Amount Of Mitral Regurgitation Research Articles

Acute contractile recovery extent during biventricular pacing is not associated with follow-up in patients undergoing resynchronization

BackgroundIt has been reported that contractility, as assessed using dobutamine infusion, is independently associated with reverse remodeling after CRT. Controversy, however, exists about the capacity of this approach to predict a long-term clinical response. This study's purpose was to assess whether long-term CRT clinical effects can be predicted according to acute inotropic response induced by biventricular stimulation (CRT on), as compared with AAI–VVI right stimulation pacing mode (CRT off), quantified at the time of implantation. MethodsIn 98 patients (ejection fraction 29±10%), acute changes in left ventricular (LV) elastance (Ees), arterial elastance (Ea), and Ees/Ea, as assessed from slope changes of the force–frequency relation obtained when the heart rate increased, and also assessed while measuring triplane LV volumes and continuous noninvasive blood pressure, were related to death or rehospitalization during a 3-year follow-up. Other covariances tested were age, gender, disease etiology, QRS duration, amount of mitral regurgitation, LV diastolic volume, ejection fraction, and the degree of asynchrony and longitudinal strain at baseline. ResultsThere was a marked increment in the Ees slope with CRT (interaction P=0.004), no Ea change, and modest Ees/Ea increase (interaction P<0.05). In Cox analysis, however, neither slope changes nor baseline values of Ees, Ea, and Ees/Ea were associated with long-term follow-up. Only ventricular diastolic volume (direct relation P=0.002) and QRS duration (inverse relation P=0.009) predicted death/rehospitalization. ConclusionsAcute contractile recovery in CRT patients is not associated with 3years prognosis. Instead, death or rehospitalization can be predicted from QRS duration and LV diastolic volume at baseline.

1061 Atorvastatin inhibits mitral regurgitation in an experimental hypercholesterolemia rabbit model

Degenerative mitral regurgitation is the most common cause of mitral regurgitation in the United States. Recent epidemiologic studies have linked degenerative mitral valve disease and risk factors for atherosclerosis. In the current study, we studied a hypercholesterolemic rabbit model with and without atorvastatin to determine the cellular mechanisms of mitral leaflet abnormalities. Methods: 48 Watanabe rabbits were assigned to one of 3 groups: cholesterol (1%) diet, cholesterol (1%) plus atorvastatin (2.5 mg/kg), and normal diet for six months. The rabbits underwent transesophageal echocardiograms and then the mitral valves were harvested. Electron microscopy, immunohistologic staining, and Real-time PCR was performed. Immunohistologic staining of the mitral valves was performed using atherosclerotic markers macrophage (RAM11), alpha -actin smooth muscle, and Proliferating Cell Nuclear Antigen (PCNA). Bone matrix expression was determined by staining for osteopontin, osteocalcin, alizarin Red and measuring alkaline phosphatase gene expression. A 4-point grading system was used to visually describe the staining on each of the slides (0=no staining, 4=high staining). Real-time PCR was performed was performed to measure alkaline phosphatase gene expression. Results: Mitral regurgitation (3+), Macrophage (3.5+/-0.7), alpha-actin (4+/-0), osteopontin (4+/-0), osteocalcin (2.5+/-0.7), PCNA (4+/-0) and alkaline phosphatase (0.479+/-0.286) were increased the mitral valves from the cholesterol treated rabbits (p<0.05 as compared to control mitral valves). Alkaline phosphatase was unchanged in the control versus cholesterol treatment groups. Atorvastatin decreased the amount of mitral regurgitation (1+), atherosclerotic proliferative changesincluding macrophage (2.5+/-0.7), osteopontin (1.5+/-0.7), osteocalcin (2.5+/-0.7), PCNA (2+/-0) and alkaline phosphatase expression (0.479+/-0.286) in these treated valves. Conclusion: Experimental hypercholesterolemia induces proliferation and osteopontin expression in the mitral valve that may potentially be modified with the use of a lipid-lowering agent.

Left ventricular dyssynchrony and dynamic functional mitral regurgitation: relationship or association?The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.

