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Query: UMLS:C0033377 (prolapse)
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To investigate the continuity between the normal and prolapsed mitral valves (MVP), two-dimensional echocardiography (2DE) and color Doppler echocardiography (CDE) were performed in 508 healthy boys aged 12 to 13 years old. The distance from the plane of the mitral annulus to the coaptation of the mitral valve "c", the maximum distance between the anterior leaflet and a straight line connecting the anterior mitral annulus and the coaptation of the mitral valve "d", and the maximum distance between the posterior mitral leaflet and the straight line connecting the posterior mitral annulus and the coaptation of the mitral valve "e" were measured in the parasternal long-axis view. The locations of the anterior and posterior mitral annuli were determined to be the hing point of the anterior leaflet on the left ventricular side and the junction of the posterior leaflet on the ventricular side, respectively. Mitral regurgitation (MR) was evaluated by CDE in the parasternal long-axis view. The ratio of the duration of regurgitation to ejection time (DT/ET) was measured by M-mode CDE in the subjects with and without MVP. The values of "c" ranged from +10 mm to -3 mm, and those of "d" from +5 mm to -4 mm (minus denotes prolapse into the left atrium). Approximately normal distributions were demonstrated with the parameters "c" and "d". The value of "e" could not be measured because of a poor image of the posterior leaflet. The incidence of MVP varied from 2.5 to 13.5% depending on the criterion for applied MVP. Fifty-nine of the 487 healthy subjects turned out to have MR (12%). Coaptation of the mitral valve deviated from the posterior commissure significantly to the left atrium more in the subjects with MR than in those without MR (2.46 +/- 1.93 vs 3.41 +/- 1.84, p < 0.01). The DT/ET ratio of the MR subjects with MVP tended to be higher than that of the boys without MVP. The presence of continuity between the normal and prolapsed mitral valves suggests that MVP may be a multifactorial disorder of the valve. Associated asymptomatic MR may be related not only to the severity of MVP but also to other factors, especially in MR of normal healthy subjects.
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PMID:[Continuity from normal to prolapsed mitral valves: two-dimensional and color Doppler echocardiographic investigations]. 184 27

A 32 year old female patient, documented clinically and echocardiographically to have a competent prolapse of the mitral valve (MVP), developed a sudden ischemic cerebrovascular accident (CVA), suggestive of embolism. There were no predisposing factors to cerebrovascular disease, except for past use of contraceptive pills. Tomographic study disclosed an ischemic right-parietal "wedge-shaped" defect. The patients's recovery, with physiotherapy and AAS, was satisfactory. The authors discuss the association of MVP and CVA, considering physiopathogenic, prophylactic and therapeutic aspects, emphasizing the need to consider MVP as a cause of CVA in young adults.
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PMID:[Mitral valve prolapse as a probable cause of cerebral ischemia. A case report]. 281 40

To certify the continuity between the normal and prolapsed mitral valves (MVP), two-dimensional and color Doppler echocardiography (2-DE and CDE) were performed for healthy 250 male subjects of 13 years old. The distance from the plane of the mitral annulus to the coaptation (c) and the grade of systolic ballooning of the anterior mitral leaflet as expressed by the maximum distance between the leaflet and the straight line connecting the anterior mitral ring with the point of coaptation (d) were measured in the long-axis 2-DE. Mitral regurgitation (MR) was evaluated by CDE. Distribution of c was between +10 and -3 mm, and d was between +5 and -3 mm (minus denotes prolapse toward the left atrium). An approximately normal distribution was found in both parameters c and d. The incidence of MVP varied from 3 to 13% according to the strictness of the criteria for MVP. Subjects with MR from the posterior commissure showed the coaptation significantly displaced toward the atrium compared with the rest of subjects (p less than 0.01). Our data suggest that MVP is a multifactorial disorder of the valve and the development of MR has some relation to the severity of MVP.
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PMID:[Continuity of normal and prolapsed mitral valves: two-dimensional and color Doppler echocardiographic investigations]. 325 4

