Acute effect of percutaneous transvenous mitral commissurotomy on ventilatory and hemodynamic responses to exercise. Pathophysiological basis for early symptomatic improvement.

BACKGROUND: Improvement of exertional dyspnea occurs immediately after percutaneous transvenous mitral commissurotomy (PTMC), but the pathophysiological basis for this early symptomatic improvement has not been elucidated. METHODS AND
RESULTS: Exercise hemodynamic measurement and exercise ventilatory measurement with arterial blood gas analysis were performed in 21 patients aged 50.4 +/- 9.5 years (mean +/- SD) with symptomatic mitral stenosis before and a few days after PTMC. Exercise ventilatory measurement were also performed in 14 normal control subjects aged 48.9 +/- 4.9 years. After PTMC, mitral valve area increased (from 1.0 +/- 0.3 to 1.7 +/- 0.3 cm2, P < .001), mean mitral gradient (from 12.2 +/- 5.2 to 5.2 +/- 2.2 mm Hg, P < .001), and mean left atrial pressure (from 18.7 +/- 6.1 to 12.1 +/- 4.0 mm Hg, P < .001) decreased. All patients experienced significant symptomatic improvement soon after PTMC. Comparison of hemodynamic parameters at the same ergometer work rate showed a significant decrease in pulmonary artery systolic pressure (from 77 +/- 18 to 67 +/- 14 mm Hg, P < .001) and diastolic pressure (from 36 +/- 10 to 28 +/- 7 mm Hg, P < .001) and a significant increase in cardiac output (from 6.4 +/- 1.4 to 8.1 +/- 1.9 L/min, P < .001). Despite the improvement in exercise hemodynamics and symptoms, exercise capacity determined by peak oxygen uptake (from 18.0 +/- 2.9 to 18.6 +/- 3.1 mL.kg-1 x min-1) and anaerobic threshold (from 11.7 +/- 2.4 to 12.0 +/- 2.4 mL.kg-1 x min-1) remained unchanged. Excessive exercise ventilation, as assessed by the slope of the regression line between expired minute ventilation and carbon dioxide output, decreased significantly from 37.2 +/- 6.7 to 33.9 +/- 5.8 (P < .001), but remained significantly higher than that in the normal subjects (27.9 +/- 3.6, P < .01). The ratio of total dead space to tidal volume and total dead space per breath during exercise decreased significantly after PTMC (P < .05). The change in excessive exercise ventilation after PTMC was correlated with the change in dead space to tidal volume ratio (r = .59).
CONCLUSIONS: Significant relief of exertional dyspnea immediately after PTMC is not accompanied by an improvement in exercise capacity. A decrease in excessive ventilation due to a decrease in physiological dead space resulting from hemodynamic improvement partly contributes to the early relief of symptoms after PTMC. However, lung compliance, which was not measured in the present study, may have changed after PTMC. This change may also contribute to the symptomatic improvement.