Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Without treatment, about 60% of atrial arrhythmia patients suffer a relapse within 3 months and 70% within one year. Antiarrhythmic treatment intended to reduce this percentage is therefore justified, on condition that it is well tolerated. Several preliminary questions have to be settled before this medical prophylaxis: 1) Justification of antiarrhythmic treatment (sometimes pointless to deal with very occasional episodes); 2) Treatment of the underlying heart disease (valve disease, cardiothyrotoxicosis, etc.) or promoting factors (potassium depletion etc.); 3) Accurate assessment of any associated conduction abnormalities, which may constitute a contraindication to antiarrhythmic treatment (WPW syndrome in the case of verapamil and the digitalis-like drugs) or require additional treatment (pacemaker); 4) Definition of the mechanism (vagal or sympathotonic) inducing arrhythmia; 5) Evaluation of the hemodynamic parameters of the underlying heart disease (size of the atria, ventricular function, coronary or valvular lesions) which may limit the efficacy of the treatment. Once these parameters have been identified, the primary treatment should be type la or lb antiarrhythmics, which have been shown to be effective, despite the fact that they are not without arrhythmic risks (the Ib antiarrhythmics are less effective and have a poor safety profile). The beta-blockers have preferential indications (hypersympatheticotonia, hyperthyroidism, hypertrophic myocardiopathy, mitral prolapse, angina etc.) and can be replaced by verapamil or bepridil if there are non-cardiac contraindications (ulcers, asthma, diabetes). Amiodarone is extremely effective, but its poor extracardiac safety restricts its long-term use. Complementary treatments (digitalis-like, anticoagulants or anti-PAF and cardiostimulant drugs) should be added if necessary. Recurrences (to be confirmed by ECG or Holter) should lead to rigorous confirmation of therapeutic compliance and observance of simple hygienic and dietary measures (no excessive exertion, elimination of stimulants etc.). With strict clinical and ECG monitoring, it would then be possible either to increase the dose levels (accompanied by plasma determinations if possible) or to switch to a treatment with more effective, but more aggressive drugs (amiodarone, flecainide) or to use drug associations (la and lb, la and II etc.). Repeated failure of such attempts should lead to a non-medical approach to treatment.
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PMID:[Preventive drug therapy of recurrence of atrial fibrillation]. 129 92

Episodic mitral regurgitation due to ischaemia of one or both papillary muscles was studied in a review of 39 cases with complementary investigations and compared with previously reported data. The condition occurred after myocardial infarction in 69 p. 100 of cases (usually after inferior infarction: 54 p. 100) associated with ischaemia of the controlateral territory; there was no history of myocardial infarction in 31 p. 100 of cases. The patients were usually elderly (73 years), often hypertensive (77 p. 100) and diabetic (62 p. 100). The clinical syndrome was that of severe anginal pain, mitral regurgitation and left ventricular failure which was critical in some cases. The ECG showed typical ST depression (4.1 +/- 1.6 mm) especially in the antero-lateral leads; left bundle branch block (28 p. 100) with left axis deviation (18 p. 100), sometimes associated with changes of chronic infarction (64 p. 100) was also recorded. Mitral regurgitation and left ventricular failure regressed almost completely in typical cases between attacks, whilst the ECG showed slight residual sub-endocardial ischaemia (ST depression of 1.5 +/- 0.4 mm) in 30 cases and/or subepicardial ischaemia observed in the anterolateral leads in 13 cases. Phonomechanographic recordings (n = 32) showed moderate mitral regurgitation (1-2/6), usually parasystolic (47 p. 100) or early and mid systolic (36 p. 100) in 87.5 p. 100 of cases between attacks, aggravated by handgrip exercise and improved by trinitrin administration. Echocardiography (n = 27) only showed mitral valve changes in 2 patients (increased density of the papillary muscle in 1 case and prolapse of the anterior leaflet in 1 case); however, segmental wall hypokinetic (51 p. 100) or dyskinetic (15 p. 100) motion, was common with increased left ventricular end diastolic dimensions (mean 56.3 +/- 8.0 mm) and decreased fractional shortening (mean 0.30 +/- 0.07) (67 p. 100). Left atrial dimensions were increased (mean 39.7 +/- 6.4 mm) in 52 p. 100 of patients. Thallium 201 myocardial scintigraphy (n = 32) showed hypofixation in 57 (36 p. 100) and a lacuna in 23 (14 p. 100) of the 160 segments analysed. Left ventricular angioscintigraphy (n = 27; 135 segments) showed hypokinesia in 72 segments (53 p. 100); 2.7 segments per patient), akinesia in 19 segments (15 p. 100; 0.7 segment per patient) and dyskinesia in 2 segments (1.5 p. 100); 0.1 segment per patient). The global ejection fraction was 46 +/- 13 p. 100. Coronary angiography (n = 8) showed significant diffuse atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Paroxysmal mitral insufficiency caused by ischemic dysfunction of the papillary muscles. Apropos of 39 cases]. 391 82

