Background: The epidemiology of rheumatic mitral disease has changed considerably in the last decade with patients presenting at older age. We aimed to determine the mechanisms responsible for reduced effort capacity in older patients with rheumatic mitral stenosis (MS). Combined stress echocardiography and cardio-pulmonary stress tests are able to divide effort into four well defined activity levels (rest, unloaded, anaerobic threshold [AT], and peak), allowing non invasive assessment of cardiac function, hemodynamics, and oxygen content difference (A-VO2 Diff) during all stages.
Methods: Left ventricular volumes, cardiac output, e`, VO2, trans-mitral gradients, mitral valve area (by continuity), and calculated A-VO2 Diff were measured at rest and during all effort stages using incremental, ramp semi-recumbent cycle exercise in 31 subjects divided into 15 patients evaluated for effort intolerance and no heart disease (EI), and 16 patients with mitral stenosis (age 61.6±15; 67% female)].
Results: There was no difference in age, gender, weight or height between the groups (P>0.4 for all). In MS, the change in VO2 during exercise was attenuated compared to patients with EI (group by time interaction p<0.0001), as well as heart rate (P=0.03), e` (P<0.0001), end diastolic volume (P=0.006), stroke volume (P=0.05), S` (P=0.0006), and ejection fraction (P=0.01). MS patients had similar RV end diastolic area (P=0.6), fractional area change (P=0.6), and A-VO2 Diff (P=0.7) to EI.
The best model to determine peak VO2 in patients with MS was based on parameters measured at peak exercise, but models based on parameters measured at earlier stages of exercise (anaerobic threshold) were superior to those employing rest parameters. Determinants of effort intolerance in MS were lower FEV1 (P=0.0005), peak E` (0.03), peak cardiac output (P=0.001), peak heart rate (P=0.01), and peak A-VO2 diff (P=0.04), but neither stroke volume, trans-mitral gradient, nor mitral valve area throughout exercise were associated with effort capacity. Combined cardio-pulmonary and echo stress enabled to non-invasively recognize several unique etiologies for effort intolerance, such as severe diastolic dysfunction (low compliance), poor physical fitness, or chrontropic incompetence in patients with MS allowing individualized therapy.
Conclusions: Combined cycle cardio-pulmonary and stress echocardiography tests allow non invasive comprehensive individualized evaluation of effort intolerance. MS patients fail to increase heart rate, LV relaxation, LV diastolic volume in spite of elevated filling pressure. In both MS and EI, heart rate and peripheral non cardiac factors play a prominent role in limiting exercise performance
