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

This case report describes a mitral systolic honk originating from the mitral valve and adjacent structures in a 52 year-old woman with mitral stenosis. The patient was hospitalized because of dyspnea. Auscultation of the heart revealed a grade 3/6 apical early systolic honk accompanied by an increased first heart sound, an opening snap and a diastolic rumble. The phonocardiogram demonstrated an early systolic honk at a frequency of 115 Hz. Intensity of the honk varied on beat to beat basis, increasing in the short preceding R-R interval compared to that in the long one. The M-mode echocardiogram showed early systolic fluttering of the mitral valve and chordae tendineae at the same frequency as the honk. The two-dimensional echocardiogram showed bulging of the anterior mitral leaflet toward the left atrium in early systole. After treatment with digitalis and diuretics, the early systolic honk disappeared in beats with preceding long R-R intervals (greater than 1100 msec). In beats without the honk, systolic fluttering of the mitral valve was not observed. The genesis of the early systolic honk is analogous to that of the honk audible in mitral or tricuspid valve prolapse. The bulging of the anterior mitral leaflet into the left atrium may produce vibrations of the mitral valve leaflets and adjacent structures.
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PMID:[Systolic honk in mitral stenosis: a case report]. 384 6

From 1974 to 1983, 37 symptomatic patients with mitral systolic click (Barlow's syndrome) underwent mitral valve repair. In 11 patients (30%), the click syndrome was associated with minor mitral regurgitation. Thirty-two patients (86%) had chest pain, 20 had arrhythmia (54%), and 20 had dyspnea as a major complaint. In 5 patients, the arrhythmia was serious, and in 2 of them, it was potentially life threatening. Mitral annuloplasty using a collar prosthesis was performed in 33 patients with posterior leaflet plication in 2, shortening of the chordae in 1, and commissural plication in 2. In 4 patients, commissural plication was performed. One of these patients also required cusp plication and shortening of the chordae, and another required repair of ruptured chordae. There were no operative or late cardiac-related deaths at a mean follow-up of 4.7 years (range, 1 to 10 years). Sixty-two percent of patients with prolapse alone and 91% of those with associated regurgitation were improved by at least one New York Heart Association Functional Class, with 60% of patients obtaining relief of one or more symptoms. In the presence of major symptoms, mitral annuloplasty offers symptomatic relief for some patients with mitral systolic click syndrome without valve incompetence, but it gives substantially better results in patients with mitral regurgitation.
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PMID:Surgical treatment of mitral systolic click syndrome: results in 37 patients. 397 Jun 9

Cyclopiazonic acid (CPA) was found to have many pharmacological properties in common with the antipsychotic drugs chlorpromazine and reserpine. Thus, in mice CPA at ip doses of 5-14 mg/kg body weight produced hypokinesia, hypothermia, catalepsy, ptosis, sedation without loss of righting reflex, tremor, gait disturbance, dyspnoea, opisthotonus, atypical convulsion and prolonged barbiturate-induced sleep. The ip LD50 of CPA was found to be 13 +/- 0.05 mg/kg. The tremors induced by near-lethal doses of CPA were associated with voluntary or forced movements (action tremors); they worsened during the days following treatment, but they were weak compared with the exhausting and continuous tremors of the whole body caused by 20 mg tremorine/kg (used for comparison). When death occurred only 24-259 min after administration of CPA (11-14 mg/kg), it was preceded by dypsnoea, cyanosis, opisthotonus and clonic leg movements and tonic extension of hind legs (convulsions). When death was delayed (2-6 days after CPA administration), it was preceded by prostration, ptosis, hypothermia, tremor and cessation of food and water intake resulting in cachexia; convulsions were not seen in this group of mice. CPA did not affect the rate of convulsion or death caused by either maximal electroshock or metrazol administration but it did delay the onset of metrazol-induced seizures. In rabbits, 10 mg CPA/kg body weight initially produced tachycardia, tachypnoea and sedation with an activated electroencephalogram. Of three rabbits given 10 mg CPA/kg one died, and in this rabbit slow delta waves were seen just before and during a brief period with clonic leg movements. In this animal death was accompanied by tonic extension of the hind legs, respiratory arrest and cardiac fibrillation; and epileptiform EEG was not seen at any time. The unexpected EEG activation with sedation in rabbits treated with CPA was similar to the effect of reserpine on EEG.
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PMID:Toxicity and neuropharmacology of cyclopiazonic acid. 404 83

In six patients with clinically unsuspected right atrial thromboemboli the diagnosis was made with two-dimensional echocardiography. Five patients had pulmonary emboli, and one had systemic embolization. Three patients had congestive cardiomyopathy, two with tricuspid regurgitation; of the remaining three, one had cor pulmonale complicated by tricuspid regurgitation, one had thrombophlebitis and one had no discernible cardiac illness. Four patients had dizziness or syncope, four had dyspnea, three had chest pain, three had hypotension and tow had cyanosis. Five patients were treated with thrombolytic or anticoagulant therapy, or a combination of the two. In three patients, surgical removal of the thrombus was undertaken because of recurrent pulmonary emboli or tricuspid regurgitation, or both, and progressive right heart failure. The thromboemboli were removed in all three, but one patient died. On two-dimensional echocardiography, four of the six patients' thromboemboli were snake-like, unattached to the right atrium and prolapsed freely across the tricuspid valve into the right ventricle in diastole and back into the right atrium in systole. The other two patients' thromboemboli were attached to the right atrium and did not prolapse across the tricuspid valve. Our cases, together with a review of other reports, suggest that right atrial thromboemboli: 1) can be accurately diagnosed by two-dimensional echocardiography; and 2) result from two different pathophysiologic mechanisms developing a) in situ, either on a foreign body or secondary to reduced cardiac output, or b) as a result of an embolus from systemic vein thromboses.
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PMID:Right atrial thromboemboli: clinical, echocardiographic and pathophysiologic manifestations. 649 Oct 71

