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

A patient with click and late systolic murmur syndrome originating in the right side of the heart is described. Prolapse of the anterior tricuspid leaflet was demonstrated by subxiphoid two-dimensional echocardiography alone. Neither of the mitral leaflets showed any evidence of prolapse on the echocardiogram. The prolapsed anterior tricuspid leaflet and mild regurgitation were confirmed by right heart cineangiogram.
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PMID:Subxiphoid two-dimensional echocardiographic detection of tricuspid valve prolapse. 51 9

Quantitative angiographic findings were reviewed in 40 patients with significant mitral regurgitation classified into three etiologic groups: group I, primary mitral regurgitation (prolapse, ruptured chordae); group II, mixed stenosis and regurgitation of rheumatic origin; and group III, cardiomyopathic mitral regurgitation. For patients in both groups I and II, left ventricular end-diastolic volume was directly related to regurgitant fraction, and ejection fraction was generally well maintained. In contrast, patients in group III had a depressed ejection fraction (less than 0.40) and end-diastolic volume that was disproportionately increased in relation to the degree of regurgitation. Left ventricular end-diastolic pressure was a poor indicator of severity of regurgitation in all patient groups. There was a significant negative correlation between forward cardiac index and regurgitant fraction. There was significant relation, although with considerable variation, between the normalized V wave and regurgitant fraction. The graphs of chamber size, ejection fraction and hemodynamic measures plotted against the severity of regurgitation in different patient groups provide a perspective for interpreting the findings in individual patients.
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PMID:Ventriculographic and hemodynamic features of mitral regurgitation of cardiomyopathic, rheumatic and nonrheumatic etiology. 55 77

The occurrence of mitral regurgitation in ankylitis is very unusual. The case reported herein is a remarkable one because the subaortic bump at the base of the anterior mitral leaflet, the mose characteristic aspect of the heart involvement in this disease, was visualized for the first time by echocardiography. Moreover, the prolapse of the mitral leaflets was documented; it allows for a new understanding as far as the mechanism of the regurgitation is concerned.
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PMID:[Mitral and aortic regurgitation: a rare association in ankylosing spondylitis (author's transl)]. 66 14

In 26 patients with mitral valve prolapse, ventricular function was evaluated by mean velocity of circumferential fiber shortening (MVCF) as measured along the basilar, middle and apical axes. Significantly increased rates of MVCF were found in patients with mitral prolapse along the basilar axis (1.75 +/- 0.23 circ/sec) and middle axis (2.09 +/- 0.34 cir/sec) (P less than 0.025 and P less than 0.05, respectively). Patients with mitral valve prolapse and regurgitation demonstrated a significant increase in MVCF along the basilar axes (1.72 +/- 0.15 cir/sec) (P less than 0.05). Asynergy apperars to have a negative effect on the MVCF along the middle axis. The MVCF was found not to be related to clinical findings, symptoms or electrocardiographic changes. The mechanism for the increase in MVCF in patients with mitral valve prolapse remains unsettled.
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PMID:Mean velocity of circumferential fiber shortening in prolapsed mitral leaflet syndrome. 91 47

Four adult women with histories of rheumatic fever and clinical findings of mitral stenosis and regurgitation had echocardiograms demonstrating moderately severe mitral stenosis (EF slope less than 20 mm/sec, mean left atrial size 3.0 cm/m2, mean anterior mitral leaflet excursion 25 mm) as well as typical mitral valve prolapse. Three patients underwent cardiac catheterization which confirmed the presence of mitral stenosis, as well as systolic prolapse and excessive scalloping of the mitral valve with no visible mitral calcium and no coronary artery disease. One patient had associated mild aortic stenosis and regurgitation. Two patients underwent mitral valve surgery which revealed anterior and posterior commissural fusion consistent with rheumatic disease and intact chordal apparatus. Both leaflets were large and the anterior leaflets were redundant. There were no vegetations. Pathology revealed myxomatous degeneration of the valve leaflets. In the absence of heavy calcification and thickening, the presence of mitral stenosis with commisural fusion does not exclude the possibility of a redundant mitral valve. When these entities coexist, systolic clicks may be absent.
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PMID:Mitral valve prolapse in rheumatic mitral stenosis. 92 8

Three cases of aortic sinus aneurysm and three cases of prolapse and regurgitation of the aortic valve associated with ventricular septal defect are discussed from an angiographic point of view. It is pointed out that aortic regurgitation into the left ventricle might be helpful for a correct diagnosis. Aortic regurgitation, in fact, is the result of an anatomically unsupported aortic valve that becomes gradually distorted by haemodynamic influences. This pathogenetic mechanism is often found in subpulmonar and infracrestal ventricular septal defect.
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PMID:[Aortic sinus aneurysm. The angiographic diagnosis (author's transl)]. 101 Jan 92

