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Query: UMLS:C0033377 (prolapse)
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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

Many reports of diabetic ophthalmoplegia have been published from the clinical points of view. However, there have been only three autopsied cases in which the ocular nerves were investigated histopathologically. A 72-year-old housewife was diagnosed to have glycosuria at the age of 67, but no medical treatment was done. She admitted to the hospital, because of acute onset of right eyelid drooping and diplopia for previous four days. She showed complete eyelid ptosis, moderate dilatation of right pupil, loss of light reaction, and extraocular muscle palsy except abduction on the right. Blood pressure was normal. A glucose tolerance test was diabetic and HbA1c was moderately increased. Her diabetes was fairly well-controlled with a diet therapy and injection of lente insulin. Two and a half months after admission, the course of illness became regressive. Seven months later, external ophthalmoplegia was disappeared and only slight anisocoria was seen. She readmitted to the hospital one year and eleven months later, because of anorexia and emaciation. She died of adenocarcinoma of the stomach without chemotherapy. The duration from onset of ocular symptoms to death was two years and one month. At postmortem examination, stomach cancer infiltrated extensively to the abdominal and pelvic viscera, but no metastasis to the nervous system or intraorbital tissues was found. There were mild to moderate atherosclerotic changes in the small-and middle-sized arteries of the kidneys, pancreas and adrenal glands corresponding to her age. Moderate atherosclerosis was found in all of the major arteries including Willis ring, siphon of the right internal carotid artery and Vertebro-basilar one.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diabetic ophthalmoplegia--a clinico-pathological study of the first case in Japan]. 269 31

Prolapse of the aortic valve (PAV) was diagnosed in 20 patients using a method of two-dimensional echocardiography. PAV primary and secondary forms were distinguished. Congenital pathology of the other cardiac valves (prolapse of the atrioventricular valves and the bicuspid aortic valve) or the aorta was observed in primary PAV. Secondary PAV was observed as a concomitant pathology in dilatation of the aortic root resulting from atherosclerosis or in an infectious process on the aortic cusps in subacute septic endocarditis. Of non-invasive diagnostic methods the most effective one was two-dimensional echocardiography which could be regarded as a verifying method in PAV.
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PMID:[Prolapse of the aortic valve]. 382 76

112 echocardiographies and 91 long-term Holter recordings were performed looking for an emboligenic cardiac lesion in patients in sinus rhythm and free of any major carotid atherosclerosis. The results were evaluated in relation to the emboligenic potential of the lesions observed. 5 positive results were obtained (4.46%) on echocardiography (3 aneurysms of the interatrial septum, 1 myxoma and 1 endocarditis) and 10 positive results (10.99%) were demonstrated on the Holter monitor. Among the 45 (40.18%) echocardiographic anomalies capable of constituting a cardiac site of origin of emboli, there were 18 cases of dilatation or hypertrophy of the left chambers of the heart, 13 cases of calcification of the aortic valve, 8 cases of prolapse of the mitral valve and 8 cases of calcification of the mitral ring. Finally, 55.35 per cent of the echocardiographic examinations and 52.74 per cent of the Holter examinations were found to be normal. Although the yield of these examinations is low, the anomalies discovered were definitely responsible for the cerebral emboli and could only have been demonstrated by such investigations.
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PMID:[Contribution of echocardiography and Holter monitoring to the diagnosis of occult sources of cerebral embolism]. 390 5

