Mitral Regurgitation In Dilated Cardiomyopathy Research Articles

Functional mitral regurgitation in dilated cardiomyopathy: clinical implications and prognosis

Abstract Funding Acknowledgements Type of funding sources: None. Dilated cardiomyopathy (DCM) is a complex myocardial disease, with a high burden of symptoms and decreased life expectancy. Mitral regurgitation (MR) is a frequent comorbid condition and it is thought that it deteriorates left ventricle (LV) volume and ejection fraction. Guideline directed medical therapy for heart failure improves myocardial function and decreases morbidity and mortality, and there is ongoing interest in the application of novel percutaneous techniques like mitral edge-to-edge repair or resynchronization therapy in order to decrease cardiovascular events (CVE). Our objective was to analyze if MR is associated with late gadolinium enhancement (LGE), left ventricle (LV) or right ventricle (RV) dysfunction and cardiovascular events in patients with DCM. A retrospective, case control study was designed including 173 patients (mean age 60 years, 73% males, 36% dyslipemia, 30% diabetes, 20% hypertension, 8% current smokers) with diagnosis of DCM and cardiac magnetic resonance study in our center between 2014-2020 according to the latest European Society of Cardiology (ESC) definition and the latest updated position paper. Clinical data, use of guideline directed medical therapy and devices, cardiac imaging tests, mortality and CVE were collected and analyzed. Mitral regurgitation was calculated on CMR and was included if it was more than mild. After a mean follow up of 18 months, 53 patients (30%) suffered a CVE (16% heart failure, 14% incident arrythmia, 0,5% stroke 8% death). Patients with MR (n= 48; 28%) had worse LV ejection fraction (-4,8% mean; p=,02), worse RV ejection fraction (-5,5% mean; p=,03), more hospitalizations due to heart failure (OR 1,78; p=,01), had a trend toward increased mortality although it was not statistically significant (p=,01) and a trend towards late gadolinium enhancement (p,13). There was no association with incident arrythmias (p=,5) or stroke (p=,9) In multivariate analyses (log regression, multiple linear regression) MR was maintained as an independent predictor of worse RV ejection fraction (mean -3,9%; p=,03), and hospitalization for heart failure (OR 3,8; p=,043). There was also a trend toward increased mortality (p=,1) in our population. Figure. In patients with DCM, MR is associated with decreased LV and RV ejection fraction, hospitalization due to heart failure and has a tendency to be associated with mortality. Specific treatment for mitral regurgitation, including percutaneous edge-to-edge repair or surgery according to current guidelines, might decrease the severity of MR in these patients and that could lead to an improved prognosis and less morbidity. Further studies should review the impact of an interventional strategy in mitral regurgitation in patients with DCM. Abstract Figure. Mitral regurgitation in DCM: prognosis.

Relationship between native papillary muscle T1 time and severity of functional mitral regurgitation in patients with non-ischemic dilated cardiomyopathy

BackgroundFunctional mitral regurgitation is one of the severe complications of non-ischemic dilated cardiomyopathy (DCM). Non-contrast native T1 mapping has emerged as a non-invasive method to evaluate myocardial fibrosis. We sought to evaluate the potential relationship between papillary muscle T1 time and mitral regurgitation in DCM patients.MethodsForty DCM patients (55 ± 13 years) and 20 healthy adult control subjects (54 ± 13 years) were studied. Native T1 mapping was performed using a slice interleaved T1 mapping sequence (STONE) which enables acquisition of 5 slices in the short-axis plane within a 90 s free-breathing scan. We measured papillary muscle diameter, length and shortening. DCM patients were allocated into 2 groups based on the presence or absence of functional mitral regurgitation.ResultsPapillary muscle T1 time was significantly elevated in DCM patients with mitral regurgitation (n = 22) in comparison to those without mitral regurgitation (n = 18) (anterior papillary muscle: 1127 ± 36 msec vs 1063 ± 16 msec, p < 0.05; posterior papillary muscle: 1124 ± 30 msec vs 1062 ± 19 msec, p < 0.05), but LV T1 time was similar (1129 ± 38 msec vs 1134 ± 58 msec, p = 0.93). Multivariate linear regression analysis showed that papillary muscle native T1 time (β = 0.10, 95 % CI: 0.05–0.17, p < 0.05) is significantly correlated with mitral regurgitant fraction. Elevated papillary muscle T1 time was associated with larger diameter, longer length and decreased papillary muscle shortening (all p values <0.05).ConclusionsIn DCM, papillary muscle native T1 time is significantly elevated and related to mitral regurgitant fraction.