Numerous parameters are associated with a dismal prognosis in heart failure patients. Some of these factors may be mechanistically related, such as increased left ventricular (LV) volume, functional mitral regurgitation (MR), QRS widening, and LV dyssynchrony. Indeed, LV dilation produces distortion of ventricular geometry. The apical and outward displacement of the mitral leaflets restricts their ability to close through tethering forces. QRS widening is frequently associated with LV dyssynchrony. Both dysfunction and dyssynchrony, notably the dyscoordination of the segments containing papillary muscles 1 reduce LV-generated mitral valve closing force. Functional MR varies dynamically depending on annular size, loading conditions, and a balance of closing force and mitral valvular deformation. Dynamic MR can be reliably quantitated during exercise testing. Large exerciseinduced increases in ischaemic MR are associated with acute pulmonary oedema 2 and a high risk of morbidity and mortality. 3 In patients with normal QRS duration but reduced LV contraction, exercise-induced changes in MR are not associated neither to the degree of MR at rest nor to the changes in global LV function, but are related to the changes in local LV distortion and in mitral deformation. 4 But are the determinants of exercise-induced changes in functional MR similar in patients with LV dyssynchrony? In other words, does the reduction in closing force play a more important role in this setting? Ennezat et al. 5 tested the hypothesis that myocardial dyssynchrony at baseline contributes to worsening of functional MR during exercise. They studied 70 heart failure patients; half of the population had ischaemic cardiomyopathy. Pulsed-wave Doppler tissue imaging was performed to assess and quantify LV dyssynchrony at rest. The proximal flow convergence technique was used to quantify MR both at rest and during exercise. Exercise-induced changes in MR were individually variable and were associated with the presence and the degree of LV dyssynchrony. The authors conclude that LV dyssynchrony at rest is related to worsening of functional MR during exercise in patients with systolic heart failure. Although functional MR and dyssynchrony are obviously continuous variables, cut-off values have been proposed for delineating their significance: effective regurgitant orifice (ERO) of functional MR � 20 mm 2 , exercise-induced increase 3 in MR � 13 mm 2 or LV dyssynchrony � 65 ms, defined as the maximum delay between peak systolic velocities among basal LV segments. 6 Using, for instance, this latter cut-off value for analysing Figure 2 in the article published by Ennezat et al., 5 we see that approximately half of their patients have no ‘significant’ LV dyssynchrony. In this subgroup, the absence of correlation between LV synchronicity and changes in mitral ERO is obvious; two-thirds of the patients exhibited a decrease in ERO during exercise and only one had a large (.13 mm 2 ) exercise-induced increase in MR. The correlation between the two parameters is apparent in the other half of the population who presented with significant LV dyssynchrony; no patient had a decrease in mitral ERO during exercise and seven (roughly 20% of this subgroup) developed a large exercise-induced increase in ERO. In the overall population, LV dyssynchrony at rest and exercise-induced changes in systolic mitral annular diameter were the two parameters independently associated with exercise-induced changes in functional MR. LV dyssynchrony was associated with changes in MR severity in patients with ischaemic and non-ischaemic cardiomyopathies. Exerciseinduced changes in annular diameter were related to changes in MR only in patients with non-ischaemic cardiomyopathy. The dynamic component of chronic functional MR, revealed by exercise testing has clinical implications. Some patients exhibit small changes in the amount of MR; others have a sizeable decrease in ERO mainly because of recruitable contraction of the basal LV segments. 4 These patients have a good long-term prognosis. 3 In contrast, a large rise in MR during exercise is associated with more frequent hospital admission for decompensated heart failure or flash pulmonary oedema. Repetitive acute exacerbation of functional MR accentuate left atrial and LV overload and