In spite of two decades of research, the precise relationship of anatomic mitral valve prolapse (floppy valve) to the neuroendocrine disorder (MVP syndrome) remains unclear. In all likelihood they are two separate genetic disorders which travel together in some fashion. Mitral valve prolapse is a common disorder but progressive mitral regurgitation usually occurs late in life and in only a few patients. Other complications such as bacterial endocarditis, stroke, and sudden death are far less common but can occur at younger ages. The neuroendocrine syndrome in civilian life is mainly seen in young females (interestingly the peak incidence years correspond to peak female sex hormone output) but can be seen in males when subjected to unusual stress such as military service. More recent echocardiographic studies have questioned whether all prolapsing valves are truly abnormal. It has been shown that echographic prolapse can be produced in normal subjects by reducing venous return and impaired venous return may be present in some patients with the MVP syndrome. However, clicks and murmurs are apparently not heard when normal valves prolapse. It is our opinion that the presence of a click or typical murmur requires some anatomic abnormality of the mitral valve. One wonders if minimal valve abnormality (noted and dismissed by Davies) is the valve abnormality present in many young females with MVP syndrome, and that it may remain a mild abnormality throughout life. Recent psychiatric studies suggest that MVP is present in 30% of patients with Panic Disorder. It is not clear that this psychiatric syndrome is the same thing as the MVP syndrome. In Devereux's study, anxiety proneness was no different in the MVP cohort than in relatives without MVP. It is possible that diagnostic mixing of two similar but separate disorders has occurred, as has been the case since World War I. Perhaps the most important question is whether young patients with MVP syndrome and no echocardiographic criteria for "floppiness" will develop progressive mitral regurgitation or other complications in later life. In other words, how often is MVP syndrome in a young individual without echocardiographic evidence of a floppy valve a precourser to eventual progressive mitral regurgitation? Are there two different populations? Because of the long course of the disorder, several more years of observation (and, it is hoped, prospective longitudinal study) will be required to answer this question.
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PMID:The mitral valve prolapse epidemic: fact or fiction. 330 18

A 40-year-old man was admitted to our hospital in May 1982 for evaluation of a heart murmur. A standard 12-lead electrocardiogram (ECG) showed an abnormal Q wave in lead III. Echocardiography revealed prolapse of the anterior mitral valve leaflet (MVP), but neither dilatation nor wall motion abnormalities of the left ventricle (LV) were observed. Thallium-201 scintigraphy revealed an abnormal thallium uptake at the apex and inferior wall. He had no episode of acute myocardial infarction or myocarditis, but complete right bundle branch block suddenly appeared, and he was hospitalized in October 1984. He had no coronary artery lesions, and only mild mitral regurgitation on left ventriculography. The motion of the interventricular septum and apex was reduced on echocardiography and a persistent perfusion defect was observed at the inferior wall and the interventricular septum on T1-201 scintigraphy. In December 1985, he experienced an Adams-Stokes attack due to complete atrioventricular block. Echocardiographically, the left ventricle became enlarged and the wall motion abnormality and a perfusion defect on T1-201 scintigrams were of relatively severe degree. Thus, left ventricular dilatation and wall motion abnormality may progress in some cases of MVP as it did in this one. We consider this case a very interesting one in speculating on the relationship between MVP and DCM.
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PMID:[Regression of mitral valve prolapse to a state masquerading as dilated cardiomyopathy: a case report]. 350 16

MVP is a common condition with rare life-threatening implications. Recent follow-up studies over several years in children, and young and middle-aged adults failed to suggest increase in prolapse in most of the subjects. Older individuals with MVP appear to have increased complications, primarily due to mitral regurgitation. Echocardiography supports the diagnosis of MVP made by auscultation in over 90% of individuals, with excellent reproducibility. MVP is more common in young women than young men. The prevalence of prolapse decreases with age in women; it is relatively constant in men. Although complications are rare, MVP is the most common underlying disorder in rupture of the chordae tendineae. These spontaneous ruptures are usually unassociated with infective endocarditis. Familial studies indicate that isolated MVP is an autosomal dominant condition with variable expression. It is recommended that first-degree relatives of patients with isolated prolapse be examined. Infective endocarditis is uncommon, but it is recommended that antibiotic prophylaxis be implemented in patients with prolapse and evidence for mitral regurgitation. Prolapse is frequently associated with autonomic imbalance, primarily an increased catecholamine sensitivity. The use of beta blockers may reverse symptoms secondary to this abnormality. Sudden death is exceedingly rare despite marked arrhythmias in many patients. On the basis of retrospective studies, sudden death is associated with floppy valves, marked mitral regurgitation, and arrhythmias. There is no evidence that any class of antiarrhythmic agents can prevent the rare sudden deaths in these patients.
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PMID:Mitral valve prolapse: recent advances in diagnosis and therapy. 372 Feb 68