Left Atrial Volume Determinants in Patients with Non-Ischemic Dilated Cardiomyopathy.

BackgroundLeft atrial volume (LAV) is a predictor of prognosis in patients with heart failure.ObjectiveWe aimed to evaluate the determinants of LAV in patients with dilated cardiomyopathy (DCM).MethodsNinety patients with DCM and left ventricular (LV) ejection fraction ≤ 0.50 were included. LAV was measured with real-time three-dimensional echocardiography (eco3D). The variables evaluated were heart rate, systolic blood pressure, LV end-diastolic volume and end-systolic volume and ejection fraction (eco3D), mitral inflow E wave, tissue Doppler e´ wave, E/e´ ratio, intraventricular dyssynchrony, 3D dyssynchrony index and mitral regurgitation vena contracta. Pearson´s coefficient was used to identify the correlation of the LAV with the assessed variables. A multiple linear regression model was developed that included LAV as the dependent variable and the variables correlated with it as the predictive variables.ResultsMean age was 52 ± 11 years-old, LV ejection fraction: 31.5 ± 8.0% (16-50%) and LAV: 39.2±15.7 ml/m2. The variables that correlated with the LAV were LV end-diastolic volume (r = 0.38; p < 0.01), LV end-systolic volume (r = 0.43; p < 0.001), LV ejection fraction (r = -0.36; p < 0.01), E wave (r = 0.50; p < 0.01), E/e´ ratio (r = 0.51; p < 0.01) and mitral regurgitation (r = 0.53; p < 0.01). A multivariate analysis identified the E/e´ ratio (p = 0.02) and mitral regurgitation (p = 0.02) as the only independent variables associated with LAV increase.ConclusionThe LAV is independently determined by LV filling pressures (E/e´ ratio) and mitral regurgitation in DCM.

Editorial Comment: Mitral repair for functional mitral regurgitation in idiopathic dilated cardiomyopathy: a good operation done well may help

In this issue, De Bonis et al. [1] described a very interesting retrospective series of 54 patients with idiopathic dilated cardiomyopathy who underwent mitral valve repair for severe functional mitral regurgitation. No patients had coronary artery disease. These patients, very typically, had severe mitral regurgitation, class III–IV New York Heart Association failure with large ventricles, poor ejection fractions, and many had atrial fibrillation and tricuspid regurgitation. In this series, as has been shown by others, the patients underwent correction of their mitral regurgitation with low in-hospital mortality (5%). The actuarial survival at 6.5 years was 70%. The survival was further improved if the patients had either atrial fibrillation ablation or cardiac resynchronization therapy. In follow-up, patients showed improvement in their left ventricular geometry, ejection fraction and in NYHA class. Most importantly, in this series, the freedom from recurrence of significant mitral regurgitation was 90% at 6.5 years. Functional mitral regurgitation is a complication of idiopathic dilated cardiomyopathy, occurring secondary to left ventricle geometrical distortion from stenting, inferobasilar migration, apical displacement, annular dilation and posterior leaflet restriction, with altered ventricular shape and/or regional LV wall dysfunction. Mitral regurgitation (MR) leads to a vicious cycle of LV volume overload, geometric distortion and progressive MR. MR complicating congestive heart failure (CHF) predicts poor survival [2]. Mitral reconstruction surgery to treat MR in dilated cardiomyopathy has been undertaken with an acceptably low operative mortality [3, 4]. However, MR surgery for these patients remains controversial, as substantial residual or recurrent MR has been noted, and may mitigate any benefits. In fact, some series show an early (6 months) recurrence rate of significant MR of up to 50%, which certainly negatively influences or obscures potential survival advantage [5, 6]. When reviewing literature series of both surgical and percutaneous outcome studies on patients with MR in dilated idiopathic cardiomyopathy, one should be critically aware of the negative impact, mechanism and rates of recurrent MR. At present, many of the mechanisms of recurrent functional MR have been elucidated and include annular level and subvalvular components. Predictors of recurrent MR have included LV size >65 mm, a coaptation depth of >1 cm below the annular plane and angulation of the mitral valve apparatus, all of which indicate a degree of LV distortion [6]. We have also learned that the intertrigonal distance is not stable, with dilatation occurring along both the insertion of the posterior leaflet, but also in the anterior portion. This intertrigonal portion dilates and, although at one time, was considered to be a stable ‘measurable’ standard by which to size annuloplasty rings, we now know from a landmark paper of Hueb et al. [7] that this is not the case. Therefore, our previous method of sizing was incorrect and ‘undersizing’ rings has become the standard for these functional MR patients. This may partly explain the operation ‘failing’ and recurrence of mitral regurgitation in functional MR patients when using too large ‘standard-sized’ rings or when using a partial or flexible rings. Perhaps, the most important mechanistic predictor of recurrent mitral regurgitation is an increased anterior–posterior or septal– lateral mitral annular diameter. This CHF-related change has been shown not only in animal models, but also in humans. Three-dimensional magnetic resonance imaging and echo studies showed that the mitral annulus flattens and significantly increases its anterior-posterior (AP) diameter. Kongsaerepong et al. [8] found that the strongest predictor of a recurrent MR, following mitral repair, was a residual large AP diameter, i.e. a ‘too large’ ring size. Finally, Spoor et al. [9] demonstrated that the use of flexible rings (which flex and allow the largest AP diameter) as opposed to a rigid complete ring was associated with a five times higher recurrent mitral regurgitation rate. At present, numerous rigid, complete rings with stable AP dimension reduction are available [10]. In this present series, all patients were uniformly treated with an undersized rigid complete ring. The authors noted an extremely low long-term rate of recurrent MR, with excellent LV remodelling and survival. The use of a rigid complete ring has been adopted for these functional MR patients by a majority of surgeons and is becoming our best practice standard. Of course, many factors in these difficult patients determine the long-term outcome including patient comorbidities, some of which (atrial fibrillation, tricuspid regurgitation, cardiac resynchronization therapy) have been shown by these authors to be beneficial when corrected. In dealing with functional MR in idiopathic cardiomyopathy, it has been noted that a good operation when done poorly will not help; however, the manuscript by De Bonis et al. reveals that a good operation done well will help these functional MR patients.

