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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transient ischaemic focal cerebral attacks (TIA's) are due to: 1) atherosclerosis when embolism may take place or perhaps transient occlusion of the internal carotid artery or mural or transiently occlusive thrombus of an intracranial artery stenosis or transient systemic hypotension. In recent years embolism may have been overdiagnosed; 2) cardiac embolism due to dysrythmias, myocardial infarction, endocarditis, valvular prosthesis, etc.; 3) miscellaneous causes, often difficult to demonstrate such as tortuosity of the extracranial cerebral arteries, dissecting aneurysms, changes in cerebrovascular resistance; 4) not unfrequently no cause is found, especially in young patients.
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PMID:[Pathogenesis of focal, transitory cerebral ischemic accidents]. 60 29

About 15% of patients with cancer have cerebrovascular lesions, resulting from 4 kinds of disorders sometimes intermingled in advanced disseminated cancer: coagulation disorders, direct effects of the tumor, infections and therapeutic measures. Infarction, hardly less frequent than hemorrhage, mostly complicates lymphoma and carcinoma. Hypercoagulation states, such as chronic disseminated intravascular coagulation, nonbacterial thrombotic endocarditis, and nonmetastatic cerebral venous thrombosis account for about 50% of cases. Tumor emboli, as seen in intravascular malignant lymphomatosis, arteritis related to aspergillus, granulomatous angiitis with or without herpes zoster and radiation-induced atherosclerosis are rarer. Cerebral hemorrhages, excluding bleeding from the metastases of choriocarcinoma and melanoma are mainly associated with leukemia by acute disseminated intravascular coagulation as in promyelocytic leukemia, by leukostasis or by pancytopenia. Both infarction and hemorrhage rarely reveal the neoplasia. Lesions are often small and disseminated, and therefore produce a picture of diffuse acute or subacute encephalopathy rather than acute focal deficits. Finally, there may be no relationship between the cerebrovascular event and the neoplasia, and atherosclerosis or traumatic subdural hematoma may well be the causal factor.
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PMID:[Cerebrovascular complications of cancers]. 130 55

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

"Mycotic" aneurysm was originally described by Osler in 1885. It occurs in a normal or atherosclerotic artery from septic emboli in patients with infective endocarditis. However, now the term "mycotic" aneurysm is applied to all cases of aneurysms caused by any organisms. From September 1988 to November 1990, four cases of ruptured mycotic aneurysm were diagnosed at our institute. Three were males and one was a female; they were elderly with atherosclerosis of the aorta. The diagnosis was established by computed tomography (CT) scan, bacteriology or operative findings. Two of the patients underwent emergency operation; only one survived. In general, the diagnosis of mycotic aneurysm is based on the classical features of fever, abdominal or chest pain, positive blood culture and a pulsatile mass. Because the clinical manifestations are often variable, a patient may present with chronic sepsis (esp. Salmonella sp) of unknown origin with deterioration to a fatal outcome from the aneurysmal rupture, which is a rare cause of retroperitoneal abscess or pericardial effusion. The principles of management, including high clinical suspicion, an accurate diagnosis by imaging studies (arteriography or CT scan), prolonged effective antibiotic therapy, arterial ligation or wide excision of the infected lesion, intraoperative Gram's stain and culture, extra-anatomic bypass grafting through clean tissue planes, and prolonged postoperative follow-up, are indispensable to reduce morbidity and mortality.
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PMID:Mycotic aneurysm rupture: report of four cases. 136 21

Based on the clinical, instrumental and biochemical findings, out of 104 patients with septic endocarditis 11 (10.6%) were diagnosed to have myocardial infarction. It was provoked by coronary artery embolism, the covering of the coronary artery ostium by vegetation from the aortal cusp, a decrease of perfusion pressure in atherosclerosis stenosed coronary arteries because of marked insufficiency of the aortal cusp. In more than half the cases, the clinical picture of myocardial infarction was atypical, painless. Echocardiographic demonstration of the vegetations near the coronary artery ostium permits forecasting the possibility of its covering with vegetation, the threat of the occurrence of acute coronary insufficiency, which may appear an additional indication for heart valve replacement.
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PMID:[The mechanisms of the development and diagnosis of myocardial infarct in septic endocarditis]. 144 Mar 11

