Values for Mitral Valve Annulus Dimensions in Normals and Patients with Mitral Regurgitation

Objectives. The present study was designed to investigate the dimensions of mitral valve annulus in the presence of mitral regurgitation. Method. Fifty-four patients were examined. On transthoracic echocardiographic images, we performed linear measurements in the parasternal plane in order to define the size of the left ventricle, left atrium, and mitral valve annulus. We compared these findings with those obtained in 16 control subjects. Results. Twenty-one patients with mild or moderate mitral regurgitation demonstrated no significant change of the mitral valve annulus compared with the control group (P > 0.05). Seventeen patients with severe mitral regurgitation (grade of 4) had a significant increase of the dimensions of the mitral valve annulus, left ventricle, and left atrium (P < 0.05). The etiology of mitral regurgitation was degenerative in 32 patients, rheumatic in 2 patients, and mitral valve prolapse in 4 patients. All patients had normal left ventricular systolic function. Thirty-one patients were in normal sinus rhythm, and seven were in atrial fibrillation. Conclusions. The measurement of the diameter of the mitral valve annulus is feasible with transthoracic echo-cardiography. In addition to the evaluation of mitral valve leaflets and subvalvular apparatus, the measurement of the mitral valve annulus is important in the evaluation of mitral regurgitation, as its enlargement is indicative for severe mitral regurgitation .     

Classic mitral valve prolapse causes enlargement in left ventricle even in the absence of significant mitral regurgitation

Aim: The aim of this study was to evaluate whether left ventricular size was increased in patients with classic bileaflet mitral valve prolapse (MVP) in the absence of significant mitral regurgitation (MR). Method: Patients with classic bileaflet MVP were included as the case group. Two different control groups were established. The first control group was composed of the patients with mild MR caused by the reasons except MVP. The second control group consisted of healthy individuals whose echocardiograms were normal. The patients with moderate or severe MR and having abnormality in the other valves were excluded. Results: There were 20 patients in each group. Systolic and diastolic diameters and volumes of left ventricle (LV) in the MVP group were significantly higher than those in the control groups. In 10 of the patients in the MVP group, LV internal diastolic diameter (LVIDD) values were measured as ≥5.7 cm, whereas increased LVIDD value was detected in only one patient in the other two control groups. There was a significant difference in terms of the presence of increased LVIDD values between the MVP group and the control groups. Despite this enlargement in the LV dimension, the LV ejection fractions were found similar in all groups. Furthermore, it was found that the lengths of both anterior and posterior mitral leaflets in MVP group were significantly higher than those in the control groups. Conclusion: The LV diameters and volumes of patients with classic bileaflet MVP were found to be increased even in the absence of significant MR. These results need to be supported by large‐scale clinical studies. (Echocardiography 2012;29:123‐129)     

Valve Strain Quantitation in Normal Mitral Valves and Mitral Prolapse With Variable Degrees of Regurgitation

ObjectivesThe aim of this study was to quantitate patient-specific mitral valve (MV) strain in normal valves and in patients with mitral valve prolapse with and without significant mitral regurgitation (MR) and assess the determinants of MV strain.BackgroundFew data exist on MV deformation during systole in humans. Three-dimensional echocardiography allows for dynamic MV imaging, enabling digital modeling of MV function in health and disease.MethodsThree-dimensional transesophageal echocardiography was performed in 82 patients, 32 with normal MV and 50 with mitral valve prolapse (MVP): 12 with mild mitral regurgitation or less (MVP ? MR) and 38 with moderate MR or greater (MVP + MR). Three-dimensional MV models were generated, and the peak systolic strain of MV leaflets was computed on proprietary software.ResultsLeft ventricular ejection fraction was normal in all groups. MV annular dimensions were largest in MVP + MR (annular area: 13.8 ± 0.7 cm²) and comparable in MVP ? MR (10.6 ± 1 cm²) and normal valves (10.5 ± 0.3 cm²; analysis of variance: p < 0.001). Similarly, MV leaflet areas were largest in MVP + MR, particularly the posterior leaflet (8.7 ± 0.5 cm²); intermediate in MVP ? MR (6.5 ± 0.7 cm²); and smallest in normal valves (5.5 ± 0.2 cm²; p < 0.0001). Strain was overall highest in MVP + MR and lowest in normal valves. Patients with MVP ? MR had intermediate strain values that were higher than normal valves in the posterior leaflet (p = 0.001). On multivariable analysis, after adjustment for clinical and MV geometric parameters, leaflet thickness was the only parameter that was retained as being significantly correlated with mean MV strain (r = 0.34; p = 0.008).ConclusionsMVs that exhibit prolapse have higher strain compared to normal valves, particularly in the posterior leaflet. Although higher strain is observed with worsening MR and larger valves and annuli, mitral valve leaflet thickness—and, thus, underlying MV pathology—is the most significant independent determinant of valve deformation. Future studies are needed to assess the impact of MV strain determination on clinical outcome.     

