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

Echocardiography was performed in 25 consecutive patients with angina pectoris and angiographically demonstrable coronary artery disease. Left ventricular echograms detected late or pansystolic mitral valve bowing suggesting of mitral valve proplapse in 6/25 (24%). Left ventricular angiography showed prolapse of the posterior mitral leaflet in 15/25 (60%), including 5 detected by echocardiography. Significant triple vessel coronary disease was present in 11 of 15 patients with prolapsed mitralvalve. In each of the latter a greater than 90 per cent obstructive lesion was noted in at least one coronary artery: right coronary artery, 9 subjects (82%); left circumflex coronary artery, 5 patients (33%); and left anterior descending coronary artery, 4 patients (27%). Of 15 subjects with angiographic evidence of mitral valve prolapse, 13 had left ventricular asynergy-inferior or inferoposterior in 8 subjects (62%) and anterior or anteroapical in 5 subjects (38%). Eleven subjects had vectorcardiographic evidence of transmural myocardial infarction-inferior or inferoposterior in 9 (82%) and anteroseptal in 2 (18%). A single subject with mitral valve prolapse had mild mitral regurgitation. It is concluded that: (1) coexisting prolapse of the posterior mitral valve leaflet and coronary artery disease is usually associated with triple vessel obstructive lesions, (2) severe right coronary disease, inferior left ventricular wall asynergy, and inferior myocardial infarction are important angiographic and vectorcardiographic correlates, and (3) echocardiography will detect such mitral valve prolapse in only one-third of affected cases.
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PMID:Mitral valve prolapse in patients with coronary artery disease. Echocardiographic-angiographic correlation. 83 37

Angiographic clinical correlations were made in 59 patients with prolapsed mitral leaflet syndrome. Eight had nonejection systolic clicks (group I), 20 had early, mid or late systolic murmurs with or without a systolic click (group II), and 31 had pansystolic murmurs (group III). Isolated prolapse of posterior leaflet (PL) scallops occurred in 42 and 17 had combined leaflet prolapse. The study demonstrated the following: (I) Group II patients usually had isolated PL prolapse with a predominant biscallop involvement while a high incidence of triple scallop prolapse and combined mitral leaflet prolapse occurred in group III. (II) Severe mitral regurgitation and a greater incidence of atrial fibrillation were seen in patients with triscallop prolapse and combined mitral leaflet prolapse. Mitral regurgitation was milder in patients with single and biscallop prolapse and, when severe, was associated with ruptured chordae. (III) ST-T wave abnormalities in the inferior leads were most frequent in patients with isolated PL prolapse. (IV) Systolic and diastolic asynergy occurred in 41 patients, most frequently in group II but also relatively frequently in group III (19 of 31). Segmental anterior dysfunction with normal ejection fraction was found in 18 patients, of whom 13 had early anterior wall relaxation. (V) Patients without asynergy were slightly older than those with it. More in the former group had severe mitral regurgitation and were clinically disabled from it.
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PMID:Idiopathic prolapsed mitral leaflet syndrome. Angiographic-clinical correlations. 97 64

Left ventricular structure, function, and the coronary circulation were studied in a subset of patients with mitral valve leaflet prolapse. This group of 26 patients (21 females, five males, with mean age of 46 years), had the syndrome identified as idiopathic mitral valve prolapse (IMVP), which was characterized by a systolic click-murmur, clinical symptoms that were highly variable in duration and intensity, angiographically-documented mitral prolapse, and no obvious associated systemic or cardiovascular disease. Mitral regurgitation was of moderate degree in four, mild in 14, and absent in eight. The left ventricular (LV) end-diastolic volume index was elevated in ten of 25 (40%), the LV mass index was elevated in six of 17 (35%), but the LV anterior wall thickness was increase in only one of 17. Three major patterns of ventricular contraction were identified: 1) normal in seven; 2) abnormal, usually an inferior deformity and/or anterior asynergy, in eight; and 3) hyperkinetic in 11. Normal resting left ventricular function, assessed as an ejection fraction greater than 55%, was present in 17 of 25 (68%). Selective coronary arteriography was essentially normal in all 25 patients studied. An ischemic ECG response was detected during only one of 12 maximal treadmill exercise tests and in none of ten atrial pacing stress tests (AP). Myocardial lactate extraction did not change significantly during AP in six patients. We conclude that cardiomyopathy does not appear to be a primary cause or an important associated component of the IMVP syndrome. Abnormalities of the coronary circulation or of myocardial metabolism were not demonstrated by available methods. A proposed pathophysiological mechanism to explain the clinical and angiographic findings in IMVP is discussed.
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PMID:The pathophysiology of idiopathic mitral valve prolapse. 114 11