We report a retrospective, clinicopathologic study of 139 patients who died during treatment of a severe burn. Fifty-three percent of the patients had central nervous system (CNS) complications-infections, cerebral infarcts and hemorrhages, metabolic encephalopathies, central pontine myelinolysis, and cerebral trauma. Children and adults were equally affected. Sixteen percent of the patients had a CNS infection. Candida species, Staphylococcus aureus and Pseudomonas aeruginosa caused almost 80% of them. S. aureus and candida caused cerebral microabscesses and septic infarcts. P. aeruginosa caused meningitis and infarcts due to meningitis. CNS infections arose as a result of spread from a systemic source. The major risk factors for CNS infection were an extensive burn, S. aureus endocarditis, and a burn wound infection due to candida or P. aeruginosa. Patients with burns of less than 30% of the surface area of their body, those without a systemic infection, and those in the first week after their burn were at low risk. Eighteen percent of the patients had cerebral infarcts. In almost half the patients, the infarcts were caused by septic arterial occlusions or other complications of the burn, viz, disseminated intravascular coagulation (DIC) and septic shock. In only one-third of the patients were infarcts due to atherosclerosis, atrial fibrillation, or other causes prevalent in the general population. Intracranial hemorrhages were only one-fifth as frequent as infarcts and were due to DIC and thrombocytopenia, caused by bacteremia. Diagnosis during life was difficult, because the neurologic picture of focal cerebral lesions and meningitis was indistinguishable from that of metabolic encephalopathies, and because many patients had more than 1 neurologic complication. However, our results suggest that a clinical approach that includes analysis of risk factors for CNS infection, cerebral imaging, examination of cerebrospinal fluid, and tests for DIC can lead to a neurologic and microbiologic diagnosis in most patients.
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PMID:Central nervous system complications of thermal burns. A postmortem study of 139 patients. 152 3

The patient, a 51-year-old man, was receiving immunosuppressants for 2 yr after renal allotransplantation. He had heart failure with aortic regurgitation, fever, anemia and a history of odontectomy on admission. He was resistant to medical treatments and died from cerebral emboli. On autopsy, vegetation of the aortic valve was identified. Progression of atherosclerosis, which may have been due to steroids and chronic rejection, was prominent. This report is the first case of infective endocarditis following organ transplantation in Japan. Such complications as infective endocarditis and atherosclerosis will be on the rise with the increase of numbers or organ transplantations.
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PMID:Post transplanted infective endocarditis. 180 48

An overview is given over etiology and prognosis of cerebral ischemias until the age of 40. In a time period of 19 years, 168 patients were diagnosed with cerebral ischemia until the age of 40 (91 females, 77 males). The most frequent etiology is premature atherosclerosis in patients with vascular risk factors (up to 50%). Cardiogenic embolism is responsible for 1 to 34% of the cases: cardiac valve diseases and endocarditis being the most frequent sources. In 2 to 19% a vasculitis is diagnosed. While infectious arteritis is especially frequent in countries of the third world, immunovasculitides are common in Europe and the USA. Noninflammatory vasculopathies include spontaneous or traumatic dissection, fibromuscular dysplasia and vascular malformations. A migrainous stroke is especially frequent in female smokers with intake of oral contraceptives. During pregnancy both sinus thrombosis and arterial ischemia occur. Hematologic causes for ischemia are polycythemia, thrombocytosis and genetic diseases (sickle cell anemia, AT3-deficiency). Cerebral ischemia may occur in connection with the ingestion of ergot-derivates. The prognosis of cerebral ischemia in young adults is better than in older stroke-patients.
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PMID:[Cerebral ischemia in young adults]. 193 40

Infective aneurysm showing dilatation of all three coronary sinuses of Valsalva due to infective endocarditis is extremely rare. We present the first report of such a case complicated by left single coronary artery. The patient was a 55-year-old man with a past history of untreated diabetes mellitus, cerebral infarction, aortic regurgitation and high-grade fever. He was admitted with a complaint of easy fatigability. In a treadmill exercise test, asymptomatic ischemic depression of the ST segment was observed. Two-dimensional echocardiography revealed marked dilatation of all three sinuses of Valsalva, and a mural thrombus within the dilated right sinus of Valsalva. On magnetic resonance imaging, an abnormal signal in the markedly dilated right sinus of Valsalva was revealed. Coronary arteriography showed left single coronary artery (L1 type by Sharbaugh's classification). The histopathological features of the affected aorta were thought to represent the healing stage of infective endocarditis. With regard to the myocardial ischemia in this patient, it was thought to have arisen mainly through aortic regurgitation and coronary atherosclerosis due to single coronary artery, and partly influenced by untreated diabetes mellitus.
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PMID:A rare case of infective aneurysm involving all three sinuses of Valsalva complicated by left single coronary artery. 202 86

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99


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