Possible mechanisms of mitral regurgitation in dilated hearts: A study using transesophageal echocardiography

Hypothesis: This study was undertaken to clarify the mechanisms of mitral regurgitation (MR) in dilated hearts. Methods: in all, 68 patients with dilated heart and MR, including 26 patients with dilated cardiomyopathy (DCM), 24 with prior anterior myocardial infarction (A-MI), and 18 with prior posteroinferior myocardial infarction (I-MI), as well as 25 normal subjects were examined by transesophageal two-dimensional and color Doppler echocardiography. Results: The maximum area of the MR signal in the DCM group correlated positively with the anteroposterior diameter of the mitral annulus at late systole. Although the coaptation edge length of the anterior and posterior mitral leaflets appeared shorter in dilated hearts than in the hearts of controls, a significant difference did not exist. The length of the coaptation edge correlated negatively with the maximum area of the MR signal in all dilated hearts, and characteristic systolic displacement of the coaptation point of both mitral leaflets occurred. The MI groups demonstrated anterior and posterior displacement in the direction of the short axis of the left ventricle in the A-MI and I-MI groups, respectively. However, the DCM group demonstrated inferior displacement toward the long axis of the left ventricle; its magnitude correlated positively with the maximum area of the MR signal. Conclusion: A major cause of MR in dilated hearts is mitral malcoaptation due to displacement of the coaptation point of the mitral leaflets along the long or short axis of the left ventricle. This is caused by left ventricular enlargement and/or asynergy of the left ventricular wall, rather than by a decrease in mitral coaptation edge length due to mitral annular dilation.     

High Occurrence of Mitral Valve Prolapse in Cardiac Catheterization Patients with Pure Isolated Mitral Regurgitation

ABSTRACT. Danielsen R, Nordrehaug JE, Vik-Mo H (Department of Clinical Physiology, Haukeland Hospital, University of Bergen, Bergen, Norway). High occurrence of mitral valve prolapse in cardiac catheterization patients with pure isolated mitral regurgitation. Acta Med Scand 1987; 221:33–8. The aetiological spectrum of angiographically verified pure isolated mitral regurgitation (MR) was studied in 48 consecutive adult patients (35 males). Severe MR was found in 35 patients (73%) and moderate MR in 13 patients (27%). Mitral valve prolapse (MVP) syndrome was found in 21 patients (44%). These were younger than the rest of the study population (55±13 vs. 62±6 years, p<0.05) and 15 (71%) of them were men. Endocarditis and chordal rupture occurred in 19% and 43% of the MVP patients. Sixteen patients (33%) had MR secondary to myocardial infarction while only three patients (6%) had MR of rheumatic aetiology. Bacterial endocarditis, hypertensive heart disease, hypertrophic obstructive car-diomyopathy and mitral annulus calcification were less frequently found. Mitral valve replacement was done in 20 (57%) of the patients with severe MR and MVP was the underlying disease in 15 (75%) of these patients. In conclusion, MVP is a frequent cause of pure isolated MR and of mitral valve replacement. In contrast to the preponderance of young females amongst MVP patients in population surveys, most of the MVP patients with MR in this study are middle-aged and elderly men.     

Left Ventricular Shape Deformation and Mitral Valve Prolapse in Chronic Pulmonary Hypertension

