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

Secondary valve prolapse emerges in a variety of heart diseases: coronary heart disease, dilated and hypertrophic cardiomyopathies, acquired valvular heart disease, infectious endocarditis, pulmonary hypertension, etc. Valve prolapse results from dilation of valvular fibrous rings, dysfunction of papillary muscles, mitral lesions in valvulitides. Secondary valve prolapse in dilatation of valvular opening entails manifest disorders of systemic and intracardiac hemodynamics except for cases of aortic root dilatation. In decreased valvular opening secondary valve prolapse is not associated with considerable shifts in hemodynamics. Secondary valve prolapse suggests primary structural and functional defects in the heart rather than promotes the development of circulatory insufficiency.
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PMID:[Secondary prolapse of heart valves]. 237 Jul 83

68 cases with 76 left ventriculographies, including rheumatic mitral valvular disease, congestive and hypertrophic types of cardiomyopathy, endocardial cushion defect, atrial and ventricular septal defects, coronary heart disease and mitral valve prolapse were analyzed with respect to the morphological and functional changes of the mitral valve and its appendages. Dynamic study with cineradiographic technic was the chief method used in this investigation. Except for ventricular septal defect, all the above-mentioned disease entities showed one or several of the changes of the mitral valvular apparatus including stenosis, insufficiency, displacement, cleft, deformity, prolapse and functional disorder. Regurgitation associated with mitral insufficiency exhibiting specific manifestations in different conditions was analyzed and its method of grading discussed. Mitral valve prolapse with its suggested method grading and functional disorder of the mitral valve were also discussed in detail.
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PMID:[Angiographic diagnosis of lesions of the mitral valve and its appendages]. 252 46

In 51 consecutive patients with acute transitory cerebral ischaemia cross-sectional echocardiograms, 24-hour electrocardiograms (ECG) and exercise ECGs were recorded. The subsequent observation period averaged 13 (3-30) months. The echocardiogram was abnormal in 27 of 46 patients (58%). A holosystolic mitral-valve prolapse was found in eight: cerebral ischaemia recurred in five. There was no correlation between arrhythmias in the 24-hour ECG and renewed cerebral ischaemia. In addition to the 14 patients who--according to history and resting ECG--had already had a myocardial infarction, the exercise ECG revealed probably coronary heart disease in a further 11, i.e. half of the patients had coronary heart disease. Renewed attacks of cerebral ischaemia occurred in 13 patients during the follow-up period; four patients died, all of them also having had coronary heart disease. Because of the high prevalence of coronary heart disease (often previously undiagnosed) in the whole group, routine exercise ECGs are recommended for patients with transitory ischaemic attacks, protracted ischaemic neurological deficit or "minimal stroke", while 24-hour ECG monitoring does not seem essential. Randomized trials are needed to determine whether patients with cerebral ischaemia and echocardiographic evidence of mitral-valve prolapse should be treated prophylactically.
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PMID:[Patients with transient ischemic attacks. Their cardiac status and its prognostic significance]. 335 33

Mitral valve prolapse frequently resembles coronary heart disease. Retrospective clinical, ECG and angiographic analysis of 100 consecutive patients with mitral prolapse and normal coronary arteries, but complaining of anginal pain, shows how difficult it is to establish the correct diagnosis. When resting, 44% of patients have nonspecific ECG disorders of repolarization phase. During periods of chest pain 3 patients experienced transient ST segment changes very similar to acute myocardial ischemia. The exercise test was positive in 39% of cases, and in 2 patients during exercise a sudden drop in blood pressure suggested coronary perfusion failure. In all patients the coronary arteries were normal, but left ventriculography showed mitral valve prolapse predominantly on the posterior leaflet. At rest, 35% of patients had diastolic compliance failure, 32% had left ventricular hyperkinesia and only in 3% was slight hypokinesia present. Finally, early systolic relaxation of the anteroapical wall was observed in 75% of patients.
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PMID:[Mitral prolapse syndrome: clinical, electrocardiographic and angiocardiographic correlations. Study of 100 patients with healthy coronary vessels]. 396 47

