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1.
Artigo | IMSEAR | ID: sea-188504

RESUMO

Background: The subvalvular apparatus arrangementcan causeventricular torsion& deformation during cardiac cycle and interruption of papillary annular complex. As a result there was impairment of normal left ventricular strain pattern.[2] In patients with mitral stenosis, the left ventricle is small. Preservation of subvalvular apparatus thus become important in moderation of left ventricular volume in long term in patients with mitral stenosis undergoing mitral valve replacement.Methods: This cross sectional study was performed on the 32 consecutive subjects in department of cardiac surgery and cardiology of BSMMU with rheumatic mitral stenosis undergoing MVR from Jan 2013 to June 2014.Mode of surgery was determined by morphology of subvalvular apparatus which dictated the extent of the preservation. The patients were divided into two groups- Group I- With preservation of subvalvular apparatus &Group II- No preservation- where SVA was completely excised. In 2D and M Mode echocardiographic measurements:Mid-wall circumferential end systolic LV stress as calculated for ellipsoid, LV mass, the mid wall circumferential end systolic LV stress is calculated by mirsky’s formula.9,10 Results: Patients with sub valvular apparatus resection (group I) had deterioration with postoperative ejectionfraction in compare to group-II. Left ventricular circumferential wall stress analysis showed increased wall stress in group II after MVR. Conclusion: The increased left ventricular wall stress is responsible for poor outcome in non-preserved group after MVR. The wall stress increases further in midterm follow up which may explain the mechanism of long term poor out come in patients with mitral stenosis.

2.
Artigo em Inglês | IMSEAR | ID: sea-181940

RESUMO

Background: Cardiac resynchronization therapy (CRT) had shown great promise in improving hospitalization and mortality of the patients suffering from refractory heart failure (HF) inspite of optimal medical management. The goal of CRT is to reduce cardiac mechanical dyssynchrony, thereby enabling the heart to contract more efficiently. Mechanical ventricular dyssynchrony as estimated by electrical dyssynchrony, is assessed with the QRS duration. But electrical and mechanical dyssynchrony are not well correlated in all HF patients. The dyssynchrony might have been related to the underlying etiology of HF. Objective: To compare the concordance of mechanical and electrical dyssynchrony in both ischemic and nonischemic cardiomyopathy patients. Methods: Doppler echocardiography and strain echocardiography was performed in 76 patients presenting with heart failure due to ischemic cardiomyopathy (n=40) or nonischemic cardiomyopathy (n=36) with left ventricular ejection fraction<35% & New York Heart Association class III–IV, regardless of their QRS duration. Interventricular dyssynchrony was assessed by the time interval between preaortic and prepulmonary ejection times. Intra-ventricular dyssynchrony was assessed by using conventional Doppler and strain echocardiograpy. Obtained from the three standard apical view (TMinMax) and (2) the standard deviation of the averaged time-to-peak strain (TPS-SD, ms) and (3) time to peak myocardial systolic velocity (Ts-SD) of same segments. Result: The correlation coefficient between QRS duration and mechanical interventricular dyssynchrony was significant (r=0.57, P=0.001) in patients with non-ischemic cardiomyopathy and insignificant (r=0.175, p=0.281) in patients with ischemic cardiomyoparhy. The correlation coefficient between QRS duration and mechanical intraventricular dyssynchrony was significant in patients with nonischemic cardiomyopathy (r= 0.69, P = 0.001 for TMin Max; r=0.57, P= 0.001 for TPS-SD; r=0.48, p=0.003 for TS-SD) and insignificant in patients with ischemic cardiomyopathy (r=0.153; p=0.345 for TMin Max; r=0.178; p=0.273 for TPS-SD r=0.139; p=0.392 for TS-SD). Conclusion: This study showed that the relationship between electrical and mechanical dyssynchrony is dependent on the underlying etiology of heart failure.

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