Mitral valve prolapse frequently resembles coronary heart disease. Retrospective clinical, ECG and angiographic analysis of 100 consecutive patients with mitral prolapse and normal coronary arteries, but complaining of anginal pain, shows how difficult it is to establish the correct diagnosis. When resting, 44% of patients have nonspecific ECG disorders of repolarization phase. During periods of chest pain 3 patients experienced transient ST segment changes very similar to acute myocardial ischemia. The exercise test was positive in 39% of cases, and in 2 patients during exercise a sudden drop in blood pressure suggested coronary perfusion failure. In all patients the coronary arteries were normal, but left ventriculography showed mitral valve prolapse predominantly on the posterior leaflet. At rest, 35% of patients had diastolic compliance failure, 32% had left ventricular hyperkinesia and only in 3% was slight hypokinesia present. Finally, early systolic relaxation of the anteroapical wall was observed in 75% of patients.
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PMID:[Mitral prolapse syndrome: clinical, electrocardiographic and angiocardiographic correlations. Study of 100 patients with healthy coronary vessels]. 396 47

The authors report 2 cases of myocardial infarction with normal coronary arteries occurring at an interval of 2 months in 2 brothers aged 32 and 34. Following an episode of angina, the younger brother, a sportsman, but a smoker, developed an antero-septal infarct at rest, which was complicated by complete persistent right bundle branch block. Ventriculography and coronary angiography were normal. Induced spasm tests were not performed. The elder brother presented an infero-apico-lateral infarct on effort, without any prodromal syndrome, which was complicated by apical akinesia. Ventriculography revealed mitral prolapse. Coronary angiography was normal and the methylergometrine test was negative. In relation to this example of familial infarction with normal coronary vessels, the authors review the features of this type of infarction reported in the literature which predominantly occurs in young people. They discuss the principal points of interest, including the incidence, the criteria of definition based on the coronary angiography, the elements of the prognosis, the pathophysiological mechanisms and the possibility of a genetic predisposition.
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PMID:[Myocardial infarction with normal coronary vessels in young subjects. Apropos of 2 cases with an interval of 2 months in 2 brothers aged 32 and 34]. 400 92

The etiology and clinical significance of asynchronous relaxation of the left ventricle during isovolumic relaxation period was studied. Fifty patient with angina pectoris, 50 with myocardial infarction, 40 with normal heart, 20 with mitral stenosis and 10 with mitral prolapse syndrome were investigated. Asynchronous relaxation was observed in the following order: 72% in angina pectoris, 46% in myocardial infarction, 30% in mitral valve prolapse and 10% in both pure mitral stenosis and normal heart. In left anterior descending coronary artery disease, asynchronous relaxation was observed in 80%. Asynchronous relaxation seen before aortocoronary bypass graft to the left anterior descending coronary artery either disappeared or decreased after surgery. The contractility of the site, where asynchronous relaxation was seen, was normal in most cases and akinetic in none. The results of this study suggest the possibilities that asynchronous relaxation is at least partially related to localized myocardial ischemia and that it may be an early phenomenon of the effect of myocardial ischemia. With regard to asynchronous relaxation and hemodynamic alterations, force-velocity lissajous was analysed. Distortion of the lissajous in relaxation phase was seen in 73% who showed asynchrony. This distortion can be interpreted as indication of ununiformity of the left ventricular relaxation.
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PMID:Asynchronous relaxation of the ischemic left ventricle. 697 48

