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

Echocardiograms of 400 patients with mitral valve prolapse examined at the Peter Bent Brigham Hospital between 1974 and 1977 were reviewed. Eleven patients (3 per cent) were found to have prolapse (10 patients) or large excursion of the tricuspid valve (one patient) and large excursion of the aotric valve (four patients) or dilatation of the aotric root (seven patients) in addition to mitral valve prolapse. Two of these 11 patients underwent mitral valve replacement, and myxomatous degeneration of the valves was noted on pathologic examination. Almost half of the patients with multiple floppy valves (five of 11) had symptoms of congestive heart failure. In contrast to reported series of isolated mitral valve prolapse, in which female preponderance has been documented, 10 of the 11 patients were male. The syndrome of multiple floppy valves may represent either a unique entity or a more advanced form of the same process which underlies mitral valve prolapse.
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PMID:Multiple floppy valves: an echocardiographic syndrome. 44 57

Systolic honks have so far been synonymous with prolapse of the mitral valve leaflet. Evidence of tricuspid valve involvement in two cases is presented. These patients developed systolic honk during the deterioration of their congestive heart failure. Simultaneous recordings of echocardiograms and phonocardiograms showed fluttering of the tricuspid valve, coinciding with the systolic honk. This fluttering was not seen when honk was absent. The mechanism of production of this honk is discussed.
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PMID:Systolic honk in heart failure: its origin and mechanism of production. 49 8

The conditions associated with prolapse of the posterior leaflet of the mitral valve are multiple. The mechanisms of mitral valve prolapse as well as the pathogenesis of pain and ectopic impulse formation are reviewed. Propranolol appears to be the drug of choice for the symptomatic treatment of patients with this syndrome since it decreases myocardial oxygen demand and wall tension thus reducing or abolishing the discrepancy between myocardial oxygen demand and supply within the mitral apparatus. It has also been reported to modify the auscultatory findings associated with this condition. The frequency of this mitral valve abnormality in patients with obstructive coronary artery disease is reviewed. It appears that prolapse of the posterior leaflet scallops in patients with significant obstructive coronary artery disease represents an intermediate stage before mitral insufficiency occurs. This group of patients with papillary muscle dysfunction includes those with prolapsed leaflets without mitral insufficiency, those with systolic murmurs and compensated heart failure and others with progressive cardiac decompensation and severe mitral regurgitation.
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PMID:Mitral valve prolapse. Recent concepts and observations. 93 60

We reported 2 cases of mitral valve prolapse (MVP) associated with partial absence of the chordae tendineae. Case 1 was a 25-year-old man who was admitted to our hospital for further examinations of an apical pansystolic murmur (Levine 4/6) and the abnormal shadow on his chest radiograph. He was diagnosed as having grade 3 + mitral regurgitation (MR) by the Sellers classification and pulmonary varix by cardiac catheterization. Transesophageal echocardiography revealed MVP of the rough zone of the anterior mitral leaflet and MR blowing into the pulmonary varix. Case 2 was a 60-year-old man who was admitted to our hospital because of congestive heart failure and apical pansystolic murmur (Levine 4/6). Parasternal echocardiography revealed prolapse of both the anterior and posterior mitral leaflets and moderate MR. In both cases, absence of insertion of anterolateral commissural chordae was confirmed after surgery, and the abnormalities of chordal arrangement and insertion were considered as causes of MVP in these cases.
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PMID:[Mitral valve prolapse associated with partial absence of commissural chordal insertion: report of two cases]. 141 76