Mitral valve prolapse (MVP) has been described in patients with right ventricular pressure or volume overload. The frequency of this phenomenon and its relationship to left ventricular shape and mitral valve annulus size, as well as its reversibility in chronic pulmonary hypertension, are poorly understood. We have observed an increased frequency of MVP in a patient population with chronic thromboembolic pulmonary hypertension that often resolves after thromboendarterectomy and reduction of pulmonary hypertension. To further evaluate the relationship between MVP and left ventricular shape in pulmonary hypertension, we studied 51 consecutive patients undergoing surgery for thromboembolic pulmonary hypertension. Echocardiographic features including interventricular septal position, as measured by an eccentricity index, left ventricular size, and several mitral valve annulus dimensions were evaluated prior to surgery and during the postoperative hospitalization period. The pulmonary artery systolic pressure was elevated for all patients prior to surgery, 87 ± 21 mmHg (mean ± SD). Twelve patients (23.5%) had MVP before surgery, which resolved in ten patients postoperatively. In addition, one patient whose pulmonary hypertension improved little, developed MVP postoperatively. Those patients with MVP had a greater pulmonary artery pressure preoperatively than those without MVP (102 ±19 vs 84 ±21 mmHg). The eccentricity index for those patients with MVP (1.68±0.2) was greater than for those with no MVP (1.53 ± 0.37). No significant differences were noted between groups with MVP and without MVP according to all mitral annulus dimensions or left ventricular chamber areas. Postoperatively, eccentricity index decreased significantly in both those with MVP and without MVP (1.29 ± 0.18 and 1.20 ± 0.15, respectively) as did pulmonary artery systolic pressure (67± 22 and 47 ± 13 mmHg, respectively). Mitral valve prolapse in chronic pulmonary hypertension occurs frequently and is noted particularly in those patients with the most severe pulmonary hypertension. It appears that deformation of the left ventricle is associated with echocardiographic MVP and that reduction of pulmonary hypertension reverses this deformation and allows for resolution of MVP.     

Left ventricular function in mitral valve prolapse: Assessment with radionuclide cineangiography

Abnormalities of left ventricular contraction in patients with mitral valve prolapse have suggested a myocardial factor in this disease. To determine systolic left ventricular function in mitral valve prolapse, technetium-99m gated equilibrium radionuclide cineangiography was performed in 47 patients with this diagnosis. In 39 patients without mitral regurgitation the average ejection fraction was normal at rest (average [± standard error of the mean] 57 ± 3 percent, normal 57 ± 1 percent, difference not significant) and exceeded the lower limits of normal in all but 1 patient, whose ejection fraction was 41 percent. However, ejection fraction during maximal exercise was lower for the group of patients with mitral prolapse without mitral regurgitation than for normal subjects (average 64 ± 2 percent, normal 71 ± 2 percent, p < 0.005). In eight patients with mitral prolapse and mitral regurgitation, the average ejection fraction was normal at rest but was diminished with exercise in comparison with both normal subjects and patients with mitral valve prolapse without mitral regurgitation. Chest pain, arrhythmia and the pattern or extent of mitral valve prolapse on echocardlography were not independently associated with impaired left ventricular functional reserve. We conclude that, although many patients with mitral valve prolapse have normal left ventricular function, there is a subgroup without mitral regurgitation in whom diminished left ventricular functional reserve is suggestive of a cardiomyopathic process.     

Mitral Valve Prolapse in Marfan Syndrome: An Old Topic Revisited

Background: The echocardiographic features of mitral valve prolapse (MVP) in Marfan syndrome have been well described, and the incidence of MVP in Marfan syndrome is reported to be 40–80%. However, most of the original research was performed in the late 1980s and early 1990s, when the diagnostic criteria for MVP were less specific. Our goal was to investigate the characteristics of MVP associated with Marfan syndrome using currently accepted diagnostic criteria for MVP. Methods: Between January 1990 and March 2004, 90 patients with definitive diagnosis of Marfan syndrome (based on standardized criteria with or without genetic testing) were referred to Massachusetts General Hospital for transthoracic echocardiography. Patients' gender, age, weight, height, and body surface area at initial examination were recorded. Mitral valve thickness and motion, the degree of mitral regurgitation and aortic regurgitation, and aortic dimensions were quantified blinded to patients' clinical information. Results: There were 25 patients (28%) with MVP, among whom 80% had symmetrical bileaflet MVP. Patients with MVP had thicker mitral leaflets (5.0 ± 1.0 mm vs. 1.8 ± 0.5 mm, P < 0.001), more mitral regurgitation (using a scale of 1–4, 2.2 ± 1.0 vs. 0.90 ± 0.60, P < 0.0001), larger LVEDD, and larger dimensions of sinus of Valsalva, sinotubular junction, aortic arch, and descending aorta indexed to square root body surface area, when compared with those without MVP. When echocardiographic features of patients younger than 18 years of age and those of patients older than 18 were compared, adult Marfan patients had larger LA dimension (indexed to square root body surface area), larger sinotubular junction (indexed to square root body surface area), and more mitral regurgitation and aortic regurgitation. Conclusions: The prevalence of MVP in Marfan syndrome is lower than previously reported. The large majority of patients with MVP have bileaflet involvement, and those with MVP have significantly larger aortic root diameters, suggesting a diffuse disease process.     

