Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kawasaki disease (KD), first described in Japan in 1967 by Dr. Tomisaku Kawasaki, is an acute multi system vasculitis of infancy and early childhood characterised by high fever, rash, conjunctivitis, inflammation of the mucous membranes, erythematous induration of the hands and feet and cervical lymphadenopathy. Synonyms for Kawasaki disease include "Kawasaki syndrome" and "mucocutaneous lymph node syndrome" (MCLS, MLNS, MCLNS). Kawasaki disease was initially presumed to occur only in Japan; but now this disease is known in the whole world. The first cases in the United States were reported in Hawaii in 1976. In poland 5 cases were recognized, and first time described in 1981. The etiology of Kawasaki disease remains unknown. Toxic, allergic and immunologic causes have been suspected, but most investigators favor an infectious cause or an immune response to an infectious agent. Among classes of microorganism suspected of causing Kawasaki disease were bacteria, leptospires, fungi, rickettsiae and a number of viruses. Recently, there has been considerable interest in the possibility, that Kawasaki disease is caused by RETROVIRUSES. Although the disease is generally benign and self-limited, about 20% of children develop coronary artery aneurysms. In 5% of cases, giant aneurysm/more then 8 mm/develop, predisposing the patient to acute coronary artery thrombosis, myocardial infarction and sudden death. This is the most serious complication of KD. Other manifestations of hearth involvement, include pericarditis, myocarditis, myocardial failure and mitral regurgitation. Besides this many other clinical findings are commonly noted in KD; such as: pneumonia, diarrhea, arthritis, aseptic meningitis, otitis media, obstructive jaundice, hydrops of gallbladder and others.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Kawasaki disease]. 754 22

Esophagectomy without opening the thoracic cavity--transhiatal esophagectomy--(THE) were performed in 47 patients with malignant tumors localized at various levels of the esophagus. Pulmonary function studies were performed in all patients and they are categorized as low, moderate, or high risk for probable postoperative pulmonary complications according to the risk category system. Nine of these patients were classified as high risk, seven as moderate risk, and the rest as low risk. In all patients but four, reconstruction was accomplished by using their stomachs as a substitute. In the remaining patient, intestinal continuity was established by a left and right colonic interposition. Three patients were lost in the early postoperative period. Two patients categorized as low risk died from pulmonary thromboembolism and cardiac failure, respectively. One patient categorized in the high risk group died of coronary thrombosis. Postoperative complications included transient hoarseness due to recurrent laryngeal nerve paresis in one patient, right pleural effusion in one patient, pneumothorax in two patients, and thrombophlebitis in one patient. In the high risk patient group, there were no pulmonary complications. This clinical study demonstrated the protective effect of THE in patients with serious pulmonary problems.
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PMID:Transhiatal esophagectomy for esophageal carcinoma in Turkey: with special reference to respiratory function. 829 63

Coronary artery diseases may categorized into asymptomatic disease, angina pectoris, myocardial infarction, chronic heart failure, and sudden coronary death. Unstable angina, acute myocardial infarction, and sudden cardiac death are known as the acute coronary syndromes. Coronary atheroma is unstable in the patients with acute coronary syndromes. Stable plaques will be unstable when dynamic alterations occur. The alterations are plaque rupture, plaque hemorrhage, coronary thrombosis and vasospasm. They act each other. We analysed the histopathology of coronary arteries who died of acute myocardial infarction in 85 cases. It showed that the risk factors of plaque rupture are clusters of form cells, eccentric plaque with soft lipid rich core, and thinning of fibrous cap in atheroma. Most of these cases ruptured at edge of the atheroma.
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PMID:[Pathogenesis of acute coronary syndromes]. 978 Jul 33