Anatomic and functional features of the normal and abnormal mitral valve are reviewed. Of 1,010 personally studied necropsy patients with severe (functional class III or IV, New York Heart Association) cardiac dysfunction from primary valvular heart disease, 434 (43%) had mitral stenosis (MS) with or without mitral regurgitation (MR): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 189 (44%) patients, and associated with aortic stenosis in 152 (35%), with pure (no element of stenosis) aortic regurgitation in 65 (15%) patients, and with tricuspid valve stenosis with or without aortic valve stenosis in 28 (6%) patients. The origin of MS was rheumatic in all 434 patients. Of the 1,010 necropsy patients, 165 (16%) had pure MR (papillary muscle dysfunction excluded): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 97 (59%) patients, and associated with pure aortic regurgitation in 45 (27%) and with aortic valve stenosis in 23 (14%) patients. When associated with dysfunction of the aortic valve, pure MR was usually rheumatic in origin, but when unassociated with aortic valve dysfunction it was usually nonrheumatic in origin. Review of operatively excised mitral valves in patients with pure MR unassociated with aortic valve dysfunction disclosed mitral valve prolapse (most likely an inherent congenital defect) as the most common cause of MR. Excluding the patients with MR from coronary heart disease (papillary muscle dysfunction), mitral prolapse was the cause of MR in 60 (88%) of the other 68 patients, and a rheumatic origin was responsible in only 3 of the 68 patients, all 68 of whom were greater than 30 years of age. Mitral anular calcification in persons aged greater than 65 years is usually associated with calcific deposits in the aortic valve cusps and in the coronary arteries. Because calcium in each of these 3 sites is common in older individuals residing in the Western World, it is most reasonable to view mitral anular calcification in older individuals as a manifestation of atherosclerosis. Mitral anular calcium appears to be extremely uncommon in persons with total serum cholesterol levels less than 150 mg/dl. Mitral anular calcium may produce mild MR and, if the deposits are heavy enough, MS.
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PMID:Morphologic features of the normal and abnormal mitral valve. 633 91

Contradictory two-dimensional echocardiographic findings have been reported in relation to the role of prolapse of the mitral valve and lack of systolic leaflet coaptation in mitral regurgitation secondary to coronary heart disease. A prospective study of 22 patients with chronic coronary heart disease and mitral regurgitation showed the following: Inferior akinesia was detected in 14 (64%), fibrosis of the postero-medial papillary muscle in 10 (45%), and prolapse of the mitral valve in nine (41%). A combination of the three signs was seen in six patients (27%). Lack of systolic leaflet coaptation was seen in only two patients, both with anterior myocardial infarction. When these results are compared with those reported in the literature, it is apparent that in acute coronary heart disease, lack of leaflet coaptation is frequently visualized (P less than 0.01) and fibrosis of the postero-medial papillary muscle and prolapse of the mitral valve are lacking (P less than 0.01). A unitary explanation of all forms of mitral regurgitation in coronary heart disease is misleading; mechanisms of mitral regurgitation in coronary heart disease depend on the clinical presentation--acute or chronic, the site of infarction, and the presence of cardiac dilatation.
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PMID:Different mechanisms of mitral regurgitation in acute and chronic forms of coronary heart disease. 664 50

To assess the reliability of M-mode echocardiographic patterns of mitral valve prolapse (MVP) (echo MVP) in detection of morphologic evidence of MVP (morphologic MVP), operatively excised mitral valves and corresponding M-mode echocardiograms from 65 patients with chronic, severe, isolated, pure mitral regurgitation (MR) were studied. Of the 65 patients, 45 (69%) had echo MVP (either holosystolic or mid-to-late systolic prolapse patterns on preoperative M-mode echograms) and 42 (93%) of them had morphologic MVP; of the 3 without morphologic MVP, 2 had ruptured chordae tendineae from infective endocarditis and 1 had papillary muscle dysfunction from atherosclerotic coronary heart disease. Of the 20 patients without echo MVP, 14 (70%) had no morphologic MVP (9 had papillary muscle dysfunction from coronary heart disease, 4 had infective endocarditis on previous normal valves and 1 had rheumatic heart disease). Of the 48 patients with morphologic MVP, 42 (88%) had echo MVP and most had considerably dilated mitral anulae; the other 6 had ruptured chordae tendineae with less degrees of anular dilatation. Of the 17 patients without morphologic MVP, 3 had echo MVP (coronary artery disease in 1 and infective endocarditis on a previous normal valve in 2); of the 14 with neither echo nor morphologic MVP, 9 had papillary muscle dysfunction from coronary artery disease, 4 had infective endocarditis on previously normal valves and 1 had rheumatic heart disease. The patients with very dilated mitral anuli and leaflet areas generally had holosystolic (hammocking) patterns on echo; the patients with small anuli and leaflet areas usually had mid-to-late systolic (buckling) prolapse patterns.
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PMID:Frequency and significance of M-mode echocardiographic evidence of mitral valve prolapse in clinically isolated pure mitral regurgitation: analysis of 65 patients having mitral valve replacement. 669 Dec 50