Strain patterns in primary mitral regurgitation due to rheumatic heart disease and mitral valve prolapse

ObjectiveLeft atrial (LA) and left ventricular (LV) remodelling are the adaptive changes that occur in primary mitral regurgitation (MR) and are related to its clinical outcomes. Despite the pathophysiological differences in MR in rheumatic heart disease (RHD) and mitral valve prolapse (MVP), whether the pattern of LV and LA remodelling is different between the two conditions remains unknown. Hence, we compared the LA and LV strain pattern in MR due to RHD, the predominant etiology in developing countries topatients with MVP and age and sex-matched controls.MethodsA total of 50 patients of severe MR which included 30 MVP MR and 20 RHD MR were assessed by strain imaging by speckle tracking echocardiography (STE) and were compared with age and sex-matched controls. 2D STE was used for LA and 3D STE was used for LV strain analysis. LA and LV strain parameters were compared between MVP MR and RHD MR groups.Results30 patients with MVP and 20 with RHD were studied. 60% (n = 30) were symptomatic. Mean GLS was ?17.2 ± 4.4% compared to ?20 ± 3.2% among controls and mean LA strain was 17.35 ± 10.3% compared to 51.34 ± 11.5% among controls which were significantly lower (both p < 0.01). No significant difference in LA strain and GLS was found between MVP and RHD subgroups (LA strain 20.45 ± 11.9% and 14.63 ± 8.85%; p = 0.08; GLS - 18.25 ± 4.3% and-16.2 ± 4.6%; p = 0.12). PALS in the RHD group was lower compared to MVP(p = 0.08) which showed a trend towards significance. LV strain parameters showed no significant difference among the MVP and RHD groups.ConclusionLA and LV strain parameters showed no significant difference in MR due to either RHD or MVP. There was a trend towards lower LA strain in RHD which needs validation with large multicentric studies. The current strain parameters from MVP with the prognostic value may be applied to MR of RHD etiology, pending confirmation of our results by other groups.     

Moderate exercise does not increase the severity of mitral regurgitation due to mitral valve prolapse

Background: Mitral regurgitation (MR) secondary to ischemic heart disease (IHD) increases during exercise. We tested the hypothesis that the same is also true for MR due to mitral valve prolapse (MVP). Methods: Consecutive patients with asymptomatic MR of varying severity underwent exercise test on a supine bicycle with workload up to a maximum of 100 W. Echocardiographic measurements were performed at rest and at peak exercise. The study was designed to detect an effective regurgitant orifice (ERO) change of at least 10 mm² during exercise. Results: Twenty‐six patients (21 male, age 56 ± 12 years (mean ± SD)) were included. Patients had an ERO of 35 ± 23 mm² (mean ± SD) and regurgitation volume of 48 ± 38 mL (mean ± SD). In these patients, ERO remained unchanged (an increase of 2 ± 15 mm² during exercise, P = 0.6). The regurgitation volume (RVol) decreased with 11 ± 16 mL (mean ± SD), P = 0.003. When calculated for 1 minute, RVol increased during exercise (P = 0.01), but in relation to the total cardiac output it decreased significantly (P = 0.02). Conclusion: Exercise does not increase the severity of MR due to MVP, in contrast to MR secondary to IHD. Different disease mechanisms behind these two types of MR could explain this difference. (Echocardiography 2010;27:1031‐1037)     

Left ventricular response to isometric exercise and its value in predicting the change in ventricular function after mitral valve replacement for mitral regurgitation

