Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac involvement as pericarditis, myocarditis, and endocarditis is common in juvenile rheumatoid arthritis (JRA). Though there are many reports concerning systolic and diastolic functions of adults with rheumatoid arthritis, there are no studies on children with JRA. Thirty patients with JRA without any cardiac symptoms and 30 sex- and age-matched controls were included in the study. M-mode and pulsed-wave Doppler echocardiography were performed on each participant to assess the systolic and diastolic functions of the left ventricle. Left ventricular end-systolic diameter and volume were larger and ejection fraction and fractional shortening were decreased in the JRA group. Among the diastolic parameters, increased late flow velocity, decreased early flow velocity, and prolonged isovolumic relaxation time reflected an abnormal relaxation form of diastolic dysfunction. Mortality rate is increased in adults with rheumatoid arthritis, and ischemic heart disease is the leading cause of cardiovascular mortality. The abnormal relaxation form of diastolic dysfunction found in children with JRA is seen in ischemic heart disease. These children can therefore be candidates for ischemic heart disease in the future even though they are fully asymptomatic at present. In conclusion, children with JRA should be assessed for systolic and diastolic functions with serial echocardiography. In this way it may be possible to reduce the mortality and morbidity of the disease from cardiac causes.
 ...
PMID:Left ventricular diastolic functions in juvenile rheumatoid arthritis. 1086 17

Chagas' disease, caused by Trypanosoma cruzi, is an important cause of myocarditis and chronic cardiomyopathy and is accompanied by microvascular spasm and myocardial ischemia. We reported previously that infection of cultured endothelial cells with T. cruzi increased the synthesis of biologically active endothlein-1 (ET-1). In the present study, we examined the role of ET-1 in the cardiovascular system of CD1 mice infected with the Brazil strain of T. cruzi and C57BL/6 mice infected with the Tulahuen strain during acute infection. In the myocardium of infected mice myonecrosis and multiple pseudocysts were observed. There was also an intense vasculitis of the aorta, coronary artery, smaller myocardial vessels and the endocardial endothelium. Immunohistochemistry studies employing anti-ET-1 antibody revealed increased expression of ET-1 that was most intense in the endocardial and vascular endothelium. Elevated levels of mRNA for preproET-1, endothelin converting enzyme and ET-1 were observed in the same myocardial samples. Plasma ET-1 levels were significantly elevated in infected CD1 mice 10-15 days post infection. These observations suggest that increased levels of ET-1 are a consequence of the initial invasion of the cardiovascular system and provide a mechanism for infection-associated myocardial dysfunction.
 ...
PMID:Myocardial expression of endothelin-1 in murine Trypanosoma cruzi infection. 1106 72

With the advent of more effective therapies for human immunodeficiency virus (HIV) infection, HIV-infected patients are living longer and cardiovascular disease is becoming more obvious in this population. Patients with HIV infection represent one of the most rapidly developing groups with cardiovascular disease globally. Cardiovascular disease complicating HIV infection is likely to contribute to burgeoning healthcare costs. Pericarditis, myocarditis, cardiomyopathy, atherosclerotic coronary vasculopathy, arterial aneurysms, pulmonary hypertension, and endocarditis occur with increased frequency in these patients. Pericardial tamponade, dilated cardiomyopathy, endocarditis, and vasculopathy can lead to fatal outcomes in this population. The advent of cardiomyopathy heralds a very poor prognosis in patients infected with HIV. Coronary vasculopathy without obvious risk factors can lead to myocardial ischemia in young patients infected with the virus. Moreover, the protease inhibitors used to treat HIV infection induce a syndrome of lipodystrophy and dyslipidemia that may be associated with accelerated atherosclerosis as well as insulin resistance. All these factors contribute to increased cardiovascular morbidity and mortality in the HIV-infected population. HIV infection, opportunistic infections, secreted viral proteins such as gp120 (envelope protein) or Tat (transactivator of viral transcription), and cytokines elaborated during the course of HIV infection of the immune system all contribute to pathogenesis of these disorders. Further basic and clinical studies are required to understand the pathogenesis of cardiovascular complications and develop appropriate management strategies for these patients.
 ...
PMID:The cardiovascular and metabolic complications of HIV infection. 1117 4

