, Chang M-S, Kass DA. Effective arterial elastance as index of arterial vascular load in humans. Circulation. 1992; 86: 513–521.
Tartière J, 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.