Coronary artery steal resulting from a large unligated intercostal or pericardial side branch of the internal mammary artery graft causing postoperative angina has been previously described. Transcatheter coil occlusion of internal mammary artery side branch has successfully been performed to treat coronary steal syndrome. Unsuccessful deployment of the microcoils can be due to inadequate guiding support in the LIMA or prolapse of the delivery catheter in the side branch. We report a new approach for the precise deployment of coils in the side branch of a LIMA graft, when inadequate guiding support is present.
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PMID:Novel technique for coil embolization of intercostal branch of internal mammary artery graft. 932 17

A 60 year-old woman with progressive angina who had been submitted to saphenous bypass-graft to right coronary artery and a left mammary artery graft to anterior descending artery eight years previously, underwent implantation of a Gianturco Roubin II stent in the proximal third of the saphenous vein graft. The result was suboptimal by persistence of a residual stenosis probably due to prolapse of atherosclerotic material through the coil spaces. Another stent (Palmaz-Schatz biliar stent) was implanted at the previously stented site with no residual stenosis. Another Palmaz-Schatz biliar stent was successfully implanted in the distal body of the graft to treat another lesion (passing through the previously stents without difficulty). Stenting a stent, in selected situations, is a useful tool to optimize the angiographic result of stent implantation.
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PMID:[Stenting in a recently implanted stent in a saphenous vein graft for optimizing angiographic results]. 967 79

Coronary artery fistulas vary widely in their morphological appearance and presentation. These fistulas are congenital or acquired coronary artery abnormalities in which blood is shunted into a cardiac chamber, great vessel, or other structure, bypassing the myocardial capillary network. The majority of these fistulas arise from the right coronary artery and the left anterior descending coronary artery; the circumflex coronary artery is rarely involved. Clinical manifestations vary considerably and the long-term outcome is not fully known. The patients with coronary fistulas may present with dyspnea, congestive heart failure, angina, endocarditis, arrhythmias, or myocardial infarction. A continuous murmur is often present and is highly suggestive of a coronary artery fistula. Differential diagnosis includes persistent ductus arteriosus, pulmonary arteriovenous fistula, ruptured sinus of Valsalva aneurysm, aortopulmonary window, prolapse of the right aortic cusp with a supracristal ventricular septal defect, internal mammary artery to pulmonary artery fistula, and systemic arteriovenous fistula. Although noninvasive imaging may facilitate the diagnosis and identification of the origin and insertion of coronary artery fistulas, cardiac catheterization and coronary angiography is necessary for the precise delineation of coronary anatomy, for assessment of hemodynamics, and to show the presence of concomitant atherosclerosis and other structural anomalies. Treatment is advocated for symptomatic patients and for those asymptomatic patients who are at risk for future complications. Possible therapeutic options include surgical correction and transcatheter embolization. Historical perspectives, demographics, clinical presentations, diagnostic evaluation, and management of coronary artery fistula are elaborated.
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PMID:Coronary artery fistulas: clinical and therapeutic considerations. 1612 61

Martin Luther achieved great success in religious reformation, though he was said to have suffered from many kinds of diseases during his lifetime. Unfortunately, however, his medical history has never been reported in Japan. Since the second half of his thirties, he was suffering from severe constipation, causing hemorrhoids and anal prolapse. At the beginning of his forties he had vertigo, tinnitis and headaches, which were the signs of chronic purlent otitis media and ended in left otorrhea and pyorrhea of the left mastoiditis. Nearly at the same time, he started to suffer from anginal pain, colic and dysuria due to urinary uric acid stones, gout and left leg ulcer, which were all caused by metabolic syndromes. The last 1/3 of his life was affected by the shadow of diseases, and his religious activities were frequently disturbed. He died from myocardial infarction at the age 63, in February 1546.
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PMID:[Medical history of Martin Luther]. 2258 92

An 80-year-old man with angina pectoris abruptly developed Claude's syndrome, which consisted of left-sided partial oculomotor nerve palsy without ptosis and right-sided hemiataxia. There were no other neurological abnormalities. Cranial magnetic resonance imaging indicated an infarction of the left inferior paramedian mesencephalic artery, which may have involved the most caudal portion of the oculomotor fascicules. With anti-platelet therapy, the patient became asymptomatic within 10 days. The oculomotor fascicular arrangement in humans remains unclear. Our case suggests that in the oculomotor fascicles, the fibers to the levator palpebrae superioris may be located more in the rostral region than previously hypothesized.
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PMID:Claude's Syndrome without Ptosis Caused by a Midbrain Infarction. 2617 40


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