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

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

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

The correlation of clinical features with the operative findings in 14 patients with a floppy mitral valve is discussed. The clinical course is typified by rapidly progressive disability. An abrupt deterioration was present in five of our subjects and this may be due to rupture of chordae tendinea or stretching of the valve apparatus. The redundancy of the anterior cusp in 13 of our series may explain the absence of mid systolic clicks in all except one patient. The diagnosis of prolapse can be difficult to make prior to surgery because the prolapsed cusp may be masked by the regurgitant contrast medium. Hypokinesis and prominent inflow sacculation of the left ventricular inflow tract suggest an associated myocardial abnormality. Calcium was present in one valve and thus mitral valve calcification does not exclude the possibility of a floppy valve in patients with mitral regurgitation.
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PMID:The floppy mitral valve syndrome--a review of fourteen patients requiring valve surgery. 105 20

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

The association of prolapse of the posterior leaflet of the mitral valve with secundum atrial septal defect has recently been reported but the prevalence and features of this association have not been defined. Analysis of left ventricular cineangiograms in 54 patients have secundum atrial septal defect revealed evidence of prolapse of the posterior leaflet of the mitral valve in 20 (37 percent). In 11 patients (20 percent) there was clinical evidence of a mitral valve lesion (pansystolic murmur in 9 patients and mid-systolic click in 2 patients, 1 of whom also had a late systolic murmur); the remaining 9 patients had no auscultatory evidence of a mitral valve lesion. Thus, the incidence of clinically silent prolapse in association with secundum atrial septal defect was 17 percent (9 of 54 patients). Analysis of the angiographic findings revealed that the prolapse was triscalloped in 4 patients, biscalloped in 11 and uniscalloped in 5. Mitral regurgitation was present in 12, including the 11 patients with clinical signs of a mitral lesion. Three patients with moderate or severe mitral regurgitation had triscalloped prolapse. The association of prolapse of the posterior leaflet of the mitral valve with secundum atrial septal defect is common and may be present in the absence of any clinical evidence of a mitral valve lesion.
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PMID:Prolapse of the posterior leaflet of the mitral valve associated with secundum atrial septal defect. 111 94

Of 184 patients with acute rheumatic fever and associated mitral insufficiency encountered during a 15 year period, 34 manifested a mid-late systolic murmur or a nonejection click, or both, during the course of follow-up. The mid-late systolic murmur later disappeared in four patients whose condition is now considered normal. In one of the four, systolic prolapse of the mitral valve was demonstrated on an angiocardiogram obtained when the systolic murmur was present. Since disappearance of the murmur there has been no evidence of systolic prolapse on meticulous echocardiographic study of the mitral valve. In another child with angiographically demonstrated systolic prolapse of the mitral valve the systolic murmur has also disappeared, but systolic prolapse is still evident on echocardiographic study. None of the 34 patients with a mid-late systolic murmur manifested the T wave abnormalities commonly associated with the familial variety of mitral valve prolapse.
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PMID:Late systolic murmur of rheumatic mitral insufficiency. 111 97

Among 95 patients with angina pectoris and angiographically documented coronary artery disease (CAD), prolapse of the scallops of the posterior leaflet of the mitral valve (PLMV) was noted in 30 patients. Left ventriculograms in the right anterior oblique (RAO) projection revealed isolated prolapse of the posteromedial commissural scallop (PMCS) in 12 patients and the anterolateral commissural scallop (ALCS) in two patients. Seven patients had prolapse of both PMCS and ALCS, three had prolapse of the PMCS and middle scallop (MS), and six had prolapse of all three scallops of the PLMV. Left ventricular dilatation with increase trabeculations was observed in 19 patients. Contractility determined in a quantitative fashion by segmental motion analysis was markedly impaired in 29 patients. None of the patients had angiographic evidence of mitral insufficiency. Left ventricular dysfunction was documented in 28 patients by either elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index (CI) or decreased ejection fraction (EF). In two patients in whom left ventricular contractility improved after aortocoronary by pass, previously prolapsed scallops could not be identified in the postoperative ventriculogram. Prolapsed PLMV is a frequent angiographic finding in patients with angiographically observed CAD. Impaired contractility of the ventricular myocardium and papillary muscles, left ventricular dilatation, and hypertrophy appear to play a significant role in the pathogenesis of this abnormality through distortion of the directional axis of the papillary muscles, asynergic contraction of the related free wall of the left ventricle, and changes in the normal spatial alignment necessary for mitral valve closure. The syndrome of papillary muscle dysfunction in patients with coronary artery disease represents a wider clinical spectrom than previously described.
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PMID:Mitral valve prolapse and coronary artery disease. Clinical, hemodynamic, and angiographic correlations. 114 6

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

Echocardiographic and phonocardiographic findings in 35 patients with Marfan's Syndrome and ten patients without Marfan's or other clinically apparent connective tissue disorders but with angiographic and echocardiographic evidence of mitral prolapse are reported and compared. Echocardiography revealed aortic root dilatation and/or mitral valve prolapse in 97% of the patients with Marfan's Syndrome. Aortic root dilatation was found in 60% of this group (74% of males, 33% of females) while mitral valve prolapse was found in 91% (87% of males, 100% of females). The incidence of aortic dilatation and mitral prolapse in patients with Marfan's syndrome was essentially equal in children and adults of the same sex. None of the nine adults or one child with mitral prolapse but without evidence of Marfan's Syndrome or other clinically apparent connective tissue disorder had aortic root enlargement. Ausculatory examination and phnocardiography revealed abnormalities in 54% of the patients with Marfan's Syndrome. Aortic regurgitation was found in 23% of this group (35% of males, 0% of females) while mitral regurgitation and/or mitral clicks were found in 46% (39% of males, 58% of females). Aortic regurgitation was much more frequent in adult males with Marfan's Syndrome (7/14, 50%) than male children (1/9, 11%), while the incidence of abnormal mitral sounds was essentially the same in adults (33% of males, 60% of females) and children (43% of males, 57% of females) of the same sex with Marfan's Syndrome. Abnormal mitral sounds were more frequent in patients without Marfan's who had mitral prolapse (90%) than in those with Marfan's (46%). It appears that cardiac abnormalities are a consistent manifestation of Marfan's Syndrome and that ultrasound is a more sensitive indicator of these abnormalities in such patients than ausculation or phonocardiography.
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PMID:Aortic root dilatation and mitral valve prolapse in Marfan's syndrome: an ECHOCARDIOgraphic study. 115 78

Twenty-three patients with the syndrome of midsystolic click--late systolic murmur were investigated by right and left heart catheterization, cineangiography and echocardiography. Most of the patients had symptoms such as atypical chest pain and arrhythmias. Except in one patient, slight to moderate mitral incompetence was found at rest or during stress testing by infusion of aramine or rapid atrial pacing (2 patients). In all cases, an abnormal systolic mitral valve motion was found in left ventricular cineangiography. In 14 of 15 technically satisfactory echocardiograms a systolic prolapse of one or both mitral leaflets was observed. A minority of the patients had localized abnormal wall motion in the postero-basal area or moderate generalized hypokinesis.
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PMID:[Proceedings: Left ventricular cineangiography and echocardiography in patients with the mesosystolic click-telesystolic sound syndrome]. 121 35


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