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

Nine adult patients with large pericardial effusions (PE) demonstrated echocardiographic motion abnormalites of cardiac valves in systole. In four cases (Group 1), the abnormal findings consisted of prominent systolic anterior movements of the mitral valve resembling those seen in idiopathic hypertrophic subaortic stenosis. In Group 2(five cases), typical mitral valve prolapse patterns with large posterior midsystolic displacements well below the C point were observed. Additional abnormalities in Group 2 included tricuspid valve prolapse patterns (four cases), early systolic movement of the aortic valve toward closure (three cases), midsystolic notching of the pulmonary valve (two cases) and abnormal or attenuated motion of the aortic root in all patients. Marked decrease or resolution of PE resulted in complete disappearance of all the observed abnormalities. These findings appeared to be related to large fluid collections behind the left atrium and abnormal movement of the heart in the pericardial space. In the presence of PE, therefore, the echocardiographic observation of abnormal valve motion may not be clinically significant.
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PMID:Echocardiography of cardiac valves in pericardial effusion. 94 81

Severe prolapse of the mitral valve leaflets was seen at left ventricular angiography in 16 of 92 patients with a secundum type atrial septal defect studied prospectively from 1970 to 1974. The patients were aged 15 to 69 years; angioplasty or mitral valve replacement was carried out in nine. In 9 of 122 patients aged 15 to 55 years who were operated on for closure of a secundum type atrial septal defect between 1956 and 1969, mitral regurgitation due to prolapse but with intact chordae tendineae was seen at operation. In three of these patients chordal rupture was seen at a second operation 2 to 6 years later. The outlook in the syndrome of mitral valve prolapse may be less benign than is usually believed.
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PMID:Association of ostium secundum atrial septal defects with mitral valve prolapse. 95 60

Myocardial lesions are frequently seen at necropsy after fatal carbon monoxide poisoning. Clinically, while there have been numerous reports of chest pain and electrocardiographic changes associated with acute carbon monoxide poisoning, other evidence for left ventricular abnormality has not been reported. The echocardiographic findings in five cases of non-fatal poisoning are presented here. Abnormal left ventricular wall motion was shown by echocardiography in 3 cases. Motion returned to normal in 2 of the 3 in follow-up tracings. Echocardiograms on 3 of the 5 patients showed mitral valve prolapse. Though the mitral valve prolapse may have been present before the poisoning, the reported high incidence of papillary muscle lesions in fatal cases suggests a possible relation of the prolapse to the effects of the carbon monoxide poisoning.
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PMID:Echocardiographic findings after acute carbon monoxide poisoning. 97 96

Previous parallel echocardiographic-angiocardiographic studies have proven specificity and sensitivity of ultrasonography in diagnosing prolapse of the mitral valve. Echocardiograms and phonocardiograms from 68 patients with mitral valve prolapse were studied. Echocardiograms suggestive of mitral valve prolapse were obtained in 66 patients. The typical abnormality consisted of an abrupt posterior displacement of the mitral valve leaflets, either late systolic or pansystolic. Moreover a new pattern not previously described was observed, i.e. an abrupt isolated early systolic posterior motion of the mitral leaflets ("early prolapse"). Phonocardiography, on the other hand, showed a variable spectrum of acoustic findings: non-ejection systolic click and/or late systolic murmur, pansytolic murmur, early systolic click,ejectioarly systolic click, ejection murmur, in variable association, and finally no abnormal sound at all ("silent prolapse"). The authors conclude that mitral valve prolapse may be suspected, whatever the auscultatory finding. Echocardiography provides a useful, non invasive method for detecting those forms which also present an uncommon auscultatory pattern.
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PMID:[Variable aspects in mitral valve prolapse. Echographic and phonocardiographic studies of 68 cases (author's transl)]. 97 57

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

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

The echocardiographic findings in 12 patients with tricuspid valve prolapse are presented. Eight of these patients had associated mitral valve prolapse. Only one of the above patients had the characteristic physical signs of tricuspid incompetence. Two types of abnormality were noted on the echocardiogram of the tricuspid valve. In eight patients, the systolic segment of the tricuspid valve showed an initial horizontal motion followed by a posterior motion in midsystole. Four patients exhibited posterior motion of the tricuspid valve in early systole, which reached a maximum in midsystole, and this was followed by an anterior motion, thus producing a hammock-like configuration. We conclude that echocardiography is useful in the diagnosis of tricuspid valve prolapse. Since this condition may be associated with clinically significant tricuspid incompetence or bacterial endocarditis, its recognition is of clinical importance.
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PMID:Echocardiographic detection of tricuspid valve prolapse. 112 85

Simultaneous electrocardiograms, phonocardiograms, and echocardiograms were recorded in 21 patients with mitral valve prolapse. Four patients with holosystolic mitral valve prolapse on echocardiogram had smaller resting end-diastolic volumes than the remaining 17 patients with late systolic echocardiopraphy prolapse (p greater than 0.01). Thirteen of the 17 patients with late systolic prolapse had phonocardiograhically recorded auscultatory phenomena. The initial vibrations of the auscultatory phenomena occurred after the onset of echocardiographic prolapse, but prior to maximal echocardiographic mitral valve prolapse. Amyl nitrite was administered to all patients. Three of the 17 patients with late systolic prolapse developed holosystolic prolapse, while the remaining 14 retained the late systolic prolapse pattern during amyl nitrite inhalation. In these 14 patients, the onset of mitral prolapse occurred earlier in systole due to decrease in the duration of systole prior to onset of mitral valve prolapse (p greater than 0.001). This corresponded with the occurrence of auscultatory phenomena earlier in systole. Twelve patients had left ventricular volumes recorded during amyl nitrite inhalation and all showed a decrease in left ventricular volumes (greater than) 0.001). These findings confirm the temporal relationship of mitral valve prolapse and onset of auscultatory phenomena in these patients. It suggests that the movement of auscultatory phenomena earlier in systole during amyl nitrite inhalation is related to earlier prolapse of the mitral valve, and that a decrease in ventricular valume is a tenable explanation for the earlier onset of prolapse.
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PMID:Simultaneous echocardiographic phonocardiographic recordings at rest and during amyl nitrite administration in patients with mitral valve prolapse. 113 61

Idiopathic prolapse of the mitral valve is a common disorder, but many cases are clinically subtle. Thoracic skeletal abnormalities, reported recently to accompany the syndrome, may serve as an easily identifiable clinical indicator. The prevalence of these abnormalities was defined in 24 patients with proved prolapse of the mitral valve. The valvular syndrome was defined clinically, by echocardiography and, in seven cases, by left ventricular angiography. The skeletal deformities were defined clinically and radiographically. Pectus excavatum was present in 62 percent of the patients, "straight back" in 17 percent and severe scoliosis in 8 percent. Eighteen of the 24 patients (75 percent) had a definite thoracic skeletal deformity. The association of idiopathic prolapse of the mitral valve with these skeletal deformities may represent a forme fruste of Marfan's syndrome. Patients with "straight back" and pectus excavatum should be examined clinically and perhaps by echocardiography to exclude idiopathic prolapse of the mitral valve; when murmurs are present, a diagnosis of "pseudoheart disease" should not be made before mitral valve prolapse has been excluded.
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PMID:Thoracic skeletal abnormalities in idiopathic mitral valve prolapse. 114 95

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


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