Transcatheter Self-Expandable Aortic Valve Implantation After Undersized Mitral Annuloplasty

No data are available in the literature regarding the effectiveness and safety of transcatheter aortic valve implantation in patients who underwent previous mitral valve ring repair. Concerns exist related to the possible interference between the percutaneous aortic valve and the mitral annuloplasty ring. We report our experience with percutaneous aortic self-expandable valve implantation in a 76-year-old woman affected by severe aortic stenosis, previously operated on for "undersized" mitral annuloplasty repair of severe functional mitral regurgitation in dilated cardiomyopathy. No deformation of the nitinol tubing of the CoreValve device (CoreValve, Inc, Irvine, CA), neither distortion nor malfunction nor change of the conformation of the mitral ring occurred. No change in mitral function and regurgitation was evident at echocardiography monitoring, which was performed during the implant.

Diastolic dysfunction and left atrial enlargement as contributing factors to functional mitral regurgitation in dilated cardiomyopathy: Data from the Acorn trial

Functional mitral regurgitation (MR) is commonly seen in dilated cardiomyopathy (DCM), which may result from left ventricular (LV) dilatation and alteration in the geometric relationship of mitral valve apparatus. However, not all patients with DCM show significant MR and left atrial (LA) enlargement. The aim of this study was to assess responsible factors for developing mitral valve regurgitation. Of 300 patients enrolled in the Acorn trial, baseline echocardiography studies were available in 288, of whom 144 were excluded because of a variety of reasons. Echocardiographic data were examined for the remaining 144 patients in sinus rhythm with DCM, but without organic mitral valve disease and ischemic heart disease. Mitral regurgitation was assessed by color-flow imaging. All echocardiographic parameters were indexed to body surface area. Of 144 patients, 87 had MR grade > or =2 (group 1) and 57 had MR grade 0 or +1 (group 2). Group 1 had larger tenting area, tenting height, tethering distance, LA volume index, and mitral annular area than group 2 (all P < .001); LV volume index and ejection fraction were similar between groups. The major determinant of MR severity was tenting area (r = 0.49, P < .001), and this was best related to mitral annular area (r = 0.85, P < .001). Mitral annular area was most strongly associated with LA volume (r = 0.56, P < .001). In addition, LA volume index was highly correlated with LV diastolic dysfunction (r = 0.58, P < .001), both in total and in group 2 only. For patients with DCM in the Acorn trial, MR severity was associated with LA volume and mitral annular area but not with LV volume. Mitral annular area and LA volume were closely related, even in patients without significant MR. These findings suggest that LA enlargement caused by advanced diastolic dysfunction may contribute to causing significant MR by augmenting mitral annular dilatation in DCM.

