Author + information
- Received July 16, 2004
- Revision received September 28, 2004
- Accepted October 4, 2004
- Published online July 19, 2005.
- Martin Briand, MS⁎,
- Jean G. Dumesnil, MD, FACC⁎,
- Lyes Kadem, Eng, PhD⁎,†,
- Antonio G. Tongue, MD⁎,
- Régis Rieu, Eng, PhD†,
- Damien Garcia, Eng, PhD‡ and
- Philippe Pibarot, DVM, PhD, FACC⁎,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Philippe Pibarot, Laval Hospital, 2725 Chemin Sainte-Foy, Sainte-Foy, Quebec, Canada, G1V-4G5
Objectives We sought to determine to what extent systemic arterial compliance (SAC) might impact on afterload and left ventricular (LV) function in patients with aortic stenosis (AS).
Background Although AS and reduced SAC may often coexist in the same patient, their relative impact on LV function is not well understood.
Methods Systemic arterial compliance was calculated as the ratio of stroke volume index to arterial pulse pressure in 208 patients with at least moderate AS. As a measure of global afterload, we calculated the valvulo-arterial impedance (Zva), which theoretically accounts for the effects of both AS and SAC.
Results Patients were divided into four groups: group 1, moderate AS and normal SAC (n = 77; 37%); group 2, moderate AS and low SAC (n = 50; 24%); group 3, severe AS and normal SAC (n = 45; 22%); and group 4, severe AS and low SAC (n = 36; 17%). The prevalences of LV diastolic and systolic dysfunction were 60% and 6% in group 1, 86% and 12% in group 2, 82% and 16% in group 3, and 94% and 31% in group 4. In multivariate analysis excluding Zva, energy loss index and SAC were both independent predictors of LV dysfunction, but when Zvawas entered into the analyses, it became the only hemodynamic variable to be independently associated with LV dysfunction.
Conclusions Reduced SAC is a frequent occurrence in elderly patients with AS, where it independently contributes to increased afterload and decreased LV function. Systemic arterial compliance should be taken into consideration when evaluating these patients with regard to diagnosis and treatment.
This work was supported by a grant of the Canadian Institutes of Health Research (MOP-10929), Ottawa, Ontario, Canada. Dr. Pibarot is the director of the Canada Research Chair in Valvular Heart Diseases, Canadian Institutes of Health Research, Ottawa, Ontario, Canada. Mr. Briand is the recipient of a PhD student scholarship from the Fonds de Recherche en Santé du Québec, Montreal, Quebec, Canada.
- Received July 16, 2004.
- Revision received September 28, 2004.
- Accepted October 4, 2004.
- American College of Cardiology Foundation