Edgar Argulian1, Vikram Agarwal2, Harikrishna Makani2, Eyal Herzog2, Farooq A Chaudhry3. 1. Division of Cardiology, Mount Sinai St Luke's Hospital, Mt Sinai Health System, New York, New York. Electronic address: earguli@alum.emory.edu. 2. Division of Cardiology, Mount Sinai St Luke's Hospital, Mt Sinai Health System, New York, New York. 3. Zena and Michael A. Wiener Cardiovascular Institute, Mt Sinai Hospital, Mt Sinai Health System, New York, New York.
Abstract
BACKGROUND: Ventricular-arterial stiffening is a part of the aging process that is amplified by various comorbidities. It affects normal cardiovascular reserve and limits exercise capacity. The aim of this study was to explore the association of physiologic determinants of ventricular-arterial interaction with exercise capacity in patients referred for exercise echocardiography with exertional dyspnea. METHODS: A total of 93 patients with exertional dyspnea without chest pain were evaluated using the Bruce protocol. Patients with left ventricular ejection fractions < 50% and those with exercise-induced myocardial ischemia were excluded. Poor exercise tolerance was defined as inability to achieve 8 metabolic equivalents. RESULTS: Thirty-seven patients (40%) had poor exercise tolerance. These patients were older (mean age, 60 vs 54 years, P = .01), more likely to carry the diagnosis of hypertension (84% vs 41%, P < .01), and more likely to be treated with antihypertensive medications. In multivariate logistic regression analysis, left atrial volume index (P = .04) and arterial elastance (P < .01) were significant predictor of poor exercise capacity, while left ventricular ejection fraction, tissue Doppler indices, and global longitudinal strain were not significant. CONCLUSIONS: Effective arterial elastance determined noninvasively before stress echocardiography appears to be an independent predictor of exercise tolerance in patients with exertional dyspnea.
BACKGROUND: Ventricular-arterial stiffening is a part of the aging process that is amplified by various comorbidities. It affects normal cardiovascular reserve and limits exercise capacity. The aim of this study was to explore the association of physiologic determinants of ventricular-arterial interaction with exercise capacity in patients referred for exercise echocardiography with exertional dyspnea. METHODS: A total of 93 patients with exertional dyspnea without chest pain were evaluated using the Bruce protocol. Patients with left ventricular ejection fractions < 50% and those with exercise-induced myocardial ischemia were excluded. Poor exercise tolerance was defined as inability to achieve 8 metabolic equivalents. RESULTS: Thirty-seven patients (40%) had poor exercise tolerance. These patients were older (mean age, 60 vs 54 years, P = .01), more likely to carry the diagnosis of hypertension (84% vs 41%, P < .01), and more likely to be treated with antihypertensive medications. In multivariate logistic regression analysis, left atrial volume index (P = .04) and arterial elastance (P < .01) were significant predictor of poor exercise capacity, while left ventricular ejection fraction, tissue Doppler indices, and global longitudinal strain were not significant. CONCLUSIONS: Effective arterial elastance determined noninvasively before stress echocardiography appears to be an independent predictor of exercise tolerance in patients with exertional dyspnea.
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