One hundred and eighty-two patients (100 females, 82 males) with mitral valve prolapse (MVP) confirmed by echocardiography are described. Their ages range from 12 to 87 years (mean 48 years). The symptoms of breathlessness, pain in the chest and palpitations were analysed. They were associated with left ventricular failure, co-existing ischaemic heart disease and arrhythmias in some, but in a proportion the symptoms were thought to be due to psychoneurosis. Seventy-two patients (40 per cent) were referred because of complications of MVP. In 67 patients (37 per cent) the condition was discovered by chance and in 43 patients (24 per cent) neurotic symptoms had led to referral to hospital. A systolic click was heard in 117 patients (54 per cent); 41 patients (23 per cent) had a late systolic murmur and 30 patients (16 per cent) had a pansystolic murmur. The incidence of murmurs rose with increasing age, and pansystolic murmurs were more frequent in males. Thirty-two patients (18 per cent) had neither a click nor a murmur. Twenty-four patients (13 per cent) had associated supraventricular tachycardia and 22 (12 per cent) atrial fibrillation. Twelve patients (7 per cent) had severe mitral incompetence and eight (4 per cent) developed bacterial endocarditis. Only three patients had symptoms suggesting cerebral ischaemia. Twelve patients (7 per cent) had associated aortic incompetence. Twenty-two patients had had an inguinal hernia, the incidence in males over 50 being 26 per cent. Twenty-six patients (14 per cent) had non-specific T wave changes in the electrocardiogram. Echocardiography showed that 112 patients (62 per cent) had mid-systolic buckling of the posterior leaflet and 70 patients (38 per cent) had holosystolic prolapse. In view of the high incidence of complications it is felt that the long-term prognosis not as good as has been generally believed.
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PMID:Mitral valve prolapse: an assessment of clinical features, associated conditions and prognosis. 661 38

A 59 year old man presented with dyspnea and a new murmur of aortic regurgitation. Two-dimensional echocardiography demonstrated a to and fro motion of the intimal flap as it prolapsed into the left ventricle and was thrust into the aorta during diastole and systole, respectively. At surgery, the echocardiographic and angiographic findings were confirmed and a proximal aortic dissection was identified. Prolapse of an intimal flap from the aorta into the left ventricular outflow tract represents a new two-dimensional echocardiographic sign of aortic dissection.
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PMID:Two-dimensional echocardiographic recognition of an aortic intimal flap prolapsing into the left ventricular outflow tract. 673 46

In singly- and group-housed cats, an intraventricular injection of 6-hydroxydopamine (6-OHDA) in doses up to 1.0 mg, after a latent period of 1 to 3 days, evoked motor responses including tremor, ataxia, rigidity, weakness with adynamia and clonic-tonic convulsions. However, the intraventricular administration of 6-OHDA in a dose of 2.0 mg in group-housed cats, also after a latent period of 1 to 3 days, caused aggression, a restlessness, irritability, rage, fear, threat, attack, fighting and flight. These responses were accompanied by autonomic signs of mydriasis and dyspnoea and motor changes including tremor, ataxia, rigidity, weakness with adynamia and clinic-tonic convulsions. In the singly-housed cat only the latter motor phenomena were observed after the higher dose. Intraventricular injection of reserpine (0.5-1.0 mg) in both singly- and group-housed cats produced catalepsy, sedation, miosis, ptosis, defecation and micturition as well as motor responses of tremor, rigidity and akinesia. It is concluded that although 6-OHDA and reserpine evoke different behavioral effects, the motor changes are similar.
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PMID:Comparison of behavioral changes in cats treated with intracerebroventricular 6-hydroxydopamine and reserpine. 719 23

Our purpose was to determine the incidence of mitral valve prolapse in patients with anxiety neurosis or panic disorder, with symptoms including recurrent anxiety attacks, dyspnea, palpitations, chest pain, dizziness, and paresthesias. Twenty-one patients and 20 age- and sex-matched normal controls were studied. Objective cardiac abnormalities were significantly (p < 0.05) more frequent in the patient group as compared to the control group; these comprised echocardiographic prolapse, ST-T abnormalities on resting ECG, premature ventricular contractions on exercise ECG, and the combination of echo prolapse with clicks/murmurs of exercise-induced PVC. We conclude that patients with anxiety neurosis or panic disorder may also have evidence of an organic abnormality--the mitral prolapse syndrome.
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PMID:Mitral valve prolapse in anxiety neurosis (panic disorder). 740

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

A left-sided diaphragmatic defect in the centrum tendineum of a 27-year-old female patient, who complained about dyspnea and hemoptysis, will be reported concerning symptoms, diagnostic procedure and operative therapy. This presumably congenital diaphragmatic defect caused an organ prolapse into the pleural cavity probably enhanced by an increased intraabdominal pressure during pregnancy and delivery. The defect was primarily closed after laparotomy. No plastic surgical reconstruction with autologous or homologous materials was necessary.
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PMID:[Congenital diaphragmatic hernia with symptoms in adulthood]. 777 48


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