In the present study: (a) physiopathology, (b) clinics, and (c) therapy of cardiothyreosis are discussed. (a) The hyperkinetic syndrome, the earliest clinical sign in thyrotoxicosis (vasodilatation, increase in inotropism, automatism, etc.), is mediated by a two-fold increase in the number of beta-receptors, and supported by an adequate synthesis of ATP and creatinphosphate (CP) in the young and, to a lesser extent, in the elderly. Genetical heart reserves are mobilized, thus significantly increasing the number and the size of mitochondria and also the enzymatic equipment (such as: the alpha-glycerophosphate-dehydrogenase, malic, pentosic cycles, etc.), a.s.o. Due to an excessive adrenergic action (glycogenolysis, an excessive oxygen consumption, up to necrosis, the ATP and CP syntheses dramatically drop; the phosphorus/oxygen ratio decreases to 2 (normal = 4). In this condition, the high functional cardiovascular performances are also impaired (the submaximal effort capacity is attained at a smaller and smaller oxygen consumption; Propranolol 2 mg i.v. decreased the cardiac output by above 30% (vs 10%--normal); electrocardiogram presents aspects of "coronary disease", tachycardia, etc.). An ultrastructural damage occurs: from "mitochondrial disease", partial lysis of myofibrils, to myofibrosis (revealed postmortem), in spite of a reduced degree of coronary atherosclerosis. Ultrastructural and biochemical experimental data support this point of view. (b) The incidence, precocity and severity of the thyrotoxic heart increase with age and the existence of a previous cardiovascular pathology. Cardiothyreosis is not present under 27 years; in 4,353 patients its incidence is of 25% (arrhythmia--21%, heart failure--12%, coronary insufficiency--1-3%). Of a major interest are tachyarrhythmias which may lead to a high mortality by hypodiastolic congestive heart failure, heart failure with secondary hyperaldosteronism, thromboembolic episodes and ventricular fibrillation. Thyrotoxicosis favours the disease of papillary muscles--mitral prolapse and insufficiency, reversible especially in children. (c) The treatment of thyrotoxic heart is an etiologic one (medical, surgical, radioactive--the last two being preferable after the adequate medical therapy). In particular, cardiothyreosis requires a reinforced irradiation (10,000 rads instead of 7,000 rads) in smaller 131I doses. The protection against the increased nocivity of catechols in thyrotoxicosis is very important (which explains the high mortality in the thyrotoxic "storm") and requires propranolol; doses above 2 mg/kilo body/day are recommended. In the elderly, the sensitivity to propranolol decreases: verapamil i.v. is more efficient in paroxysmal tachyarrhythmias (flutter, atrial fibrillation) and in those occurring intra-operatively during halothane narcosis. The anticoagulant therapy is administered in tachyarrhythmias with high ventricular rate, especially in the elderly, to avoid the embolic risk, higher in defibrillation condition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiothyreosis. 182 Oct 70

Surgical management of the conal (supracristal) ventricular septal defect differs significantly from the management of the perimembranous (infracristal) ventricular septal defect. The absence of a portion of the conal septum can lead to prolapse of the right cusp of the aortic valve, which predisposes these patients to aortic insufficiency. Between January 1980 and December 1989, 36 children with conal ventricular septal defect underwent intracardiac repair. Diagnosis was by echocardiography, cardiac catheterization, and intraoperative exploration. Preoperative evaluation showed that 26 patients (72%) had aortic valve prolapse and 16 (44%) had aortic insufficiency. Pulmonary-to-systemic flow ratios ranged from 1:1 to 3.5:1 (mean 2.0:1.0). Ten patients (27%) were believed to have clinical congestive heart failure. Age at the time of operation ranged from 2 weeks to 18 years (mean 5.5 years). Operative exposure was through the pulmonary artery (26), aorta (4), right ventricle (3), or right atrium (3). Simultaneous aortic valve suspension for aortic insufficiency was performed in four patients. Operative survival was 100%. Follow-up is complete in all patients and ranges from 0.5 to 9 years (mean 4.3 years). All patients are in normal sinus rhythm. No residual ventricular septal defects have been identified. Twenty-three of 36 patients (64%) have no evidence of aortic insufficiency; 12 of 36 (33%) have trivial or mild aortic insufficiency. One patient with initial severe aortic insufficiency underwent repeat aortic valvuloplasty 3 years after ventricular septal defect closure and aortic valve suspension. No patients have required aortic valve replacement. Surgical management of the conal ventricular septal defect differs from that of the perimembranous ventricular septal defect in two critical aspects. The operative approach should be through the pulmonary artery. This allows the best exposure of the remaining conal septum and the pulmonary and aortic valve leaflets, facilitating closure of the defect without injury to the valves or conduction system. Conal ventricular septal defects should undergo early closure, regardless of shunt volume, to prevent progressive aortic insufficiency.
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PMID:Surgical management of the conal (supracristal) ventricular septal defect. 186 2