The evaluation of syncope occurring during exercise or occurring spontaneously in highly trained individuals presents a unique diagnostic challenge. It is of critical importance to exclude potential life-threatening disorders such as hypertrophic cardiomyopathy, long QT syndrome, right ventricular dysplasia, anomalous coronary artery distribution, valvular heart disease, myocarditis, or exercise-induced arrhythmia. This review is not directed towards identifying, treating, or determining athletic eligibility of individuals with such disorders. Rather, we endeavour to discuss the pathophysiology of exercise-induced neurocardiogenic syncope and to address the role of head upright tilt testing in evaluating syncope in athletic individuals in whom proper evaluation has excluded the presence of ischaemic heart disease or primary structural or electrical heart disease.
 ...
PMID:Exercise-induced neurocardiogenic syncope: clinical data, pathophysiological aspects, and potential role of tilt table testing. 1122 99

Among the cardiomyopathies,--dilated cardiomyopathy (dcm), hypertrophic cardiomyopathy, restrictive cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy--, dcm is the most frequent entity. Its prevalence in the United States amounts to 36 cases per 100,000 inhabitants, men being almost 3-fold more involved than women. The etiology of dcm is very heterogenous; 50% of the cases are due to idiopathic dcm whereas the other half comprises a broad spectrum of various etiologies such as myocarditis, ischemic heart disease, peripartal cardiomyopathy, hypertension, HIV infection, toxic cardiomyopathy and others. In 20 to 30% of the cases of idiopathic dcm a genetic transmission of the disease has been found. Another 20 to 30% of idiopathic dcm are associated with inflammatory and immunological phenomena. Infectious myocarditis with enteroviruses, especially with coxsackie-virus type B has been suggested to be an important trigger for an immune-mediated dcm. In both, familiar dcm and infection with coxsackie-virus B, an impairment of constituents of the myocardial cytoskeleton has been shown. This is regarded as a possible pathogenetic mechanism in the development of dcm.
 ...
PMID:[Epidemiology-etiology of dilated cardiomyopathy]. 1126 35

Congestive heart failure may be produced by a variety of disorders, including dilated cardiomyopathy, hypertension, and ischemic heart disease. We have developed experimental models of these diseases, and found gene expressions of proinflammatory cytokines increased in the hearts of these animals. Various drugs for heart failure modulate the production of cytokines in experimental models of heart failure. Pimobendan, an inhibitor of phosphodiesterase III prolonged survival, attenuated inflammatory lesions, and decreased the production of cytokines and nitric oxide. Recent studies have shown that these inhibitory effects are due to inhibition of activation of NF-kappaB. In contrast, digitalis increased the production of cytokines and exacerbated myocarditis. Interleukin-10 prolonged survival, attenuated myocardial injury, and appears promising as a treatment of heart failure due to viral myocarditis. Endothelin-1 plays an important pathophysiological role in heart failure, and treatment with an endothelin antagonist had a cardioprotective effect in experimental models of heart failure.
 ...
PMID:The role of inflammatory mediators in the failing heart: immunomodulation of cytokines in experimental models of heart failure. 1130 31

Left ventricular assist devices (LVAD) may improve cardiac function. The pathogenesis of this phenomenon, called 'reverse remodelling', is not completely elucidated. To examine the hypothesis that LVAD support eliminates tissue stress by reducing local hypoxia, the distribution of heme oxygenase-1 (HO-1), a stress protein inducible by hypoxia, was examined in vivo and in vitro. The immunoreactivity for HO-1 was semi-quantitatively analysed in left ventricular tissue of 23 patients (14 dilated cardiomyopathy (DCM), six ischaemic heart disease (IHD), three myocarditis/congenital heart disease) with end-stage heart failure before and after LVAD support, while two unused donor hearts served as controls. Control hearts stained almost negative for HO-1, while failing hearts showed immunoreactivity mainly in cardiomyocytes, but also in endothelial cells, some smooth muscle cells and fibroblasts. Hearts with IHD showed significantly higher HO-1 immunoreactivity than hearts with DCM or myocarditis/congenital heart disease. After LVAD support, the HO-1 content decreased significantly in the DCM and IHD group and was significantly higher in the subendocardium than in the subepicardium. In vitro, under hypoxic conditions, neonatal rat cardiomyocytes showed an increase of HO-1 protein content up to sixfold above the normal level, which returned to normal values after normoxic cultivation. Mechanical support reduces the HO-1 content of the failing heart and HO-1 is inducible in vitro under hypoxia and is reversible under normoxia. This supports the concept that restoration of cardiac normoxia by mechanical unloading, particularly in the subendocardium, may be in part responsible for the phenomenon of 'reverse remodelling'.
 ...
PMID:Reduction of hypoxia-inducible heme oxygenase-1 in the myocardium after left ventricular mechanical support. 1201 48

