Abnormal blood-pressure response to exercise and oxygen consumption in patients with hypertrophic cardiomyopathy. |
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Authors: | Quirino Ciampi Sandro Betocchi Maria Angela Losi Adele Ferro Alberto Cuocolo Raffaella Lombardi Bruno Villari Massimo Chiariello |
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Affiliation: | Department of Clinical Medicine, Federico II University School of Medicine, Naples, Italy. |
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Abstract: | BACKGROUND: Abnormal blood-pressure response during exercise occurs in about one third of patients with hypertrophic cardiomyopathy (HCM), and it has been associated with a high risk of sudden cardiac death. We assessed the hemodynamics of exercise in HCM patients with abnormal blood-pressure response by using ambulatory radionuclide monitoring (VEST) of left-ventricular (LV) function, and exercise tolerance by oxygen consumption. METHODS: Twenty-two HCM patients underwent treadmill exercise during VEST monitoring. A cardiopulmonary exercise test was performed a few days after. The VEST data were averaged for 1 minute. Stroke volume, cardiac output, and systemic vascular resistance were expressed as percent of baseline. Exercise tolerance was assessed as maximal oxygen consumption. RESULTS: In eight HCM patients (36%) with an abnormal blood-pressure response, end-systolic volume increased more (52% +/- 21% vs 31% +/- 28%, P = .012), and the ejection fraction (-31% +/- 17% vs -14% +/- 22%, P = .029) and stroke volume (-21% +/- 21% vs 3% +/- 28%, P = .026) fell more, than in patients with normal response. Cardiac output increased less in the former patients (49% +/- 44% vs 94% +/- 44%, P = .012). Systemic vascular resistance decreased similarly, irrespective of blood-pressure response (-28% +/- 26% vs -34% +/- 26%, P = N.S.). Percent of maximal predicted oxygen consumption was lower in HCM patients with an abnormal blood-pressure response (63% +/- 11% vs 78% +/- 15%, P = .025). CONCLUSIONS: In HCM patients, abnormal blood-pressure response was associated with exercise-induced LV systolic dysfunction and impairment in oxygen consumption. This may cause hemodynamic instability, associated with a high risk of sudden cardiac death. |
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