Mitral regurgitation in dilated cardiomyopathy: value of both regional left ventricular contractility and dyssynchrony

Mitral regurgitation (MR) is common and independently predicts mortality in patients with left ventricular (LV) systolic dysfunction. Its management remains challenging because of the complexity and variety of potential mechanisms implicated. We sought to determine which LV functional characteristics are the most important determinants of the severity of the MR associated with dilated cardiomyopathies. We performed echocardiographic studies in 87 consecutive patients with dilated cardiomyopathy. The degree of MR was quantified according to guidelines. LV, left atrial and mitral annulus dimensions, mitral valve tenting, estimated filling pressures, regional myocardial contractility, and dyssynchrony (using regional strain (epsilon) analysis) were recorded too. Determinants of significant MR was thus assessed using multivariate models. Mitral regurgitant volume correlated with mitral annulus diameter (P<0.001), mitral valve tenting height (P<0.001), LV volumes (P=0.004), LV ejection fraction, mid-lateral wall peak of epsilon (P=0.01), and its delay (P<0.001). That inter-relation between the mitral annulus, the ventricle shape, contractility, and dyssynchrony was founded in the multivariate analysis. As a matter of fact, the model predicting the best the MR volume (R=0.78) included: mitral annulus diameter, dyssynchrony, tenting heigh and contractility of the LV mid-lateral wall (measured by epsilon). The MR of the dilated cardiomyopathy is multifactorial. Our data suggest that analysing only LV geometry and mitral orifice is insufficient to correctly describe functional MR determinant. LV contractility and dyssynchrony are essential too.

Evolution of tricuspid regurgitation after mitral valve repair for functional mitral regurgitation in dilated cardiomyopathy☆

To assess the evolution of tricuspid regurgitation (TR) in dilated cardiomyopathy (DCM) patients submitted to mitral repair for functional mitral regurgitation (MR). Ninety-one DCM patients (mean age 61+/-11.3) submitted to MV repair (+/-tricuspid repair) for functional MR were included. Preoperative EF was 30.9+/-6.5%, left ventricular (LV) end-diastolic volume 113+/-31.5 ml/m(2), LV end-systolic volume 81.8+/-26.7 ml/m(2), functional MR > or =3+/4+. TR was classified as < or =1+/4+ in 57 patients (62.6%), 2+/4+ in 21 (23%) and > or =3+/4+ in 13 (14.2%). Most of the patients were in NYHA class III or IV. A tricuspid annuloplasty was associated to mitral repair whenever preoperative TR was > or =3+. Therefore 13 patients (14.2%) underwent concomitant tricuspid annuloplasty whereas the remaining 78 (with preoperative TR < or =2+) did not. At follow-up (mean 1.8+/-1.2 years), 12% of the patients (11/91) had still 3-4+ TR due to failure of the tricuspid repair or progression of untreated < or =2+ TR. Freedom from TR > or =3+ was 78+/-8.8% at 3.5 years. Among the 78 patients not submitted to tricuspid repair, 14 (18%) showed a progression of TR severity equal or greater than two grades. The multivariate analysis identified grade of TR at discharge (OR 5.4, p=0.01) and preoperative RV dysfunction (OR 19.6, p=0.02) as the only independent predictors of TR > or =3+/4+ at follow-up. A significant number of patients submitted to mitral repair for functional MR present > or =3+ TR at follow-up as consequence of progression of untreated TR or failure of tricuspid repair. A more aggressive and effective treatment of functional TR in this setting should be pursued.

Intraventricular Dyssynchrony may Play a Role in the Development of Mitral Regurgitation in Dilated Cardiomyopathy

Background: The development of functional mitral regurgitation (MR) in dilated cardiomyopathy (DCM) has been attributed to altered left ventricular (LV) geometry and annular dilatation. We propose the hypithesis that intraventricular dyssynchrony may play a role in the development of MR in DCM.

Chordal Tethering: A Unique Cause of Structural Mitral Regurgitation in Dilated Cardiomyopathy

Mitral regurgitation in dilated cardiomyopathy is usually considered "functional," and many such patients are treated medically. Surgery is often offered as a last resort in select patients who have failed medical therapy. We report a patient with dilated cardiomyopathy with ventricular tachycardia and ventricular dyssynchrony and "structural mitral regurgitation" due to chordal tethering, which was managed surgically using a minimally invasive approach.

