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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Left ventricular endomyocardial biopsy specimens were obtained at cardiac catheterisation in 11 patients with mitral-leaflet prolapse, chest pain, and normal coronary arteries. Specimens were examined for birefringence before and after contraction induced by adenosine triphosphate and were also subjected to histochemical analysis. Biopsy specimens from a control group of patients with rigorously defined normal left ventricular function and another control group with poor left ventricular function were also studied. Biopsy specimens from patients with mitral-leaflet prolapse showed a markedly subnormal birefringence response to adenosine triphosphate, with the group mean value intermediate between values for controls with normal and poor left ventricular function. Histochemical studies in the prolapse group also revealed an abnormal pattern, particularly for monoamine-oxidase activity. This is further evidence of a cardiomyopathy in this symptomatic subgroup of patients with mitral-leaflet prolapse.
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PMID:Biopsy evidence of left ventricular myocardial abnormality in patients with mitral-leaflet prolapse and chest pain. 8 76

A cardiac history, a physical examination, an electrocardiogram, phonocardiograms in the supine and standing positions, and an M-mode echocardiogram were obtained in 100 randomly selected, presumably healthy, male medical students (mean age, 26 years). Four percent met standard echocardiographic criteria for mitral valvular prolapse. No midsystolic clicks or late systolic murmurs were appreciated in this group, and none complained of chest pain or palpitations. To elucidate further the clinical implication of the echocardiographic pattern of mitral valvular prolapse, 24-hour ambulatory ECGs, multistage exercise tests, and scintiscans of myocardial perfusion at rest and after exercise (using radioactive 13nitrogen-labelled ammonium) were obtained, with normal results. The absence of life-threatening arrhythmias and exercise-induced abnormalities in these four asymptomatic subjects without abnormal physical findings suggests that the echocardiographic pattern of mitral valvular prolapse in such individuals may represent a variant of normal which does not require extensive evaluation.
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PMID:A prospective study of mitral valvular prolapse in young men. 43 82

Despite what was considered adequate pharmacological treatment, the condition of six patients with severe mitral valve prolapse but with trivial or no mitral regurgitation deteriorated. These patients had marked weakness, chest pain, dyspnea, and arrhythmias. Because these patients found their condition to be intolerable, the prolapsed mitral valve was repaired. Electrocardiography, treadmill stress testing, and left ventirculography performed following operation showed complete repair of the valve and significant improvement over the preoperative findings in all six patients. Repair of the floppy mitral valve did not eradicate all abnormalities; however, it did significantly improve the chest pain, weakness, dyspnea, and arrhythmias in all six patients. Five patients no longer require any medication. The prolapsed mitral valve contributed significantly to the symptoms and arrhythmias, but it could not have been the sole cause for these patients' signs and symptoms. With complete correction of the prolapse in all six patients, few of the signs and symptoms of the disease persisted. Repair of severe mitral valve prolapse without mitral regurgitation is recommended only for those patients who continue to be severely symptomatic from chest pain, dyspnea, or ventricular arrhythmias after an extensive trial of adequate medical therapy.
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PMID:Surgical correction of severe mitral prolapse without mitral insufficiency but with pronounced cardiac arrhythmias. 45 34

A patient with congenital complete absence of the left pericardium had a late systolic murmur and an intermittent non-ejection systolic click. A post-exercise ECG showed ST-segment depression and T-wave inversion, compatible with that described in the billowing mitral leaflet syndrome. Left ventricular cine-angiography confirmed prolapse of the mitral valve. It is suggested that an associated billowing mitral leaflet syndrome may be responsible for chest pain, variable auscultatory features and abnormal ECGs in some patients with absent left pericardium.
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PMID:Billowing mitral valve syndrome in association with absent left pericardium: a case report. 60 94

Mitral leaflet prolapse syndrome has been associated with anginal chest pain, atypical chest pain, electrocardiographic abnormalities and positive stress electrocardiograms. These features overlap those of ischemic heart disease. Furthermore, coronary artery disease is frequently associated with mitral leaflet prolapse. This study evaluated the usefulness of stress myocardial scintigraphy in distinguishing these two disorders. Thirty-two patients with an angiographic diagnosis of mitral leaflet prolapse were studied. Of the 22 patients (8 men and 14 women, mean age 48 years) with a normal coronary arteriogram, 5 had "typical" angina pectoris, 6 had resting electrocardiographic abnormalities and 6 had a positive stress electrocardiogram; all 22 patients had a normal stress myocardial scintigram. Of the 10 patients (7 men and 3 women, mean age 55 years) with at least 70 percent stenosis of one coronary artery, 6 had "typical" angina pectoris, 1 had resting electrocardiographic abnormalities and 7 had a positive stress electrocardiogram. Nine of these 10 patients had one or more demonstrable perfusion defects on stress myocardial scintigrams. It is concluded that mitral leaflet prolapse syndrome is not associated with regional myocardial ischemia as demonstrated with stress scintigraphy, and that stress scintigraphy, a noninvasive technique, is useful in distinguishing the mitral prolapse syndrome from mitral prolapse associated with coronary artery disease.
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PMID:Stress myocardial imaging in mitral leaflet prolapse syndrome. 70 87

