Chronic mitral regurgitation: Predictive value of preoperative echocardiographic indexes of left ventricular function and wall stress

“…The resultant chronic MR and the consequent changes in LV volume, mass, geometry, and function closely parallel those seen in clinical disease. [8][9][10][11][12][13]19,20,[25][26][27][28]40 Changes in diastolic function were assessed in a serial longitudinal fashion; baseline function was compared with changes in function caused by chronic MR and then after MVR in sure gradient and LV stress at mitral valve opening by guest on May 13, 2018 http://circ.ahajournals.org/ Downloaded from the same animal. The hemodynamic and mechanical measurements made using simultaneous echocardiography and catheterization allowed assessment of changes in both diastolic function itself and many (but not all) of the determinants or mechanisms causing these changes in diastolic function.…”

Section: Diastolic Functionmentioning

confidence: 99%

Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

et al. 1993

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Background. Mitral regurgitation (MR) causes an augmentation in left ventricular (LV) diastolic function, increasing early diastolic filling rate and decreasing LV stiffness. Whether these changes in diastolic function persist, return to normal, or become abnormal after mitral valve replacement (MVR) is unknown.Methods and Results. Simultaneous LV echocardiography and catheterization studies were performed in six dogs in the baseline state (baseline), 3 months after creation of MR (chronic MR), and 3 months after MVR. Chronic MR caused LV dilation (end-diastolic dimension increased from 4.5±0.1 cm in baseline to 5.8+0.1 cm in chronic MR,p<0.05) and eccentric LV hypertrophy (LV-to-body weight ratio increased from 3.6±0.2 g/kg in baseline to 4.9±0.4 g/kg in chronic MR, p<0.05). Chronic MR caused an increase in LV early diastolic filling rate (peak rate of increase in minor-axis dimension increased from 11±1 cm/sec in baseline to 18+1 cm/sec in chronic MR,p<0.05), did not change the time constant of myocardial relaxation (T was 31±4 msec in baseline and 30±2 msec in chronic MR), and caused a decrease in the modulus of regional chamber stiffness from 7.7± 1.2 in baseline to 2.4±0.03 in chronic MR,p<0.05. MVR caused the resolution of LV dilation (end-diastolic dimension returned to normal [4.8±0.2 cm]), but three months after MVR, regression of LV hypertrophy was incomplete (LV-to-body weight ratio remained

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“…Follow-up clinical status was evaluated by a combination of personal or telephone interview and review of medical and vital records. All patients were followed until death or to currently defined predictors of significantly compromised prognosis commonly employed as bases for mitral valve surgery, i.e., new onset of heart failure symptoms (Functional Class≥2) (15), LV ejection fraction rest <10% higher than the lower limit of normal for the testing modality (<60% by echo [16]), new onset atrial fibrillation (17), or echocardiographic LVIDs≥45mm (18), an accepted criterion when the study was performed, and LVIDs>40mm, a more recently suggested criterion for surgery (19) that was not employed at the time this study was undertaken. Echocardiographic effective regurgitant orifice area, recently reported to have significant prognostic impact (20), was not measured in our laboratory during this study.…”

Section: Baseline and Follow-up Assessmentsmentioning

confidence: 99%

Prognostic Value of Exercise Tolerance Testing in Asymptomatic Chronic Nonischemic Mitral Regurgitation

Supino

Borer

Schuleri

et al. 2007

The American Journal of Cardiology

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In many heart diseases, exercise treadmill testing(ETT) has useful functional correlates and/or prognostic value. However, its predictive value in mitral regurgitation(MR) is undefined. To determine whether ETT descriptors predict death or indications for mitral valve surgery among patients with MR, we prospectively followed, for 7±3 endpoint-free years, a cohort of 38 patients with chronic severe nonischemic MR who underwent modified Bruce ETT; all lacked surgical indications at study entry. Their baseline exercise descriptors also were compared with those from 46 patients with severe MR who, at entry, already had reached surgical indications. Endpoints during follow-up among the cohort included sudden death(n=1), heart failure symptoms(n=2), atrial fibrillation(n=4), LVEF<60%(n=2), LV systolic dimensions(IDs)≥45 mm(n=12) and LVIDs>40mm(n=11), LVEF<60%+LVIDs 45 mm(n=3), and heart failure+LVIDs 45mm +LVEF<60%(n=1). In univariate analysis, exercise duration(p=.004), chronotropic response(p=. 007), percent predicted peak heart rate(p=.01) and heart rate recovery(p<.02) predicted events; in multivariate analysis, only exercise duration was predictive(p<.02). Average annual event risk was 5-fold lower(4.62%) with exercise duration≥15 minutes vs. <15 minutes(average annual risk=23.48%, p=.004). Relative risks among patients with and without exercise-inducible ST segment depression were comparable(≤1.3 [NS]) whether defined at entry and/or during follow-up. Exercise duration, but not prevalence of exercise-inducible ST segment depression, was lower(p<. 001) among patients with surgical indications at entry vs. initially endpoint-free patients. In conclusion, among asymptomatic patients with chronic severe nonischemic MR and no objective criteria for operation, progression to surgical indications generally is rapid. However, those with excellent exercise tolerance have a relatively benign course. Exercise-inducible ST segment depression has no prognostic value in this population.We followed, for 7±3 endpoint-free years, 38 patients with chronic severe nonischemic mitral regurgitation (MR) who underwent modified Bruce exercise treadmill testing (ETT) to determine whether ETT descriptors predict death or indications for mitral valve surgery. At study entry, all lacked surgical indications. Exercise duration independently predicted subsequent events; event risks among patients with and without exercise-inducible ST segment depression were comparable. We conclude that among asymptomatic patients with chronic severe nonischemic MR Address for Correspondence: Jeffrey S. Borer, M.D., New York-Presbyterian Hospital New York Weill Cornell Center, 525 East 68 th Street, New York, N.Y. 10021, 212-746-4646=phone, 212-746-8448=fax, canadaD45@aol.com=email Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulti...

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Chronic mitral regurgitation: Predictive value of preoperative echocardiographic indexes of left ventricular function and wall stress

Cited by 191 publications

References 26 publications

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Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

Prognostic Value of Exercise Tolerance Testing in Asymptomatic Chronic Nonischemic Mitral Regurgitation

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