To assess the value of intraoperative transesophageal echocardiographical Doppler color flow imaging (TEE-DCFI) during cardiac valvular surgery, 85 consecutive patients with 102 diseased valves for surgery were studied with pre-and post-operative TEE-DCFI. There were 34 women and 51 men with an age range of 15 to 55 years (mean age, 34.91 +/- 9.33 years). The etiology of valve lesion was rheumatic in 57 (AV 10, MV 47), prolapse in 9 (AV 2, MV 7), endocarditis in 21 (AV 12, MV 3, PV 2, prosthetic infection 4), prosthetic dysfunction in 14 (AV 5, MV 9), congenital in 1 (TV). Preoperative TEE-DCFI findings were helpful either in completing with some new information or changing the operation plan in 29 valves (28.43%) including abscess at aortic root in 1, perforation of aortic valve in 2, perforation of mitral valve leaflets in 5 patients with aortic valvular endocarditis, regurgitation or perivalvular leak of prosthetic valve in 4 MVs and 4AVs, left atrial thrombus detected in 8 and excluded in 3 patients with MV disease, small calcified vegetation on PV with normal valve function in 2 patients with congenital heart disease. Postoperative TEE-DCFI evaluation was performed in 53 patients with 70 diseased valves. There was only one mild regurgitation of mitral bioprosthesis and one mild perivalvular leak of aortic prosthesis detected among 40 replaced prosthetic valves. Of 30 valves repaired 23 (77%) valves had trivial or mild residual regurgitation (Group A) and 7 (23%) had moderate residual regurgitation (Group B). Postoperative congestive heart failure was seen in 6 (26.09%) of Group A and 5 (71.43%) of Group B (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The value of using transesophageal echocardiographic Doppler color flow imaging in patients undergoing cardiac valvular surgery]. 208 76

To determine whether non-rheumatic (NR) aortic regurgitation (AR) has the same clinical and postoperative courses as rheumatic (R) AR, we performed a retrospective study using pre- and postoperative M-mode echocardiograms in 23 patients who underwent aortic valve replacement (AVR) under myocardial protection with hypothermic cardioplegia. The etiology of AR was diagnosed by two-dimensional echocardiography. The NR-AR group consisted of nine patients including four with aortic valve prolapse (AP) and five with bicuspid valve (BV), and the R-AR group included 14 patients. Patients with preoperative end-diastolic dimensions (EDD) of less than 6.0 cm were excluded from this study. The indication for AVR was NYHA functional class III or severer. The severity of preoperative NYHA functional class was similar among these three groups. During the 18-month follow-up period (range 2-32 months), there were no post-operative deaths nor congestive heart failure. Ages at surgery ranged from 17 to 54 years; 10 (71%) of 14 patients with R-AR were 40 years old or older, while seven (78%) of nine with NR-AR were under 39 years old (p less than 0.05). The pre-operative left ventricular end-diastolic pressure (LVEDP) in patients with BV-AR was highest among these three groups (R-AR: 14.5 +/- 3.9 mmHg, AP-AR: 9.5 +/- 4.1 mmHg, BV-AR: 22.0 +/- 2.7 mmHg, p less than 0.05). There was no significant difference in pre-operative M-mode echocardiographic results, except for the end-systolic dimension (ESD) between R-AR (5.20 +/- 0.55 cm) and BV-AR (4.78 +/- 0.18 cm) (p less than 0.05). The EDD one month after AVR was still abnormal (greater than or equal to 5.4 cm) in seven of the 14 patients with R-AR, and three of the four patients with AP-AR but none of the patients with BV-ARs (p less than 0.05 vs AP-AR). All patients with pre-operative ESD of less than 5.2 cm had normal EDD one month after AVR. In conclusion, the clinical course of NR-AR is different from that of R-AR. Furthermore, AP-AR regresses more differently after AVR than does BV-AR. Therefore, it is important to consider the etiology of chronic AR in determining the timing of surgery.
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PMID:[Is the clinical course of non-rheumatic aortic regurgitation the same as that of rheumatic aortic regurgitation?]. 213 25