The response to electrocardiographically monitored submaximal exercise stress testing has been studied in 44 patients with mitral leaflet prolapse (MLP). With exercise, ventricular premature contractions occurred in 7, ventricular tachycardia in 1, and atrial fibrillation in 1. Exercise was terminated short of target heart rate in 18 patients, because of chest pain (5), fatigue (7), ventricular arrhythmia (4), dizziness (1) or ST segment depression (1). 23 patients developed postexercise ST segment abnormalities, of whom 5 had 'ischemic' patterns and arteriographically proven coronary artery disease (CAD); among the 18 others, the ST segments were depressed and minimally downsloping in 2, slowly ascending from depressed J point in 3, horizontal for greater than or equal to 80 msec with J depression of less than 1 mm in 12, and cupped in 1. The incidence of arrhythmias provoked by submaximal exercise stress testing in patients with MLP was lower than suggested in previous reports. In all 5 cases where MLP and CAD coexisted, the classical 'ischemic' electrocardiographic response to exercise was not obscured. Even in the absence of CAD, postexercise ST segment abnormalities were common with MLP (18/39 = 46%) and differed from the progressively resolving ST segment deviation characteristic of CAD with angina. Exercise testing can safely be recommended, subject to standard contraindications, in patients with MLP and yields useful information.
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PMID:The electrocardiographic response to exercise in 44 patients with leaflet prolapse. 71 Apr 93

For half a century the systolic click and late systolic murmur lay dormant as innocent auscultatory curiosities. The thirteen years since Barlow related these phenomena to mitral leaflet prolapse have witnessed an astonishing information explosion. We have sought to bring together the accumulated data in this review. An Historical Perspective traces the evolution from the now abandoned "pericardial" or "extracardiac" phases, through the leafletchordal phase (redundancy), the myocardial phase (segmental left ventricular contraction abnormalities), to the anular phase (dilatation and faulty systolic contraction). Functional Anatomy is dealt with in terms of pathology, pathophysiology, hemodynamics, angiocardiography, echocardiography, and physical and pharmacological interventions. Clinical Manifestations are concerned with prevalence, natural history, symptoms, physical signs, electrocardiographic abnormalities and roentgen fingings. The four Major Complications- sudden death, infective endocarditis, spontaneous rupture of chordae tendineae, and progressive mitral regurgitation- are examined. Associated Cardiac Diseases, i.e., Marfan's syndrome, ostium secundum atrial septal defect and atherosclerotic coronary artery disease, are discussed, and a section on Treatment deals chiefly with prophylaxis for infective endocarditis and the management of arrhythmias and chest pain. A final section on Evolving Information considers etiologic concepts, the nature of left ventricular contration abnormalities, the cause of chest pain, the relationship to Marfan's syndrome and ostium secundum atrial septal defect, and the effect of aging and sex differences on leaflet chordal redundancy.
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PMID:Mitral valve prolapse. 77 40

Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
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PMID:Mitral valve prolapse. 77 95

This study evaluates propranolol's effect on symptoms, arrhythmias, and exercise tolerance in 16 patients with mitral valve prolapse. Three patients (19 per cent) experienced symptomatic deterioration with propranolol therapy, seven (44 per cent) were unchanged, and six (37 per cent) noted an over-all symptomatic improvement, primarily due to a reduction in palpitation. Symptomatic improvement continues in these six patients an average of 12.5 months after beginning propranolol therapy. Treatment with propranolol alleviated chest pain in only two of eight patients and it did not improve the ability to perform treadmill exercise. Fatigue did not improve, and in three patients appeared for the first time during propranolol therapy. Premature ventricular contractions were reduced by at least 75 per cent in five of nin patients (56 per cent), and paroxysmal ventricular tachycardia was eliminated in three of four patients. We conclude that propranolol is not uniformly effective in patients with mitral vale prolapse. A trial of propranolol may be instituted fro patients with mitral valve prolapse who have severe symptoms and/or arrhythmias, but the drug should only be continued in those who demonstrate clinical and/or antiarrhythmic response.
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PMID:Propranolol for patients with mitral valve prolapse. 84 37

A man evaluated for disabling chest pain was found to have isolated anatomically corrected transposition of the great vessels. Angiography demonstrated right and left atrioventricular (A-V) valve prolapse and normal coronary arteries. Atrial pacing produced chest pain, ischemic electrocardiographic changes, abnormal myocardial lactate metabolism and marked elevation of the left ventricular end-diastolic pressure; all of these changes returned to normal on termination of pacing. The association of corrected transposition and bilateral A-V valve prolapse and the possible causes of myocardial ischemia in this patient are discussed.
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PMID:Chest pain and bilateral atrioventricular valve prolapse with normal coronary arteries in isolated corrected transposition of the great vessels. Clinical, angiographic and metabolic features. 90 44


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