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.
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PMID:Does "physiologic" mitral valve prolapse occur with acute blood loss? 382 87

The etiology of cerebrovascular disease (CDV) in young patients is difficult to establish if the common causes of a focal neurological deficit are excluded by appropriate investigations. Since in some observations prolapse of the mitral-valve (MVP), alterations of platelet function, or both have been linked with cerebral ischemic events, we studied the in vivo platelet release reaction and the incidence of MVP in 47 patients (12 males, 35 females) under 45 years of age with TIA or stroke of unknown cause and in an age- and sex-matched control group. The mean plasma beta-thromboglobulin (beta-TG) level of the patients (mean = 54.9 +/- 31.4 ng/ml) was significantly higher than that of the controls (mean = 20.6 /- 6.9 ng/ml, p less than 0.001). MVP was demonstrated in 13 of 47 patients in contrast to 4 of the controls (p less than 0.01). However, the beta-T levels of patients with MVP (n = 13, 52.9 +/- 25.5 ng/ml) did not differ from those of patients without MVP (n = 34, 55.7 +/- 33.7 ng/ml) significantly (p less than 0.4). Our results confirm that the incidence of MVP is higher in young patients with cerebral ischemia of unknown cause than in asymptomatic controls. The significantly elevated plasma beta-TG concentrations in the patient's group indicate an increased platelet activity in vivo. Since there was no significant difference between beta-TG levels of patients with and without MVP, the mitral-valve abnormality can not be the cause for the altered platelet activity.
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PMID:Cerebral ischemia in young patients: it is associated with mitral valve prolapse and abnormal platelet activity in vivo? 621 70

Echocardiographic studies have recently documented high incidence of mitral valve prolapse in cases with papillary muscle dysfunction (PMD). However, any pathologic evidence has not been yet described. To evaluate the incidence and the degree of morphologic prolapse of the mitral valve, we examined 76 cases of mitral regurgitation which were pathologically proved to have PMD among 3,000 consecutive autopsy cases over 60 years of age. The morphologic evidence of "mitral valve prolapse" was defined as overshooting of the mitral leaflet into the left atrium beyond the degree of normal hooding. Papillary muscle dysfunction was classified into three types; Type A due to old myocardial infarction, Type B due to acute myocardial infarction, and Type C induced by other factors such as cardiomyopathies. The following results were obtained: Morphologic "mitral valve prolapse" was found in 19 among the 76 cases (25%) of PMD, but marked "prolapse" was found in only one case. The incidence of morphologic "prolapse" did not show any difference among the types of PMD (cf. Fig. 1). The site of "prolapse" was mainly in the region of posteromedial commissure of the mitral valve. Echocardiographic study of 39 cases with PMD showed mitral valve prolapse in only two cases who belonged to the eight cases having morphologic "mitral valve prolapse". This study suggests that prolapse formation of the mitral valve secondary to PMD can be differentiated morphologically from those following primary myxomatous degeneration of the mitral leaflets as observed in cases with MVP.
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PMID:[A study on prolapse of the mitral valve in autopsy-proved papillary muscle dysfunction]. 653 94

The past decade has seen a notable resurgence of interest in the systolic click-murmur syndrome. Previously regarded as extracardiac and benign, it is now clear that these auscultatory findings are central to a disorder characterized by abnormal systolic herniation (prolapse) of the mitral leaflets into the left atrium. Although it may be the result of diverse etiologies, the usual case represents an idiopathic, hereditary disorder of the valve leaflets with pathologic findings similar to those in Marfan's syndrome. The condition is very common and generally benign, and asymptomatic; however, a wide variety of clinical manifestations has been described, with a clinical picture at times indistinguishable from that of coronary artery disease. The small subset of patients at risk for malignant arrhythmias and sudden death has yet to be fully characterized. Although noninvasive techniques generally suffice for the diagnosis of MVP, left ventricular cineangiography is the definitive procedure. It remains for future studies in symptomatic and asymptomatic patients to define the relation between severity of MVP, its clinical manifestations, and its prognosis.
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PMID:Mitral valve prolapse--a review. 698 85


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