Fifty consecutive patients with a newly acquired systolic murmur and severe cardiac decompensation following a recent myocardial infarction (27 with an anterior and 23 with an inferior infarct) were studied by a combination of two-dimensional echocardiography, spectral Doppler and Doppler color flow mapping. The initial ultrasound study defined a ventricular septal rupture in 43 patients and severe isolated mitral regurgitation in 7 patients (5 with papillary muscle rupture and 2 with severe papillary muscle dysfunction). All 50 patients had subsequent confirmation of the diagnosis by either cardiac catheterization or surgical inspection, or both. Two-dimensional echocardiography alone directly visualized a septal defect in only 17 (40%) of the 43 patients with ventricular septal rupture. In all 43 patients the mitral valve appeared normal on imaging. In six of the seven patients with isolated mitral regurgitation, two-dimensional echocardiography correctly demonstrated the structural abnormality of the mitral valve (five with flail anterior leaflet and one with posterior leaflet prolapse). The addition of Doppler color flow mapping greatly improved the diagnostic information in both patient groups. In all 43 patients with ventricular septal rupture, Doppler color flow mapping demonstrated both an area of turbulent transseptal flow and a diagnostic systolic flow disturbance within the right ventricle. In the seven patients with isolated papillary muscle rupture or dysfunction, Doppler color flow mapping not only demonstrated the presence of mitral regurgitation in all cases, but also identified the specific mitral leaflet abnormality by defining the direction of the regurgitant jet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Doppler color flow mapping in the diagnosis of ventricular septal rupture and acute mitral regurgitation after myocardial infarction. 232 47

It has been reported that Kawasaki syndrome is accompanied with mitral regurgitation or aortic regurgitation in some cases. To elucidate the incidence and the natural history of valvular heart disease in Kawasaki syndrome, we analyzed the patients who were detected to have a new heart murmur after the onset of Kawasaki syndrome. From 1973 to 1988, we have experienced 13 cases with valvular heart disease in 1215 cases of Kawasaki syndrome, 12 cases with mitral regurgitation (1.0%) and one with aortic regurgitation (0.1%). Valvular lesions were confirmed by angiography or pulsed Doppler echocardiography. The age at onset of Kawasaki syndrome, the duration of fever, the maximum erythrocyte sedimentation rate, and the incidence of coronary artery lesions in these cases were compared with the same variables in 30 cases of without valvular lesion in Kawasaki syndrome. There were no statistical difference between the cases with valvular heart disease and without valvular heart disease about the age of onset (mean +/- SD 10.2 +/- 12.7 months vs 20.8 +/- 18.4 months; N.S.) and the maximum erythrocyte sedimentation rate (87.7 +/- 29.0 mm/h vs 87.2 +/- 35.6 mm/h; N.S.). Whereas the duration of fever in cases of valvular heart disease was more extended than those without valvular heart disease (20.3 +/- 8.1 days vs 10.3 +/- 4.3 days; p less than 0.001), and the incidence of coronary artery lesions in the cases of valvular heart disease was significantly higher than those without valvular heart disease (12/13 cases vs 7/30 cases; p less than 0.001), thus suggesting that the cases of valvular heart disease were subject to a severe case of Kawasaki syndrome. All valvular heart disease appeared within 1 month after the onset of Kawasaki syndrome, except in one case whose heart murmur was noticed 5 years after the onset. The heart murmur disappeared within 2 months after the onset of valvular heart disease in 5 cases, however in another 7 cases, the heart murmur persisted more than 2 years (mean; 5.3 years to date) or one has died of acute congestive heart failure due to mitral regurgitation. All cases with persistent valvular disease revealed mitral or aortic valve prolapse. Our data suggest that the cause of valvular heart disease might be different by the time of onset and duration of valvular heart disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Valvular heart disease in Kawasaki syndrome--incidence and natural history. 263 47


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