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

Anatomic and functional features of the normal and abnormal mitral valve are reviewed. Of 1,010 personally studied necropsy patients with severe (functional class III or IV, New York Heart Association) cardiac dysfunction from primary valvular heart disease, 434 (43%) had mitral stenosis (MS) with or without mitral regurgitation (MR): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 189 (44%) patients, and associated with aortic stenosis in 152 (35%), with pure (no element of stenosis) aortic regurgitation in 65 (15%) patients, and with tricuspid valve stenosis with or without aortic valve stenosis in 28 (6%) patients. The origin of MS was rheumatic in all 434 patients. Of the 1,010 necropsy patients, 165 (16%) had pure MR (papillary muscle dysfunction excluded): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 97 (59%) patients, and associated with pure aortic regurgitation in 45 (27%) and with aortic valve stenosis in 23 (14%) patients. When associated with dysfunction of the aortic valve, pure MR was usually rheumatic in origin, but when unassociated with aortic valve dysfunction it was usually nonrheumatic in origin. Review of operatively excised mitral valves in patients with pure MR unassociated with aortic valve dysfunction disclosed mitral valve prolapse (most likely an inherent congenital defect) as the most common cause of MR. Excluding the patients with MR from coronary heart disease (papillary muscle dysfunction), mitral prolapse was the cause of MR in 60 (88%) of the other 68 patients, and a rheumatic origin was responsible in only 3 of the 68 patients, all 68 of whom were greater than 30 years of age. Mitral anular calcification in persons aged greater than 65 years is usually associated with calcific deposits in the aortic valve cusps and in the coronary arteries. Because calcium in each of these 3 sites is common in older individuals residing in the Western World, it is most reasonable to view mitral anular calcification in older individuals as a manifestation of atherosclerosis. Mitral anular calcium appears to be extremely uncommon in persons with total serum cholesterol levels less than 150 mg/dl. Mitral anular calcium may produce mild MR and, if the deposits are heavy enough, MS.
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PMID:Morphologic features of the normal and abnormal mitral valve. 633 91

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48

Infections are an increasing problem in the elderly population, because of the often atypical presentation and the more frequent occurrence of complications, which lead to increased morbidity and mortality. The increased prevalence of infections in the elderly is due to a number of factors: increased exposure to micro-organisms (especially in nursing homes); degeneration of various organs (atherosclerosis, pulmonary emphysema, diverticulosis, prolapse); decreased immune response; concomitant diseases (e.g. diabetes mellitus) and (or) use of medication. There is often a delay in the diagnosis because the presentation of infection in the elderly is frequently atypical and symptoms are attributed to old age, rather than to infection. Treatment may be hampered by increased resistance of micro-organisms, interaction with other drugs and toxicity problems.
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PMID:[Infections in elderly patients]. 955 Jul 96

This study tested the hypothesis that stroke patients without a cardiac source of embolism suspected by clinical examination can be risk stratified by transesophageal echocardiography. Forty ischemic stroke patients without atrial fibrillation, prosthetic valves, ejection fraction < 20%, or recent myocardial infarction underwent multiplane transesophageal echocardiography: 24 (designated high risk) had > or = 1 of the following: left heart thrombus, vegetation, mass or spontaneous echo contrast, mobile ascending aortic or arch debris, patent foramen ovale, atrial septal defect or aneurysm, mitral annular calcification, mitral valve thickening, prolapse or mitral valve strands. End points were death, recurrent stroke, transient ischemic attack, myocardial infarction or peripheral embolism. Thirty-eight patients (95%) (23 high, 15 low risk) were followed for 14 +/- 8 months: 9 (24%) died of vascular causes including 4 who had a cardiac cause of death and 5 who had fatal strokes. Eight had recurrent strokes (4 nonfatal) and 1 nonfatal myocardial infarction occurred. Cardiovascular survival was predicted by transesophageal echocardiography: survival rates were 92% (low risk) and 63% (high risk) at 24 months (p = 0.036). Left atrial enlargement was independently associated with death from stroke (fatal stroke occurred in 25% of those with atrial enlargement compared to 8% of those with normal atrial dimension, p < or = 0.03), as was left atrial spontaneous echo contrast (50% died vs 9% without contrast, p < or = 0.03). Left ventricular hypertrophy and aortic atherosclerosis were both associated with the risk of recurrent stroke (30% of patients with ventricular hypertrophy had recurrent stroke compared to 10% with normal wall thickness (p < or = 0.05); 30% with aortic atherosclerosis had a recurrent stroke compared to none with a normal aorta (p < or = 0.05). Thus, transesophageal echocardiography clearly identifies patients at a high risk for cardiovascular mortality and morbidity after stroke despite an unsuspected source of embolism by clinical examination.
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PMID:Usefulness of transesophageal echocardiography in predicting mortality and morbidity in stroke patients without clinically known cardiac sources of embolus. 960 57

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


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