Evaluation of predictors of clinical outcome after partial left ventriculectomy

Background. Outcome after partial left ventriculectomy (PLV) is difficult to predict. Our goal was to determine if clinical measurements including exercise testing could predict outcome after PLV. Methods. Sixteen patients with dilated cardiomyopathy had left ventricular ejection fraction, left ventricular end-diastolic diameter, amount of mitral regurgitation (MR), New York Heart Association (NYHA) functional class, and cardiopulmonary exercise testing measurements measured before PLV and 3 months after PLV. Eleven patients who remained stable after PLV (group 1) were compared with 5 patients who deteriorated after PLV (group 2). Results. Similar significant improvements were seen in both groups 3 months post-PLV with respect to left ventricular ejection fraction (group 1: 0.136 ± 0.037 to 0.212 ± 0.046; group 2: 0.139 ± 0.042 to 0.179 ± 0.073) and left ventricular end-diastolic diameter (group 1: 8.5 ± 0.7 to 7.0 ± 0.6 cm; group 2: 7.6 ± 0.6 to 6.5 ± 0.6 cm). The MR grade (1.0 ± 0.6 versus 2.5 ± 0.6), NYHA functional class (1.5 ± 0.31 versus 2.5 ± 0.6), and peak oxygen consumption (17.8 ± 1.1 versus 12.2 ± 2.0) were significantly different in the two groups 3 months after PLV ( p < 0.05, analysis of variance). Conclusions. Patients that do not show significant improvement in peak oxygen consumption, NYHA class and significant decrease in the amount of MR 3 months after PLV, compared with pre-PLV, are at increased risk of clinically deteriorating.

CAN CLINICAL OUTCOME AFTER PARTIAL LEFT VENTRICULECTOMY BE PREDICTED?

984 Partial left ventriculectomy (PLV) is a surgical option for patients (Pts) with idiopathic dilated cardiomyopathy (IDC). Outcome after PLV is difficult to predict. The goal of our study was to determine if LV ejection fraction (LVEF), LV end diastolic diameter (LVEDD), amount of mitral regurgitation (MR), NYHA class and peak oxygen consumption (PVO2) measured before and 3 months after PLV would predict clinical outcome. 16 Pts with IDC underwent PLV (14 males, mean age 49.6 years, mean LVEDD 8.2 cm, mean LVEF of 13.9%, NYHA class IV despite maximal medical therapy, mean PVO2 of 13.5 ml/kg/min and mean follow-up of 11.1 months.) Variables were retrospectively compared before and after PLV in Pts who remained clinically stable after PLV (Group 1, n=11) with Pts who deteriorated after PLV (Group 2) and were relisted for cardiac transplant (n=3) or expired (n=2). (Table)TableSimilar significant improvements were seen in both groups 3 months post PLV with respect to LVEF and LVEDD. The amount of MR, NYHA Class, and PVO2 were different in the two groups (p<0.05, ANOVA), post PLV. In conclusion, analysis of pre and 3 month post PLV peak VO2, NYHA class, and MR may predict sustained improvement after PLV. Pts that do not have significant improvement in these variables post PLV may be at increased risk of clinical deterioration and may be referred earlier for cardiac transplantation.

Simulation of chronic mitral regurgitation.

In mitral regurgitation the left ventricle enlarges in order to increase its stroke volume because of the regurgitation through the mitral valve. The amount of this volume increase, and of the consequent increase in left ventricular mass, its dependent upon the amount of the regurgitant volume, but many other factors come into play, such as left ventricular pumping capability (contractility), the level of peripheral pressure, resistance and compliance of the arterial tree. The aim of this study is to predict the final left ventricular volumes and mass given the amount of mitral regurgitation. The predicted results are compared with actual data in real patients. In most cases prediction is fairly good; some discrepancies can be interpreted as an index of advanced decompensation.

Clinical experience of mitral valve reconstruction with artificial chordae implantation

To expand the application of mitral valve reconstruction for pure mitral regurgitation due to diffuse leaflet prolapse, we have employed artificial chordae implantation using GPEP strips in 9 patients and 4-0 PTFE sutures in 20 patients since November 1986. The total number of GPEP strips implanted was 20 with a range from 1 to 4 (average 2.2 per patient) and 45 pairs of PTFE sutures with a range from 1 to 6 (average 2.3 per patient). There was one hospital death (3.4%). All other patients survived operation without valve-related complications except 1 patient who required reoperation for failure of mitral valve reconstruction. In 27 survivors free from reoperation, the amount of mitral regurgitation assessed postoperatively was none or trivial in 19 patients, mild in 7 and moderate in 1. All 27 patients improved to NYHA functional class I or II. So far, our results were no less acceptable than those with conventional procedures for mitral valve prolapse.

Postural changes in left ventricular and mitral valvular dynamics in the systolic click - late systolic murmur syndrome.