Left ventricular ejection fraction (LVEF) was calculated by echocardiography and gate blood pool (GBP) in 33 patients including those with coronary heart disease, acute and old myocardiac infarction, cardiomyopathy or mitral prolapse. Fourteen of the 33 had segmental wall motion abnormalities and 19 had non-segmental wall motion abnormalities. The results of comparing echocardiography and GBP showed that the former could substitute for other invasive and expensive examinations to determine LVEF (r = 0.804-0.964 in the 5 echocardiography methods used). Mod-Simpsons method of cross-sectioned echocardiography was the most accurate echocardiographic method (r = 0.964, sensitivity 90.9%) in all patients. The Teich method of M-mode echocardiography was useful in patients who had non-segmental wall motion abnormalities only (r = 0.957, sensitivity 94.7%) but not in patients who had segmental wall motion abnormalities (r = 0.703, sensitivity 42.9%).
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PMID:[Evaluation of echocardiography for determining left ventricular function]. 795 67

Atrial septal aneurysm is a localized "saccular" deformity, generally at the level of the fossa ovalis, which protrudes to the right or the left atrium or both. For 39 months we prospectively analyzed 205 consecutive patients in whom atrial septal aneurysm was diagnosed echocardiographically. The direction and movement of atrial septal aneurysms were carefully studied in multiple views, and, according to our findings, we now propose a new classification: type 1R if the bulging is in the right atrium only, type 2L if the bulging is in the left atrium only, type 3RL if the major excursion bulges to the right atrium and the lesser excursion bulges toward the left, type 4LR if the maximal excursion of the atrial septal aneurysm is toward the left atrium with a lesser excursion toward the right atrium, type 5 if the atrial septal aneurysm movement is bidirectional and equidistant to both atria during the cardiorespiratory cycle. We found an incidence of 1.9%, a mean age of 63 years (25 to 97 years), a female/male ratio of 2:1, valvular regurgitation 74%, hypertension 64%, left ventricular hypertrophy 38%, coronary heart disease 32%, patent foramen ovale 32%, pulmonary hypertension 31%, stroke 20%, dysrhythmias 16%, valvular prolapse 15%, and atrial septal defect 3%. No differences were found between mobile and motionless types of atrial septal aneurysm. However, differences were found between predominantly left bulging or right bulging atrial septal aneurysm (134 versus 57 patients), as well as other variables. All types of atrial septal aneurysm have particular clinical or echocardiographic characteristics. The new classification is a complete, simple, and practical form. Atrial septal aneurysm is associated with congenital and acquired heart diseases but also can present as an isolated abnormality.
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PMID:Atrial septal aneurysm: a new classification in two hundred five adults. 928 54

In a 77-year-old man with a history of arterial hypertension, coronary heart disease, dilative cardiomyopathy, mitral and tricuspid insufficiency, arteriovenous block III, implantation of a pacemaker, atrial fibrillation, and heart failure, left ventricular hypertrabeculation (LVHT) was detected on transthoracic echocardiography during hospitalization for worsening heart failure. Revision of previous echocardiography did not show LVHT in any of the previous investigations why LVHT was interpreted as acquired. The additional presentation with bilateral ptosis, madarosis (absent eyelashes), bilateral hypoacusis, sore neck muscles, absent tendon reflexes, weakness for foot extension, ataxic stance, and recurrently elevated creatine kinase with normal troponin-T suggested a metabolic myopathy. Autopsy after death resulting from intractable heart failure, 17 months later, confirmed severe coronary heart disease and LVHT in the apex. The case confirms that LVHT may be acquired in single cases with neuromuscular disease and may represent an adaptive mechanism of an impaired myocardium.
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PMID:Acquired noncompaction associated with coronary heart disease and myopathy. 2045 46


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