Reduced left ventricular (LV) afterload and its effect on the resting ejection fraction may lead to over-estimation of LV function in mitral regurgitation (MR). To evaluate LV function during increased afterload of the heart, an isometric handgrip test was performed during cardiac catheterization in 15 patients with mitral regurgitation (MR group) and in 9 normal subjects (normal group). Twelve months after successful mitral valve replacement (MVR) the patients were recatheterized, and the value of preoperative stress testing in predicting the change in resting ventricular function after surgery was estimated.Isometric exercise caused an increase in end-systolic wall stress, a measure of ventricular afterload, in both the MR group and the control group (p < 0.001). The ejection fraction remained unchanged in the control group, but decreased from 0.58 ± 0.08 to 0.53 ± 0.08 in the MR group (p < 0.001). After MVR, end-systolic wall stress increased significantly (p < 0.001) and the ejection fraction decreased from 0.58 ± 0.05 to 0.51 ± 0.1 (p < 0.05). A positive correlation existed between the change in the ejection fraction during preoperative stress testing and the change in the resting ejection fraction after MVR (r = 0.65, p < 0.01). In 8 patients whose resting ejection fraction was within normal limits (> 0.55) preoperatively, the ejection fraction was depressed (< 0.55) 1 year after surgery. In all but 1 of these patients the isometric exercise revealed the reduced ventricular response to afterload stress preoperatively (decrease of the ejection fraction > 0.03 during exercise). Therefore, the isometric exercise-induced change in LV function appears to predict the influence of MVR on LV function.     

Retrograde atrial kick in acute aortic regurgitation. study of mitral and pulmonary venous flow velocities by transthoracic and transesophageal echocardiography

Background and hypothesis: The purpose of this study was the comprehensive evaluation of the changes in pulmonary venous and mitral flow velocities of patients with acute and chronic severe aortic regurgitation. Transmitral flow velocities obtained with pulsed-wave Doppler echocardiography have been used to provide information on left ventricular (LV) filling and diastolic function. Pulmonary venous flow tracings are an important adjunct to LV inflow pattern in assessing LV diastolic function. Methods: Fourteen patients with severe aortic regurgitation (8 chronic and 6 acute) and in sinus rhythm were examined by transthoracic and transesophageal pulsed Doppler echocardiography. Mitral and pulmonary flow velocities were recorded and compared. All patients had ejection fractions > 40%. Results: Early mitral flow peak velocity was higher in patients with acute regurgitation (p<0.001). The mitral A wave was absent in five patients with acute regurgitation. In contrast, a prominent reverse atrial pulmonary systolic wave AR was demonstrated in these patients. Peak diastolic velocity of the pulmonary venous flow was greater in patients with acute aortic regurgitation (0.76 ± 0.13) than in patients with chronic aortic regurgitation (0.40 ± 0.09) (p<0.001). Peak systolic velocity did not differ significantly between the two groups. The systolic fraction of pulmonary venous flow in patients with acute aortic regurgitation was lower (0.43 ± 0.05) than that of patients with chronic regurgitation (0.63 ± 0.1) (p<0.01). All patients with acute aortic regurgitation had an S/D ratio < 1, while those with chronic regurgitation had an S/D >1 (p< 0.001) and an E/A<1. Conclusion: Patients with severe acute aortic regurgitation showed a retrograde atrial kick (absence of transmitral A wave with prominent pulmonary AR wave). These patients had an S/D ratio < 1 (restrictive Doppler pattern). Patients with chronic aortic regurgitation exhibited a Doppler pattern of abnormal LV relaxation (E/A <1, S/D > 1).     

Influence of corevalve revalving system implantation on mitral valve function

Objectives : The purpose of this study is to verify whether transcatheter aortic valve implantation (TAVI) determined changes in mitral valve (MV) function, in terms of mitral regurgitation (MR) and stenosis. Background : Little data is available regarding the effects of TAVI on global MV function, often derived from analysis primarily focused on clinical and aortic related outcomes. Methods : From May 2008 to March 2010, 73 patients with severe symptomatic aortic stenosis underwent TAVI with the CoreValve ReValving System. The study population consisted of 58 patients (27 males, mean age 82 ± 7 years) who underwent transthoracic echocardiography at least ≥1 month after implantation (mean follow‐up 7.8 ± 5.4 months). Results : In patients with a left ventricular dysfunction (ejection fraction, EF, <45%) at the baseline, EF significantly increased from 37 ± 6% to 48 ± 7% after TAVI (P = 0.003). Before TAVI, 42 patients had no or mild MR, 13 mild‐to‐moderate, and 3 moderate or moderate‐to‐severe. During follow‐up, the MR degree was unchanged in the majority of patients (55%), 12% reduced, and 33% worsened. Variables associated with worsening in MR were depth of aortic prosthesis (P = 0.02 for the distance between the ventricular end and the right coronary cusp; P = 0.04 for mean distance right‐left coronary cusps) and left atrium area at the baseline (P = 0.02). After TAVI, six patients (10%) developed mild or moderate mitral stenosis, often in a native valve with anterior calcifications. Conclusions : In the majority of patients no significant changes occurred in the degree of MR in native valve, but we found that if the aortic valve was deeply implanted in the left ventricle outflow tract, a worsening in MR can be observed. A mitral stenosis development must be sought in patients with heavy calcifications of the anterior leaflet. © 2011 Wiley‐Liss, Inc.     