Intraventricular Dyssynchrony May Play a Role in the Development of Mitral Regurgitation in Dilated Cardiomyopathy

Background The development of functional mitral regurgitation (MR) in dilated cardiomyopathy (DCM) has been attributed to altered left ventricular (LV) geometry and annular dilatation. We propose the hypothesis that intraventricular dyssynchrony may play a role in the development of MR in DCM. Methods and Results Tissue Doppler echocardiography was performed in 32 DCM patients to assess the time from the onset of the QRS complex to the peak systolic myocardial strain (Ts) at 2 segments adjacent to the anterolateral and posteromedial papillary muscles from a short axis view. The time difference corrected by the RR interval (ΔTs/√RR) was used to evaluate dyssynchrony of these segments. There was no difference in the QRS duration (103 ± 29 ms versus 95 ± 22 ms, P = .38) or the presence of left bundle branch block (39% versus 14 %, P = .25) between 18 patients with MR and 14 patients without MR. However, ΔTs/√RR was significantly increased in the patients with MR, compared with those without MR (104 ± 67 ms versus 5 ± 16 ms, P < .0001). Stepwise multiple regression analysis showed that ΔTs/√RR was independent contributing factor of MR. Conclusion Dyssynchrony of myocardial segments adjacent to the papillary muscles may disturb synchronized closure of the mitral leaflets and cause MR in DCM.

Role of Echocardiography in Assessing the Mechanism and Effect of Ramipril on Functional Mitral Regurgitation in Dilated Cardiomyopathy

The objectives of this article are to determine the possible mechanism of functional mitral regurgitation in patients with dilated cardiomyopathy (DCM) and to know the effect of ramipril on left ventricle (LV) and mitral regurgitation by ECHO. Several postulates are put forth for functional mitral regurgitation in DCM, and mitral annular dilatation is said to be the primary mechanism in the past, but the exact mechanism is not clear. Though angiotensin converting enzyme (ACE) inhibitors are known to remodel the LV, their beneficial effect in patients with DCM with functional mitral regurgitation is not known. Various cardiac dimensions and degree of mitral regurgitation were measured by echocardiography in 30 normal control group and in 30 patients with DCM of various etiologies except ischemic, before and after ramipril therapy. There was a significant difference in all parameters especially sphericity of left ventricle and position of papillary muscles (P < 0.0003) in DCM patients, but mitral valve annulus did not show significant change (P < 0.3) compared to control group. In 50% of the patients, the functional mitral regurgitation totally disappeared. In 30% of patients, it came down from grade II to I or became trivial. In 20% of patients, it remained unchanged. There was remarkable improvement in sphericity, LV dimension, volumes, and EF%, which increased from 31 +/- 9.81 to 39.3 +/- 8.3% (P < 0.0003). It is concluded that echocardiography clearly demonstrates the increased sphericity of LV in DCM. The lateral migration of papillary muscles possibly plays a major role in functional mitral regurgitation. Ramipril significantly reduces not only sphericity but also functional mitral regurgitation.

1144-116 Prevalence and mechanism of functional mitral regurgitation in dilated cardiomyopathy: Baseline data from the acorn trials

1144-116 Prevalence and mechanism of functional mitral regurgitation in dilated cardiomyopathy: Baseline data from the acorn trials

Mitral valve annuloplasty for mitral regurgitation in dilated cardiomyopathy with severe ventricular dysfunction

Mitral valve annuloplasty for mitral regurgitation in dilated cardiomyopathy with severe ventricular dysfunction

Tachycardia-induced cardiomyopathy in the ovine heart: Mitral annular dynamic three-dimensional geometry