The midsystolic click-late systolic murmur syndrome is a complex entity with variable manifestations that involves a primary process causing myxomatous degeneration of the mitral valve leaflet(s) and subsequent systolic mitral valve leaflet prolapse. Other cardiac diseases may cause mitral valve prolapse and regurgitation associated with a midsystolic click that mimics this primary syndrome. The prolapsing mitral valve leaflet(s) syndrome occasionally may be familial. Most patients are asymptomatic but some complain of chest pain, palpitation, dyspnea or fatigue. Prolapsing mitral valve leaflet(s) can be distinguished from other causes of systolic clicks and mitral regurgitation murmurs by the characteristic movement of the clikmurmur complex in systole with various hemodynamic interventions. The clinical diagnosis usually can be confirmed by echocardiography, which demonstrates the abnormally prolapsdrome usually is minimal but can be progressive and lead to the need for prosthetic valve replacement. Most symptomatic patients can be managed medically but some require cardiac catheterization to evaluate the possibility of coexistent coronary artery disease, to assess the degree of mitral regurgitation and to evaluate other associated cardiac lesions. All patients with this syndrome should receive antibiotic prophylaxis prior to any surgical or dental procedures. Those patients suspected of having arrhythmias should be evaluated by continuous ambulatory ECG monitoring and dangerous arrhythmias probably should be treated. The prognosis usually is excellent, but sudden death and rapidly progressive mitral regurgitation due to ruptured chordae tendineae have been reported. Although more than a decade has elapsed since the midsystolic click-late systolic murmur syndrome was first recognized, much remains to be learned about this common but complex clinical entity.
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PMID:The systolic click-murmur syndrome: clinical recognition and management. 101 8

Marked changes in the auscultatory pattern with posture have been noted in patients with mid-systolic clicks and/or late systolic murmurs (MSC-LSM). MSC tend to move earlier in systole and LSM become longer and often louder when patients assume upright posture. Systolic prolapse of the mitral leaflets with mild regurgitation account for MSC-LSM; earlier and greater prolapse with more and prolonged regurgitation associated with a reduced left ventricular volume (LVV) in the upright position would explain the auscultatory changes. Twenty-two patients with MSC-LSM were studied supine and at 45 degrees head-up tilt, recording intracardiac pressures, cardiac outputs, systolic time intervals, and performing LV cineangiography. Systolic prolapse of one or both mitral leaflets was demonstrated in all patients. Left ventricular end-diastolic and end-systolic volumes both decreased significantly at 45 degrees in all sixteen technically satisfactory studies. Greater mitral prolapse was noted upright in 12 of 14 studies with enough sinus beats to judge. The amount of mitral regurgitation was mild in all, and changes in amount from supine to upright posture could not be discerned angiographically. THE FINDINGS, SUGGEST THAT THE AUSCULTATORY CHANGES OCCURRING WITH UPRIGHT POSTURE IN PATIENTS WITH MSC-LSM are related to greater prolapse of the mitral leaflets which is associated with a small LVV in the upright position.
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PMID:Postural changes in left ventricular and mitral valvular dynamics in the systolic click - late systolic murmur syndrome. 110 15

Two patients with a prolapse and cleft posterior mitral leaflet were studied. The first case had an associated ostium secundum type atrial septal defect. In both cases, the pansystolic regurgitation of contrast material during angiography corresponded to the pansystolic configuration of the murmur. In each instance, the systolic murmurs displayed a late systolic accentuation during the maximal prolapse of the mitral valve. The echocardiographic studies demonstrated only a late systolic prolapse which in both patients corresponded angiocardiographically to the maximum buckling of the pansystolic prolapse. Echocardiographic and angiocardiographic features of cleft posterior mitral valve leaflet are discussed.
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PMID:Prolapsing mitral valve leaflet syndrome. A spectrum that includes cleft posterior mitral valve. 126 Aug 54

A consecutive series of 912 surgically excised aortic valves was evaluated by means of macroscopic and histologic study. Pure aortic stenosis was diagnosed in 203 patients (p.) (22.25%), pure incompetence in 125 (13.72%) and combined dysfunction in 584 (64.03%). The diseases affecting the valves were: a) chronic rheumatic disease (593 p., 65%); b) dystrophic calcifications (214 p., 23%); c) noninflammatory aortic root disease (NIARD) and/or myxomatous infiltration of aortic cusps, floppy aortic valve (FAV) (55 p., 6%) d) infective endocarditis (50 p., 5.5%). Males outnumbered females with a ratio ranging from 2.4 (dystrophic calcific disease) to 1.6 (infective endocarditis). The mean age ranged from 37 +/- 7.5 (NIARD) to 61.2 +/- 6.3 (dystrophic calcific disease). Chronic rheumatic disease was the most frequent cause of stenoincompetence (542 p., 91.4%) while isolated stenosis was prevalently due to dystrophic calcification (172 p., 80.4%). The diseases causing isolated aortic incompetence were (in order of frequency): a) NIARD and/or FAV (55 p., 44%); b) infective endocarditis (50 p., 40%); and c) rheumatic disease (30 p., 16%). The 55 patients with NIARD and or FAV were divided into 3 groups: a) 23 p. with aortic root dilatation and normal cusps; b) 20 p. with aortic root dilatation and FAV; c) 12 p. with FAV but undilated aortic root. Aortic regurgitation was caused by cusp derangement in rheumatic disease (shortening, retraction) and infective endocarditis (perforations, erosions). Cusps diastasis and prolapse were the cause of regurgitation in aortic root dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Surgical pathology of the aortic valve: a morphologic study on 912 surgically excised valves]. 129 12


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