Usefulness of live/real time three-dimensional transthoracic echocardiography in the identification of individual segment/scallop prolapse of the mitral valve

In this report, we present 34 patients in whom surgical intervention was undertaken for severe mitral insufficiency due to mitral valve prolapse (MVP). Location and severity of MVP and regurgitation were assessed preoperatively by live/real time three-dimensional transthoracic echocardiography and closely agreed with the surgical findings.     

The relationship between mitral regurgitation and asynergy of the left ventricle in old myocardial infarction

To elucidate the mechanism of mitral regurgitation (MR) in patients with old myocardial infarction, two-dimensional (2D) and 2D Doppler echocardiographic examinations were performed in 92 patients. According to the sites of asynergy in the short-axis view of the left ventricle at the papillary muscle level, the patients were classified in three groups; i.e., anteroseptal (AS) group (49 cases), inferoposterior (IP) group (29 cases), and the AS + IP group (14 cases). The existence and severity of MR were evaluated by 2D Doppler echocardiography and the presence of mitral valve prolapse (MPV), by 2D echocardiography. The mitral valve ring diameter was also measured. The incidence of MR was significantly higher in the IP group (41%) and AS + IP group (43%) than in the AS group (20%) (p less than 0.05, respectively). In the IP group, 21 patients had left ventricular asynergy at the base of the posterior papillary muscle; eight did not. In the former 21 patients with asynergy, MR was detected in 12 (57%) and MVP in nine (43%), whereas neither MR nor MVP was detected in the eight patients without asynergy. The grade of MR assessed by 2-D Doppler echocardiography was significantly more severe in patients with MVP than in those without MVP (MR distance: 23 +/- 6 mm with MVP vs 11 +/- 1 mm without MVP; p less than 0.05, MR area; 312 +/- 217 mm2 with MVP vs 64 +/- 29 mm2 without MVP; p less than 0.05). MR appeared at the mitral orifice between its middle portion and the posteromedial commissure, which coincided with the site of MVP in the majority of cases. In the AS and AS + IP groups, however, such close relationships between MR and MVP were absent. In these groups, mitral valve ring diameters were significantly larger in patients with MR than in those without MR (AS group: 32 +/- 3 mm with MR vs 24 +/- 2 mm without MR; p less than 0.01, IP group: 26 +/- 2 mm with MR vs 25 +/- 2 mm without MR; NS, AS + IP group: 30 +/- 3 mm with MR vs 24 +/- 1 mm without MR; p less than 0.05). Mitral valve ring diameters in the IP group with MR (26 +/- 2 mm) were smaller than in those in the AS and AS + IP groups with MR, and did not differ from those in the IP group without MR (25 +/- 2 mm). In conclusion, posterior papillary muscle dysfunction was mainly responsible for MR in the inferoposterior infarction and the dilatation of the mitral valve ring in the infarction involving the anteroseptal wall.     

Arrhythmic profile,ventricular function,and histomorphometric findings in patients with idiopathic ventricular tachycardia and mitral valve prolapse: Clinical and prognostic evaluation