Meta-analysis of previous relatively small clinical trials, comparing intravenous magnesium with placebo in acute myocardial infarction (AMI) patients, mainly without thrombolytic therapy, demonstrated that magnesium reduced in-hospital mortality by 19%, mainly by reducing the incidence of serious arrhythmias and left ventricular heart failure by one quarter. These findings have led us to hypothesize that magnesium treatment inhibits platelet-dependent thrombosis in patients with coronary artery disease (CAD). In a prospective, double blind, and crossover study, we have recently demonstrated that oral magnesium treatment inhibits thrombus formation measured by platelet-dependent thrombosis in stable CAD patients by 35%. This effect appears to be independent of platelet aggregation and activation, and is additive to that of aspirin. High dose of intravenous magnesium can inhibit thrombus formation and is associated with suppression of platelet aggregation. Magnesium treatment can dose-dependently inhibit a wide variety of agonists of platelet aggregation, such as thromboxane A2 and stimulate prostacyclin synthesis. The molecular basis for these effects is likely modulated via reduction of intracellular calcium mobilization. Hypomagnesemia also selectively impaired the release of nitric oxide from the coronary endothelium. We have recently demonstrated that oral magnesium treatment can improve endothelium-dependent vasodilation in CAD patients with optimal lipid values. Because nitric oxide is a potent endogenous vasodilator and inhibitor of platelet aggregation and adhesion, hypomagnesemia could promote vasoconstriction and coronary thrombosis in hypomagnesemic states. These findings suggest a potential mechanism whereby magnesium may beneficially alter outcomes in CAD patients.
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PMID:The role of magnesium as antithrombotic therapy. 1110 30

Myocardial infarction with normal coronary arteries is a syndrome resulting from numerous conditions but the exact cause in a majority of the patients remains unknown. Cigarette smokers and cocaine users are more prone to develop this condition. The possible mechanisms causing myocardial infarction with normal coronary arteries are hypercoagulable states, coronary embolism, an imbalance between oxygen demand and supply, intense sympathetic stimulation, non-atherosclerotic coronary diseases, coronary trauma, coronary vasospasm, coronary thrombosis, and endothelial dysfunction. It primarily affects younger individuals, and the clinical presentation is similar to that of myocardial infarction with coronary atherosclerosis. Thrombolytics, aspirin, nitrates, and beta blockers should be instituted as a standard therapy for acute myocardial infarction. Once normal coronary arteries are identified on subsequent angiography, the calcium channel blockers could be added since coronary vasospasm appears to play a major role in the pathophysiology of this condition. The beta blockers should be avoided in cocaine-induced myocardial infarction because the coronary spasm may worsen. In myocardial infarction with normal coronary arteries, complications such as malignant arrhythmia, heart failure, and hypotension are generally less common, and prognosis is usually good. Recurrent infarction, postinfarction angina, heart failure, and sudden cardiac death are rare. Stress electrocardiography and imaging studies are not useful prognostic tests and long-term survival mainly depends on the residual left ventricular function, which is usually good.
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PMID:Myocardial infarction with normal coronary arteries: the pathologic and clinical perspectives. 1138 79

In a post-mortem analysis of 1,500 patients, aged 70 years or more, heart disease and malignancy were the two major causes of death. Coronary disease was exceedingly prevalent, almost one in five being subject to this form of heart disease, and 13% dying from its effects. The levelling of the sex ratio in coronary disease in the aged was a striking feature. The clinical manifestations of coronary thrombosis were often atypical. The incidence of demonstrable coronary thrombosis was as high as in younger age groups. The pathological findings and the incidence of local complications in coronary disease were similar to those in other age groups. Other causes of heart failure were relatively infrequent. Certain features of these conditions in old age are discussed. Cardiac amyloidosis, in the form associated with senility, occurred in a very few cases but did not contribute to heart failure.
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PMID:HEART DISEASE IN OLD AGE. 1407 70

Panic disorder serves as a clinical model for testing whether mental stress can cause heart disease. Our own cardiologic management of panic disorder provides case material of recurrent emergency room attendances with angina and electrocardiogram ischemia, triggered arrhythmias (atrial fibrillation, ventricular fibrillation), and documented coronary artery spasm, in some cases with coronary spasm being complicated by coronary thrombosis. Application of radiotracer catecholamine kinetics and clinical microneurography methodology suggests there is a genetic predisposition to panic disorder that involves faulty neuronal norepinephrine uptake, possibly sensitizing the heart to symptom generation. During panic attacks there are large sympathetic bursts, recorded by clinical microneurography in the muscle sympathetic nerve neurogram, and large increases in cardiac norepinephrine spillover, accompanied by surges of adrenal medullary epinephrine secretion. In other conditions such as heart failure and presumably here also, a high level of sympathetic nervous activation can mediate increased cardiac risk. The sympathetic nerve cotransmitter, neuropeptide Y (NPY), is released from the cardiac sympathetics during panic attacks, an intriguing finding given that NPY can cause coronary artery spasm. There is ongoing, continuous release of epinephrine from the heart in panic sufferers, perhaps attributable to epinephrine loading of cardiac sympathetic nerves by uptake from plasma during panic attacks, or possibly to in situ synthesis of epinephrine through the action of intracardiac phenylethanolamine-N-methytransferase (PNMT) activated by repeated cortisol responses. We have used internal jugular venous sampling and measurement of overflowing lipophilic brain monoamine metabolites to quantify brain norepinephrine and serotonin turnover in untreated patients with panic disorder. We find normal norepinephrine turnover but a marked increase in brain serotonin turnover in patients with panic disorder, in the absence of a panic attack, which presumably represents an underlying neurotransmitter substrate for the condition.
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PMID:Cardiac sympathetic nerve biology and brain monoamine turnover in panic disorder. 1524 Apr 8

