Global left ventricular function and regional wall motion in pure mitral stenosis‐Left ventricular function in pure mitral stenosis

Abstract

Summary:Global left ventricular function (LVF) and segmental wall motion of the left ventricle are registered in 113 patients presenting a pure mitral stenosis (MS) and in a control group of 50 individuals. The segmental wall motion is measured on the end-diastolic-end-systolic frames of the left ventricle, obtained from right anterior oblique (RAO) monoplane cineangiography . Measurement of the segmental wall shortening is performed using the Stanford method. Group 1 includes 68 patients (60% of the total number of patients studied). These patients show no pathological contraction abnormality. In this group, the global LVF is not different from the control group. Group 2 includes 45 patients (40% of the total) for whom contraction abnormalities are present: anterior hypokinesis in 20% of the cases (anterior area mean shortening (AAS) = 18f8%; p<O.OOl vs. group 1 and control group), and posterior hypokinesis in 20% of the cases (posterior area mean shortening (PAS) = 9.8f5.8%, p<O.OOl vs. group 1 and control group). In this group, global LVF is impaired; ejection fraction (EF) = 0.57f0.1% (p<O.OOl vs. group 1); velocity of circumferential fiber shortening group 1). Segmental contraction abnormalities appear to be the main factor involved in the global LVF impairment. Segmental wall motion abnormalities could be related to subvalvular fibrosis, or LV filling difficulties, or principally, to a possible interplay between the right and the left ventricles.

Evaluation of the effect of mitral stenosis severity on the left ventricular systolic function using isovolumic myocardial acceleration

“…The probable causes can be listed as: chronically restricted LV filling due to the structural abnormalities in the mitral valve, increased afterload, myocardial involvement during rheumatic fever, extension of the scar process from the mitral valve into the adjacent posterior basal myocardium, restriction or tethering of the posterobasal myocardium by the scarred mitral apparatus, abnormal interventricular septal motion associated with the right-ventricular overload, and the decrease in LV compliance [2,4]. Conventional ECHO methods such as M-mode and 2D ECHO can detect one fourth of the LV dysfunction in MS [2][3][4][5][6]. In recent years, the studies using TDI [3][4][5] and strain/strain rate imaging [6,7] demonstrated the presence of subclinical LV systolic dysfunction, which was not detected with the conventional ECHO methods in pure MS patients with preserved EF.…”

“…The presence of impaired left ventricular (LV) systolic function, determined by M-mode and/or two--dimensional (2D) echocardiography (ECHO), is noted in 25-30% of the patients with MS [2][3][4][5][6]. Recently, in the studies using tissue Doppler imaging (TDI) [7][8][9] and strain/strain rate imaging [10,11], which are more sensitive methods compared to the conventional ECHO, the occurrence of subclinical Mehmet Erturk et al, Severity of mitral stenosis and left ventricular function LV systolic dysfunction was confirmed even in MS patients with preserved ejection fraction (EF).…”

Subclinical left ventricular systolic dysfunction in patients with mild-to-moderate rheumatic mitral stenosis and normal left ventricular ejection fraction: an observational study

“…The tethering of posterobasal myocardium or restriction caused by scarred mitral apparatus has been implicated in segmental dysfunction of LV (35). In a recent study performed by Özdemir et al (36) global and segmental LV dysfunction in MS patients was shown by using S and SRs imaging.…”

Evaluation of left ventricular systolic function with pulsed wave tissue Doppler in rheumatic mitral stenosis

“…As a result they specified that the main pathological mechanism responsible for LV function disturbance was myocardial involvement due to rheumatic process in rheumatic pure MS [30]. Colle et al [31] revealed that rheumatic MS patients had anterior and posterior hypokinesia and mean shortening of hypokinetic segments was lower in MS patients than in normal individuals. They also showed that patients who had contractile abnormality had lower EF and circumferential myofibril shortening velocity.…”