Background: Ring annuloplasty has been used to correct annular dilatation and mitral regurgitation in dilated cardiomyopathy, but little is known about the dynamic precise 3-dimensional geometry of the mitral annulus in this condition. Methods: Nine sheep had radiopaque markers sewn to the mitral annulus, creating 8 distinct segments beginning at the posterior commissure (segments 1-4, septal mitral annulus; segments 5-8, lateral mitral annulus). Biplane videofluoroscopy and transesophageal echocardiography were performed before and after rapid pacing (180-230 min−1 for 15 ± 6 days) sufficient to develop tachycardia-induced cardiomyopathy and mitral regurgitation. Mitral annular segment contraction was defined as the percentage difference between maximum and minimum lengths. Mitral annular area and mitral annular septal-lateral and commissure-commissure diameters and 3-dimensional shape were determined from marker coordinates. Results: With tachycardia-induced cardiomyopathy, end-diastolic mitral annular area, septal-lateral diameter, and commissure-commissure diameter increased by 36% ± 14%, 25% ± 12%, and 9% ± 5%, respectively (P <.01), whereas mitral regurgitation increased from 0.3 ± 0.2 to 2.2 ± 0.9 (P <.0001). All annular segments dilated at end-diastole with tachycardia-induced cardiomyopathy, except the segment between the midseptal annulus and the left fibrous trigone. Annular segment contraction was significantly decreased with tachycardia-induced cardiomyopathy in the lateral, but not in the septal, regions. Three-dimensional reconstruction of annular shape revealed a saddle shape of the annulus at baseline; this shape was also measured with tachycardia-induced cardiomyopathy, but there was some flattening of the septal annulus. Conclusions: With tachycardia-induced cardiomyopathy, the mitral annulus dilated substantially, being more in the septal-lateral than in the commissure-commissure dimension. Greater annular segmental dilatation and decreased contraction occurred in the lateral annulus. The saddle shape of the annulus was retained but flattened.J Thorac Cardiovasc Surg 2003;125:315-24

Rupture of posteromedial papillary muscle as a mechanism of death in dilated cardiomyopathy

The pathogenesis of mitral regurgitation in dilated cardiomyopathy is ascribed to several mechanisms. The authors describe the case of an adult male with idiopathic dilated cardiomyopathy who developed myocardial infarction in the absence of coronary atherosclerosis and died from acute lung edema following rupture of a papillary muscle of the left ventricle. The possibility of coronary embolism could not be ruled out.

Mechanism of Mitral Regurgitation in Dilated Cardiomyopathy

Dilated cardiomyopathy is a condition characterized by chamber dilatation and impaired systolic function, resulting in the clinical manifestations of congestive heart failure. Mitral regurgitation occurs with varying frequency in dilated cardiomyopathy, and its detection depends on the diagnostic modality utilized. The presence of mitral regurgitation imposes an additional burden on the failing ventricle, and appears to be an independent prognostic indicator of mortality. The mechanism of mitral regurgitation in dilated cardiomyopathy is complex, controversial, and incompletely understood. The mitral apparatus consists of the left atrial wall, mitral annulus, mitral leaflets, chordae tendineae, papillary muscles, and left ventricular wall, and each of these components and the intimate interrelationship between these structures may contribute to the development of mitral regurgitation. Left atrial enlargement, reduced left atrial contractility, mitral leaflet retraction, abnormal vector of chordal tendineae pull, papillary muscle dysfunction (either asynergic contraction or malalignment), mitral annular dilatation, and changes in the size, shape, and function of the left ventricle have been suggested as possible mechanisms for the development of mitral regurgitation in dilated cardiomyopathy. The primary event in the development of mitral regurgitation appears to be left ventricular dilatation and dysfunction. Controversy persists as to whether the associated mechanism is annular dilatation, papillary muscle or free left ventricular wall dysfunction, or a combination of all, but recent echo‐Doppler studies reviewed in this article support the notion that annular dilatation is the predominant mechanism. Improved understanding of the mechanism of mitral regurgitation in dilated cardiomyopathy may lead to a more aggressive approach with regard to pharmacological therapy, thus impacting on survival in this group of patients. (ECHOCARDIOGRAPHY, Volume 8, March 1991)

Noninvasive quantification of mitral regurgitation in dilated cardiomyopathy: Correlation of two Doppler echocardiographic methods

The presence and severity of functional mitral regurgitation were quantified by Doppler echocardiography in 17 patients with dilated cardiomyopathy and no evidence of primary valvular disease. Mitral regurgitant fraction was greater than 20% in 11 of the 17 patients, and exceeded 40% in four patients. Total stroke volume, calculated from the difference between end-diastolic and end-systolic volumes obtained by two-dimensional echocardiography, correlated well with mitral valve inflow determined by Doppler echocardiography ( r = 0.90, p < 0.001). Similarly, mitral regurgitant volume, calculated as the difference between echocardiographic total stroke volume and forward aortic volume obtained by Doppler echocardiography, correlated well with regurgitant volume calculated as the difference between mitral valve inflow and forward aortic flow, both determined by Doppler echocardiography ( r = 0.90, p < 0.001). Accordingly, functional mitral regurgitation can be conveniently demonstrated in patients with dilated cardiomyopathy by two different Doppler echocardiography methods, whose results are closely correlated. Mitral regurgitant fraction is greater than 20% in two thirds of the patients with a dilated cardiomyopathy.