The renin-angiotensin-aldosterone system (RAAS) is critical in regulating systemic blood pressure, water and electrolyte balance, and pituitary gland hormones. These physiologies appear to be primarily mediated by the angiotensin II/AT(1) receptor subtype system. Overstimulation of this system can predispose cardiovascular disease (CVD) characterized by excessive vasoconstriction, fibrosis, and cardiac remodeling. If untreated, the patient typically displays a continuum of pathophysiologic conditions progressing from atherosclerosis to left ventricle hypertrophy (LVH), coronary thrombosis, myocardial infarcts, with heart failure as an endpoint. Intervention with antihypertensive therapy is necessary to inhibit this progression. RAAS blocking drugs appear to be the most effective approach. Diastolic heart failure patients benefit from treatment with angiotensin converting enzyme (ACE) inhibitors and angiotensin AT(1) receptor blockers (ARBs). Elderly CVD patients evidence age-related changes in body composition that alter the distribution and half-life of medications, thus presenting special challenges to treatment. The presence of comorbidities such as diabetes, renal dysfunction, liver insufficiency further complicates any therapeutic strategy. In addition, noncompliance because of cognitive impairment, depression, confusion due to the complexity of dose regimens, and lack of an appropriate social support system can disrupt positive outcome. The present review discusses the roles of an overactive RAAS and sympathetic nervous system as primary contributors to CVD. In addition, treatment strategies are discussed, focusing on middle aged and elderly hypertensive and heart failure patients.
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PMID:Pathways involved in the transition from hypertension to hypertrophy to heart failure. Treatment strategies. 1798 82

A 44-year-old man with HES who developed a large thrombus in the right ventricle as well as multiple occlusive coronary thrombi died of cardiac failure. Autopsy showed that a large thrombus in the right ventricle was associated with eosinophilic endocarditis. In addition, an occlusive thrombus formed in the circumflex and right coronary arteries with eosinophilic infiltrate in the walls. The findings suggest a causal relationship between coronary thrombosis and eosinophilia. To the authors' knowledge this is the first report to document the clinical and histological findings of coronary thrombosis in a patient with HES.
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PMID:Hypereosinophilic syndrome associated with occlusive coronary thrombosis and right ventricular thrombus. 1819 65

Anaphylactic shock can sometimes take the appearance of heart failure, in relation to an acute coronary syndrome, even with normal coronary arteries, that we illustrate by two observations. We firstly report the case of an anaphylactic shock caused by succinylcholine, after anesthesia induction for inguinal hernia surgery in a 50-year-old man with cardiovascular risks, who presented with ventricular fibrillation followed by a cardiac arrest. An acute and severe anterior coronary syndrome was suspected and treated with thrombolysis. Then the electrocardiogram normalized, as well as the left ventricular function. No significant coronary stenosis was retrospectively revealed by coronarography, and a severe coronary vasospasm induced by the anaphylactic reaction was confirmed. We also describe the case of an anaphylactoid shock caused by cisatracurium infusion, that occurred at the beginning of an adnexectomy in a 55-year-old woman without any particular history. She presented with a cardiogenic shock after intravenous administration of epinephrine. The echocardiograpghic evaluation pointed out an aspect of stress-induced cardiomyopathy, and the coronarography showed normal coronary arteries. The left ventricular dysfunction completely normalized, strongly suggesting the diagnosis of Takotsubo-like syndrome after the anaphylactic shock and its treatment. Both of these cases point out the major interest of cardiologic and allergic evaluation in case of heart failure during general anesthesia. Coronary vasospasm and stress-induced cardiomyopathy are two pathologies that may be observed during anaphylactic shock, and their diagnosis should be considered after elimination of coronary thrombosis.
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PMID:[Heart failure and anaphylactic shock. A report of two cases]. 2127 63


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