Though many publications in the field of myocarditis and cardiomyopathies have renewed interest in the value of endomyocardial biopsy, its role in the work-up of patients with cardiomyopathies, idiopathic arrhythmias and even ischemic heart disease, is still debated. Since its introduction in 1963 the technique has been developed with current routine use of a biventricular and even atrial approach. At the same time immunohistochemistry and molecular biology studies have greatly enhanced the information obtainable from myocardial samples. The authors report their experience and briefly review the pertinent literature on the current use of endomyocardial biopsy in the diagnosis and treatment of dilated, hypertrophic and restrictive cardiomyopathy, of idiopathic arrhythmias and in ischemic heart disease.
 ...
PMID:The role of endomyocardial biopsy in the diagnosis of cardiomyopathies. 1211 98

This article reviews some of the adverse effects on the heart of both cardiac and noncardiac drugs. Myocardial function is affected by antineoplastic agents, tricyclic antidepressants and other psychotropics, amebicides, radiographic contrast agents, and alcohol. Oral contraceptives (OCs) may aggravate myocardial ischemia. The acute effects of OC use probably reflect increased platelet aggregation or fibrin accumulation; the added longterm risk noted in women who have discontinued OCs up to 10 years previously suggests acceleration of atherogenesis, although the mechanism for this remains uncertain. The magnitude of the increased risk of myocardial infarction seems to depend on coexistent cardiac risk factors such as smoking and age. Adverse effects of other drugs prescribed for noncardiac disease include the production of cardiomyopathy, pericarditis and myocarditis, and tachyarrhythmias and bradyarrhythmias.
 ...
PMID:Drugs that induce heart problems. Which agents? What effects? 1226 99

Exercise-induced ventricular tachycardia in young adults may occur with various structural heart diseases or with structurally normal heart. The structural heart diseases reported to cause exercise-induced ventricular tachycardia in this patient population include arrhythmogenic right ventricular dysplasia, hypertrophic cardiomyopathy, dilated cardiomyopathy, myocarditis, congenital heart disease, and myocardial ischemia. The conditions well identified to cause exercise-induced ventricular tachycardia with structurally normal heart are congenital long-QT syndrome and familial polymorphic ventricular tachycardia. Exercise-induced ventricular tachycardia may display polymorphic, monomorphic, or bidirectional morphologies. A case of exercise-induced catecholamine-sensitive bidirectional ventricular tachycardia with alternating right and left bundle branch block patterns is reported in a young boy in the absence of structural heart disease, the conditions causing bidirectional ventricular tachycardia, and family history of such an event or sudden cardiac death. The bidirectional tachycardia typically displays right bundle branch block in right precordial leads with alternating polarity of the QRS-complex in frontal plane leads but in this case the bidirectional morphology of tachycardia was caused by alternating right and left bundle branch block-type patterns. The conditions causing bidirectional ventricular tachycardia are digoxin toxicity, ischemic heart disease, hypokalemia, myocarditis, and familial polymorphic ventricular tachycardia syndrome but the exact cause in this patient remained obscure, and the possibility of an underlying electrical or ion channel disease of the heart could not be ruled out.
 ...
PMID:Exercise-induced bidirectional ventricular tachycardia with alternating right and left bundle branch block-type patterns--a case report. 1236 69


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>