Md. Tischler et al., OBSERVATIONS SUGGESTING A HIGH-INCIDENCE OF EXERCISE-INDUCED SEVERE MITRAL REGURGITATION IN PATIENTS WITH MILD RHEUMATIC MITRAL-VALVE DISEASE AT REST, Journal of the American College of Cardiology, 25(1), 1995, pp. 128-133
Objectives. The aim of this study was to determine the hemo dynamic ef
fects of upright bicycle ergometry in symptomatic patients with mild,
mixed mitral stenosis and regurgitation. Background. Patients with see
mingly mild rheumatic mitral valve disease often complain of exertiona
l dyspnea or fatigue. These symptoms are usually ascribed to flea-depe
ndent increases in the gradient across the stenotic mitral valve. Alth
ough catheterization studies in these patients may demonstrate an incr
ease in mitral valve gradient proportional to an increase in cardiac o
utput, this approach does not specifically address the underlying mech
anism of any observed increases in mitral gradient or left atrial (i.e
., pulmonary capillary wedge) pressure. Exercise echocardiography is u
niquely suited to the dynamic assessment of exercise-induced hemodynam
ic changes. Methods. Fourteen symptomatic patients with exertional dys
pnea and mild mitral stenosis and regurgitation at rest performed symp
tom-limited upright bicycle ergometry with quantitative two-dimensiona
l, Doppler and color Doppler echocardiographic analysis. Results. Aver
age pulmonary artery systolic pressure in the 13 patients with adequat
e spectral signals of tricuspid regurgitation increased from 36 +/- 5
mm Hg (mean +/- SD) at rest to 63 +/- 14 mm Hg at peak exercise (p < 0
.001). The mean transmitral pressure gradient in ail patients increase
d from 4.5 +/- 1.4 mm Hg at rest to 12.7 +/- 2.7 mm Hg at peak exercis
e (p < 0.001). Five patients developed severe mitral regurgitation dur
ing exercise. Conclusions. Patients with exertional dyspnea and mild m
itral stenosis and regurgitation at rest demonstrate a marked increase
in pulmonary artery systolic pressure and mean transmitral pressure g
radient during dynamic exercise. In a subset of these patients, marked
worsening of mitral regurgitation appears to be the underlying mechan
ism of this hemodynamic deterioration. Because of the small sample siz
e, this novel observation must be considered preliminary with respect
to the true prevalence of exercise-related development of severe mitra
l regurgitation. If additional studies confirm the importance of this
phenomenon, it has important implications for the management of patien
ts with rheumatic mitral valve disease.