Background: In patients with ventricular tachycardia (VT) and apparently normal hearts, mitral valve prolapse (MVP) is discovered fairly often, raising the question of whether or not it is an occasional finding. Hypothesis: This issue was analyzed in a series of patients with VT and apparently normal hearts in order to define the prevalence of MVP in this condition, the existence of specific diagnostic features suggesting a nonrandom association between idiopathic VT and MVP, and the prognostic implications of this finding. Methods: We studied 28 consecutive patients with documented VT and no history of heart disease. Two-dimensional (2-D) echocardiogram, cardiac catheterization, morphometric examination of endomyocardial biopsy and arrhythmologic evaluation (24-h Holter monitoring, electrophysiologic study, and signal-averaged electrocardiogram) were performed. Inclusion criteria for all patients were angiographically normal coronary arteries, normal biventricular function, and absence of histologic evidence of myocarditis. Data obtained in patients found to have MVP at 2-D echo were compared with those of the remaining patients. Long-term follow-up data were also collected. Results: The prevalence of MVP in our study group was 25% (7 patients). It was not associated with leaflet dysplasia or significant regurgitation. Biventricular function (ventricular volumes and ejection fraction) was comparable in patients with and without MVP. Patients with MVP had a significantly higher prevalence of ventricular late potentials at signal-averaged electrocardiogram (86 vs. 29%, p = 0.027), more interstitial fibrosis at morphometry (8.5 ± 3.7 vs. 5.4 ± 2.7% p = 0.028), and VT of right bundle-branch block morphology (100 vs. 48%; p = 0.044). Other arrhythmologic findings were similar in the two groups. After a mean follow-up of >5 years, no patient in either group died, and none developed heart failure or severe mitral regurgitation. Conclusions: Mitral valve prolapse is frequently detected in idiopathic VT. The distinguishing features of this association are (1) VT of right bundle-branch block morphology, (2) high prevalence of ventricular late potentials, and (3) increased fibrosis on endomyocardial biopsy. Ventricular function and other arrhythmologic findings are not specific of this association. Prognosis remains substantially benign, as is true for most cases of idiopathic VT.     

Does “Physiologic” mitral valve prolapse occur with acute blood loss?

Intravascular volume changes are reported to affect the clinical and echocardiographic spectrum of patients with known mitral valve prolapse syndrome (MVPS). We tested whether acute blood loss can produce MVP in normal adults. Twenty-one subjects were studied with Doppler echocardiography before and after donating 550 ml whole blood. Two subjects demonstrated minimal (1+) prolapse postphlebotomy, but in only one echocardiographic view, and without mitral regurgitation by Doppler. Three subjects demonstrated slight, early (not late or pansystolic) mitral regurgitation after phlebotomy, but without prolapse. Left atrial dimensions decreased significantly after the blood donation but the left ventricular size was not significantly smaller. The 1+ MVP is within the range of superior systolic motion found in 35% of a normal population, free of heart disease, and without intervention. We find no evidence in our study or in the literature that pathologic degrees of MVP can be produced in normal subjects by physiologic alteration in blood volume.     

Acute Ischemic Mitral Regurgitation Treated by Percutaneous Coronary Intervention after an Accurate Diagnosis on Transesophageal Echocardiography

An 80-year-old woman with acute posterolateral myocardial infarction, cardiogenic shock, and acute heart failure was admitted to our hospital. Transthoracic echocardiography (TTE) showed dysfunction of the left ventricular inferolateral wall motion and severe mitral valve regurgitation (MR). Emergency coronary angiography revealed triple-vessel stenosis. We performed transesophageal echocardiography in the catheter room to diagnose the cause of MR. Severe tenting of the mitral valve and no rupture of the papillary muscles were revealed. We considered ischemic MR likely to improve with revascularization and performed percutaneous coronary intervention. Subsequently, the patient''s circulatory dynamics rapidly stabilized, and MR was significantly improved on follow-up TTE.     

Left ventricular performance in mitral regurgitation assessed with systolic time intervals and echocardiography

Among 22 patients with isolated mitral regurgitation of various origins, systolic time intervals (preejection period [PEP] index, left ventricular ejection time [LVET] index and PEP/LVET) and echocardiographic measures of left ventricular performance (end-diastolic diameter [Dd], end-systolic diameter [Ds], and the percent change in minor axis diameter [%ΔD]) were calculated. The patients were classified into two groups, those with a normal or supernormal %ΔD (group I, 15 patients) and those with a decreased %ΔD (group II, 7 patients).

On group analysis, prolongation of the preejection period, shortening of the left ventricular ejection time and an increase in PEP/LVET was generally characteristic of patients with mitral regurgitation. These changes were accentuated when mitral regurgitation was complicated by echocardiographic evidence of diminished left ventricular contractile performance (%ΔD less than 30 percent). An increase in PEP/LVET to greater than 0.50 was consistently associated with abnormal left ventricular performance, whereas a normal PEP/LVET ratio reflected normal or supernormal left ventricular performance.

An inverse linear relation was found between PEP/LVET and %ΔD. When compared with previous data on the relation of these variables among patients without valve insufficiency, PEP/LVET proved to be increased for any level of %ΔD in mitral regurgitation. The state of digitalization did not appear to influence the relation between PEP/LVET and %ΔD. The use of echocardiographic measurements augments the determination of systolic time intervals in the analysis of left ventricular performance in patients with mitral regurgitation.