Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methods are described (a) for the estimation of glycogen phosphorylase activity (EC 2.4.1.1) in human blood serum based on the chemical determination of liberated orthophosphate or on the enzymic determination of glucose 1-phosphate in a coupled assay system and (b) for the electrophoretic separation of isophosphorylases I, II, and III in human. Glycogen phosphorylase activities ranging from 1.5 to 18 mU/ml were found in the serum of patients with acute myocardial infarction. In contrast, no glycogen phosphorylase activity was detected in the serum of healthy persons. The enzyme appears in the serum 4 hours after the onset of the infarction and reaches a maximum after 20 to 30 hours. Acrylamide gel electrophoresis of serum after a myocardial infarction revealed only muscle isophosphorylase I, the isoenzyme characteristic of the heart. No phosphorylase activity was detected in serum of patients with angina pectoris, endocarditis, and uncomplicative congestive heart failure. From these findings it appears that the new serum enzyme test may prove to be a valuable addition to presently existing methods for the early differential diagnosis of acute myocardial infarction.
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PMID:The assay of glycogen phosphorylase in human blood serum and its application to the diagnosis of myocardial infarction. 112 38

Nonejection clicks and associated mitral systolic murmurs are common in routine cardiologic practice and can result from multiple etiologic factors affecting the complex mitral valve mechanism. Such factors include a specific syndrome the essential feature of which is that the mitral leaflets or part thereof, primarily the posterior one, are voluminous. The syndrome has stimulated widespread interest and study during the last decade and various descriptive terms, including the "billowing mitral leaflet syndrome" (BMLS), have been applied to it. A familial occurrence of the BMLS may be detected and symptoms include chest pain, palpitations, syncope, and anxiety. Arrhythmias, conduction defects, and ECG abnormalities which mimic occlusive coronary artery disease are important features which remain ill understood. It is suggested that there is a possible relationship between the so-called "athlete's heart" and the BMLS. We also postulate that the entity of acute myocardial infarction without demonstrable occlusive coronary artery disease is, in at least some instances, a complication of the BMLS-possibly on the basis of coronary spasm. More severe mitral regurgitation, infective endocarditis, or, rarely, sudden death may supervene in the BMLS but we conclude, from published data and our own experience, that the prognosis is generally good.
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PMID:The problem of nonejection systolic clicks and associated mitral systolic murmurs: emphasis on the billowing mitral leaflet syndrome. 119 42

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

To assess the usefulness and safety of transesophageal echocardiography in critically ill patients, we analysed the transesophageal echocardiography studies in 60 of such cases (age: 58 +/- 11 and 38 males). Every patient underwent a previous transthoracic echocardiogram, that was considered inadequate for diagnostic purposes. Thirty patients (50%), were on mechanical ventilation and 17 patients (28%) showed hypotension and/or shock. Forty patients (66%) were at special care units and in 31 (52%) of them, pulmonary and systemic pressures, and continuous analysis of venous pressure of oxygen were available. Indications for study were: 17 patients with clinical suspicion of aortic dissection (confirmed in 5 cases): 9 patients infective endocarditis (4 cases showed valvular vegetations); 6 patients with mitral prosthesis dysfunction (confirmed in 4 cases); complicated acute myocardial infarction (MI) in 8 patients (2 cases with mitral insufficiency, 3 with left ventricular dysfunction, 1 with right ventricular MI, 1 with left ventricular pseudoaneurysm and other with isolated inferior MI); in 11 patients the study was performed to evaluate the result of cardiac transplantation immediately (< 4 h) and it showed 2 cases of left ventricular dysfunction; 3 patients were studied for severe cardiac dysfunction of unknown etiology (a dilated cardiomyopathy was confirmed in one and ruled out in the other, and one patient showed signs of restrictive situation); there were other causes in the rest. The procedure could be completely performed in all cases. In conclusion in critically ill patients the transesophageal echocardiography has a great usefulness and minimal complications.
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PMID:[Usefulness of transesophageal echocardiography in the critical patient]. 147 Jul 40

A 65 year-old-man was admitted to our hospital complaining of orthopnea and precordial oppressive feeling. Chest roentgenogram revealed congestive heart failure. Electrocardiogram revealed acute myocardial infarction-like pattern. Serum enzymes (CPK, GOT, LDH) were slightly elevated, but serum antiviral antibodies were not elevated. Echocardiogram showed severe symmetrical left ventricular (LV) hypertrophy, but there was no abnormality of LV wall motion. He died of progressive heart failure and ventricular fibrillation on the second hospital day. A necropsy was performed within one hour of death. The heart was enlarged (690 g) with both left and right ventricular hypertrophy. The myocardium disclosed a diffuse infiltration predominantly of eosinophilic leucocytes. Histopathological study revealed giant cell formation and granulomatous lesions in the myocardium. There was no overt endocarditis or pericarditis. We concluded that the severe LV hypertrophy was due to myocardial inflammatory swelling. From these findings, we diagnosed this case as acute isolated (Fielder's) myocarditis.
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PMID:[A case of acute isolated (Fiedler's) myocarditis diagnosed by histopathological study with rapid unfortunate course]. 158 53

