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Background: Exertional dyspnea is a frequent limiting symptom in patients with chronic heart failure. Furthermore, dyspnea and a plateau in VO2(oxygen consumption) at peak exercise often co-exist in chronic heart failure, especially in patients with severe regurgitant valvular heart disease(RVHD), their relevance to hemodynamics and subjective symptoms during exercise have not been fully understood. Objectives: The purpose of this study was to examine the determinant factor of exercise capacity in patients with RVHD. Methods: We performed a symptom-limited cardiopulmonary exercise test using a sitting cycle ergometer with right heart catheterization in 20 patients with severe RVHD. VO2 and hemodynamics were measured at rest and during exercise, and symptomatic end-point at peak exercise was evaluated by using Borg’s score. Results: Of the 20 patients, 11 attained a plateau in VO2 at peak exercise(Group 1). At peak exercise, pulmonary arterial pressure(PAP) was higher, and cardiac output(CO) and VO2 were lower in Group 1 than in patients without a plateau in VO2(Group 2)(mean PAP: 60±10 vs. 48±9 mm Hg, P=0.05; CO: 8.3±2.6 vs. 11.2±2.6 l/min, P=0.01; VO2: 1059±259 vs. 1359±328 ml/min,P=0.01). In Group 1, 6 patients complaining of dyspnea rather than leg fatigue at peak exercise had lower CO(7.1±1.8 vs. 9.7±3.0 l/min, P=0.05) and higher slope of mean PAP-CO relation(P-Q slope)(10.6±3.6 vs. 5.4±1.7, P=0.01), compared with the other 5 patients with leg fatigue. Conclusions: Development of pulmonary hypertension during exercise is the important limiting factor for exercise capacity in patients with RVHD. The limitation of increase in CO concomitant with pulmonary hypertension could be an important factor in the appearance of dyspnea.
Background: Exertional dyspnea is a frequent limiting symptom in patients with chronic heart failure. Furthermore, dyspnea and a plateau in VO2 (oxygen consumption) at peak exercise often co-exist in chronic heart failure, especially in patients with severe regurgitant valvular heart disease RVHD), their relevance to hemodynamics and subjective symptoms during exercise have not been fully understood. Objectives: The purpose of this study was to examine the determinant factor of exercise capacity in patients with RVHD. Methods: We performed a symptom-limited cardiopulmonary exercise test using a sitting cycle ergometer with right heart catheterization in 20 patients with severe RVHD. VO2 and hemodynamics were measured at rest and during exercise, and symptomatic end-point at peak exercise was evaluated by using Borg’s score. Results: Of the 20 patients, 11 attained a plateau in VO2 at peak exercise (Group 1). At peak exercise, pulmonary arterial pressure (PAP) was higher, and cardiac outpu t (CO) and VO2 were lower in Group 1 than in patients without a plateau in VO2 (Group 2) (mean PAP: 60 ± 10 vs. 48 ± 9 mm Hg, P = 0.05; CO: 8.3 ± 2.6 vs. 11.2 ± 2.6 l / min P = 0.01; VO2: 1059 ± 259 vs. 1359 ± 328 ml / min, P = 0.01). In Group 1, 6 patients complaining of dyspnea rather than leg fatigue at peak exercise had lower CO (7.1 ± 1.8 vs. 9.7 ± 3.0 l / min, P = 0.05) and higher slope of mean PAP-CO relation (PQ slope) (10.6 ± 3.6 vs. 5.4 ± 1.7, P = 0.01) leg fatigue. Conclusions: Development of pulmonary hypertension during exercise is the important limiting factor for exercise capacity in patients with RVHD. The limitation of increase in CO concomitant with pulmonary hypertension could be an important factor in the appearance of dyspnea.