Mitral valve motion, left ventricular segmental contraction and severity of arterial stenosis were analyzed in 92 patients with coronary artery disease and 28 patients with "atypical chest pain" and normal coronary arterio-rams. Mitral valve motion was evaluated for the presence or absence of leaflet prolapse. Segmental contraction was evaluated by calculating the percent shortening of six chords of the left ventricle measured from right anterior oblique ventriculograms. The severity of disease in each coronary vessel (left anterior descending, left circumflex and right coronary) was graded on a scale of 1 (0 to 30 percent stenosis) to 5 (complete occlusion). Mitral valve prolapse was not suspected clinically but observed angiographically in 15 of 92 patients with coronary artery disease and in 5 of 28 patients with normal coronary arteriograms. In nine patients with coronary artery disease, the prolapse was restricted to the posterior leaflet, in five it was in both the anterior and the posterior leaflets and in one patient in the anterior leaflet only. Mitral regurgitation was noted in seven patients with coronary artery disease; it was mild in six and moderate in one. Among the patients with coronary artery disease, 12 of the 15 (80 percent) with mitral valve prolapse had left ventricular asynergy compared with 63 of the 77 (82 percent) without valve prolapse. The mean scores for severity of disease in the left anterior descending, circumflex and right coronary arteries were, respectively, 4.2, 2.5 and 3.2 in the patients with valve prolapse and 4.2, 2.2 and 3.5 in those without prolapse. In summary, there was no significant correlation between mitral valve prolapse and distribution of coronary arterial obstructions or abnormal patterns of left ventricular segmental contraction. There was a high frequency of mitral valve prolapse in patients with severe coronary artery disease and in those with normal coronary arteriograms and atypical chest pain.
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PMID:Mitral valve prolapse in coronary artery disease. 124 25

Three patients with mitral regurgitation (MR) associated with aortitis syndrome are presented. All had multiple lesions of the large sized arteries, calcification of the aorta, mild inflammatory findings, a chronic course, and congestive heart failure. MR was observed by ventriculography in all 3 patients. Case 1 had mitral valve prolapse and secondary systemic hypertension. Case 2 showed mildly thickened mitral valve leaflets and had moderate aortic regurgitation (AR). Case 3 had massive AR. The grade of MR was moderate in Cases 1 and 2, and massive in Case 3. The left ventricle was moderately dilated in Cases 1 and 2 but contracted sufficiently and symmetrically in all 3 patients. Other than the prolapse, no significant mitral valve deformity or left ventricular asynergy was evident by ventriculography. The incidence of MR was 3.1% of 128 patients with aortitis syndrome observed in our clinic. MR may be found in the late stage of aortitis syndrome. It may be caused by a mild valvular lesion related to aortitis syndrome and be exacerbated by increased hemodynamic loads such as those which occur in secondary hypertension and AR.
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PMID:Mitral regurgitation associated with aortitis syndrome. 613 11

Within one and a half year 24 patients with arrhythmias or chest pain were investigated to detect a mitral valve prolapse syndrome which was found in 9 cases by echocardiography. Within this group 6 patients complained of fatigue, dizziness, dyspnea or syncope, 6 had chest pain, 7 paroxysmal tachycardia and 2 patients premature beats. Auscultation revealed in 3 cases a systolic click, in 1 case a systolic click with late systolic murmur and in 5 cases a systolic murmur only. The ECG showed premature ventricular contractions in 2 patients, ST-T abnormalities in 6 patients. Echocardiography showed a late systolic prolapse in 6 and a pansystolic prolapse in 3 patients. In 3 cases also an angiography was performed and in this way a mitral valve prolapse detected; hemodynamics and coronary arteries were normal in all 3 cases but in one case a mitral insufficiency and in one case an asynergy of the anterior wall was found. Pathophysiology, clinical symptoms and phonocardiographic, echocardiographic and angiographic findings in mitral valve prolapse syndrome are discussed.
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PMID:[Mitral valve prolapse syndrome]. 744 4

Echocardiographic assessment of mitral regurgitation allows the diagnosis of its mechanism and cause which are major determinants in the feasibility of mitral valve repair. This assessment is based on a systematic analysis of the different structures of the mitral valve apparatus: mitral annulus (enlargement, calcification), mitral valve morphology (thickening, calcification, floppy valve, vegetations, perforation), mitral valve motion (restriction, identification of the prolapsed leaflets and scallops in patients with mitral valve prolapse or flail leaflets), subvalvular apparatus (ruptured chordae, thickening), papillary muscles, and left ventricular wall. This analysis can diagnose the mechanism of mitral regurgitation according to the Carpentier classification, and can clarify its cause: degenerative lesions (prolapse or flail leaflet with or without ruptured chordae), rheumatic lesions (thickened valves with restricted motion), endocarditis (vegetations, perforation, ruptured chordae), ischemic mitral regurgitation (restricted valve motion with inferior or posterior left ventricular wall asynergy), or functional mitral regurgitation (annular dilatation, displacement of papillary muscles with restricted leaflet motion). Transthoracic echocardiography with harmonic imaging usually allows a comprehensive assessment of functional anatomy of mitral regurgitation. Transesophageal echocardiography is indicated if transthoracic echocardiography is inadequate. It is also indicated just before surgery and as an intraoperative procedure. Real time 3D echocardiography should probably complete the evaluation of mitral regurgitation in the near future.
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PMID:[Use of echocardiography in mitral regurgitation for the assessment of its mechanism and etiology for the morphological analysis of the mitral valve]. 1275 63