The aim of this paper is to report for the first time the association between bronchiolo-alveolar carcinoma and acute myocardial infarction (AMI). Two patients suffering from this association were studied. A 59 year old male, diabetic, alcoholic and smoker was admitted because a diaphragmatic AMI. An interventricular septal defect and papillary posterior muscle rupture were confirmed at autopsy. A 0.8 cm diameter friable mass was found in the right lung superior lobe. The second case was a 69 year old male, smoker, who presented with a diaphragmatic and right ventricular posterior wall AMI. A round 1 cm diameter tumor was observed at the right lung superior lobe. It had a caseous aspect lying over a fibrous scar. Both cases had severe right coronary artery narrowings with recent occlusive thrombi. The cardiac valves were free of non-bacterial thrombotic endocarditis. Therefore the possibility of coronary embolization was discarded. As lung carcinomas produce vasospastic and thrombogenic mucins, these substances could have been responsible for the acute coronary thrombosis.
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PMID:[Acute myocardial infarction and bronchoalveolar carcinoma. Association or coincidence?]. 165 6

A growing amount of clinical and experimental evidence suggests a link between infection and atherosclerotic diseases including both myocardial and cerebral infarction. A prime example is a greatly increased risk of stroke in septicaemic patients with and without endocarditis. Controlled clinical studies have recently shown, however, that certain other milder bacterial infections are also a risk factor for infarction. A preceding febrile respiratory infection was a major risk factor for stroke in young and middle aged patients. In patients with acute myocardial infarction Chlamydia pneumoniae and dental infections seem to be risk factors according to one controlled clinical study. Several possible mechanisms could explain the observed association of infection and infarction. For instance, infection causes a hypercoagulable state which increases the risk of thrombosis. In addition, infection has profound and harmful effects on prostaglandin and lipid metabolism. Infection may also have some role in the atherosclerotic process itself by inducing damage and inflammation in vascular endothelium in the presence of hypercholesterolemia. So far, however, little clinical evidence is available to suggest that by controlling infection the risk of infarction or development of atherosclerotic lesions might be reduced except in patients with endocarditis, where the risk of thromboembolic complications rapidly diminished when the infection is controlled with antimicrobial therapy.
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PMID:Infection as a risk factor for infarction and atherosclerosis. 175 23

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.
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PMID:Etiology and pathogenesis of thromboembolism. 176 43

An extremely unusual case of myocardial infarction associated with infective endocarditis (IE) is described. A 38-year old male with a high fever was transferred to our hospital for further treatment of IE. Two-dimensional echocardiogram showed a large mycotic aneurysm of the sinus of Valsalva in contact with neighbouring structures. The patient had a rapid recovery within several days after administration of antibiotic agents. However, he then developed abrupt onset of severe precordial pain. From the echocardiogram images and biochemical evaluation he was diagnosed as having an acute subendocardial infarction. Serial echocardiograms revealed expansion of the aneurysm, extending from the myocardium of the anterolateral free wall to the lower margin of the proximal left coronary artery. The cause of acute myocardial infarction was thought to be incomplete occlusion of the coronary artery through compression by the enlarging mycotic aneurysm of the sinus of Valsalva. Urgent surgery confirmed compression of the left coronary artery by the large mycotic aneurysm as the cause of acute myocardial infarction.
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PMID:Infective endocarditis causing acute myocardial infarction by compression of the proximal left coronary artery due to a mycotic aneurysm of the sinus of Valsalva. 176 85

Coronary embolism is a known complication of bacterial endocarditis that sometimes causes acute myocardial infarction. The necessity for rapidly restoring coronary artery perfusion and the time constraints governing clinical decisions may prevent endocarditis from being diagnosed before pharmacologic or mechanical thrombolysis. This report describes the first documented cases of coronary angioplasty in two patients with acute myocardial infarction caused by bacterial endocarditis, and reviews the literature on coronary artery complications of bacterial endocarditis. The first patient developed a coronary artery mycotic aneurysm at the dilatation site; the second experienced a small intracerebral hemorrhage following reperfusion. It is, of course, unwise to generalize from two cases, but we believe that in patients who are most likely to have endocarditis as the cause of acute myocardial infarction, the impulse to follow conventional strategies for coronary reperfusion should be tempered by thoughts of possible consequences.
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PMID:Bacterial endocarditis presenting as acute myocardial infarction: a cautionary note for the era of reperfusion. 200 22


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