Marked changes in the auscultatory pattern with posture have been noted in patients with mid-systolic clicks and/or late systolic murmurs (MSC-LSM). MSC tend to move earlier in systole and LSM become longer and often louder when patients assume upright posture. Systolic prolapse of the mitral leaflets with mild regurgitation account for MSC-LSM; earlier and greater prolapse with more and prolonged regurgitation associated with a reduced left ventricular volume (LVV) in the upright position would explain the auscultatory changes. Twenty-two patients with MSC-LSM were studied supine and at 45 degrees head-up tilt, recording intracardiac pressures, cardiac outputs, systolic time intervals, and performing LV cineangiography. Systolic prolapse of one or both mitral leaflets was demonstrated in all patients. Left ventricular end-diastolic and end-systolic volumes both decreased significantly at 45 degrees in all sixteen technically satisfactory studies. Greater mitral prolapse was noted upright in 12 of 14 studies with enough sinus beats to judge. The amount of mitral regurgitation was mild in all, and changes in amount from supine to upright posture could not be discerned angiographically. THE FINDINGS, SUGGEST THAT THE AUSCULTATORY CHANGES OCCURRING WITH UPRIGHT POSTURE IN PATIENTS WITH MSC-LSM are related to greater prolapse of the mitral leaflets which is associated with a small LVV in the upright position.

Postural changes in left ventricular and mitral valvular dynamics in the systolic click-late systolic murmur syndrome

Marked changes in the auscultatory pattern with posture have been noted in patients with mid-systolic clicks and/or late systolic murmurs (MSC-LSM). MSC tend to move earlier in systole and LSM become longer and often louder when patients assume upright posture. Systolic prolapse of the mitral leaflets with mild regurgitation account for MSC-LSM; earlier and greater prolapse with more and prolonged regurgitation associated with a reduced left ventricular volume (LVV) in the upright position would explain the auscultatory changes. Twenty-two patients with MSC-LSM were studied supine and at 45 degrees head-up tilt, recording intracardiac pressures, cardiac outputs, systolic time intervals, and performing LV cineangiography. Systolic prolapse of one or both mitral leaflets was demonstrated in all patients. Left ventricular end-diastolic and end-systolic volumes both decreased significantly at 45 degrees in all sixteen technically satisfactory studies. Greater mitral prolapse was noted upright in 12 of 14 studies with enough sinus beats to judge. The amount of mitral regurgitation was mild in all, and changes in amount from supine to upright posture could not be discerned angiographically. THE FINDINGS, SUGGEST THAT THE AUSCULTATORY CHANGES OCCURRING WITH UPRIGHT POSTURE IN PATIENTS WITH MSC-LSM are related to greater prolapse of the mitral leaflets which is associated with a small LVV in the upright position.

Backward transmission of the left atrial V wave and premature pulmonary valve closure

The concept that premature pulmonary valve closure may result from severe mitral insufficiency is presented. Five patients with severe mitral valve insufficiency had pulmonary arterial mean pressure which exceeded simultaneously recorded right ventricular mean systolic pressure. A high delayed pressure wave was present in the pulmonary artery of these subjects, and in four subjects the pulmonary arterial pressure rose above the right ventricular pressure. In two of the five, the timing and morphology of this pressure wave were suggestive of early closure of the pulmonary valve by retrograde transmission of the left atrial “V” wave through the pulmonary vessels. Catheterization revealed low cardiac indices, marked left atrial systolic pressure elevation, and elevated pulmonary artery pressure. All subjects had high total pulmonary resistance, while pulmonary arteriolar resistance was normal in three and only moderately elevated in two. The respective roles played by pulmonary arteriolar resistance, compliance of the left atrium and pulmonary vasculature, the state of left ventricular function, and amount of mitral regurgitation in the production of this phenomenon are discussed.

An appraisal of the double indicator-dilution method for the estimation of mitral regurgitation in human subjects.

The amount of mitral regurgitation was estimated in 50 patients by an indicator-dilution technic and by the usual clinical, catheterization, operative, and autopsy criteria. There was a good correlation between the two estimates. Patients with significant mitral regurgitation (grade 2 or grade 3) had, with one exception, Q R / Q F ratios above 0.41. There were at least two instances where the calculated Q R / Q F was almost certainly falsely high. It seems likely that these discrepancies are related to the presence of an unusually large volume between the pulmonary artery and the femoral artery.