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

The purpose of this retrospective study was to consider impaired renal function in patients with severe congestive heart failure after converting enzyme inhibition and to emphasize the characteristics of this population. The study concerned 26 patients (pts), 72.5 +/- 8.1 years old, with a severe congestive heart failure (NYHA Class IV). Before treatment serum creatinine was slightly increased and the introduction of angiotensin converting enzyme inhibitor (ACEI) - Captopril 58.9 +/- 17.3 mg/j or enalapril 9.2 +/- 4.4 mg - impaired renal function from 132.0 +/- 50.7 mumol/l to 183.5 +/- 139.3 mumol/l (n = 26; p less than 0.05). Patients were separated in 3 groups: in group I; 15 pts, serum creatinine remained unchanged under ACEI in despite of the significant decrease of blood pressure (BP); from 140.7 +/- 24.0/82.5 +/- 13.4 to 120.3 +/- 12.8/71.8 +/- 8.7 mmHg (p less than 0.01). The cause of heart failure was an ischemic heart disease (IHD) in 15 patients (chi 2 test, p less than 0.05), a dilated cardiomyopathy in 4 pts and an aortic or mitral valvular regurgitation in 2 pts. In contrast renal function was significantly impaired in group II; serum creatinine increased from 120.8 +/- 25.2 to 189.0 +/- 80.7 mumol/l under ACEI. BP remained unchanged 136.9 +/- 29.0/78.1 +/- 4.9 and 118.7 +/- 13.6/75.6 +/- 7.6 mmHg respectively before and after treatment. There was 4 pts with dilated cardiomyopathy, 4 pts with mitral or aortic valvular regurgitation and only one with IHD. The introduction of an ACEI in two pts--group III--with severe tricuspid regurgitation induced an acute and reversal renal failure (serum creatinine at 600 mumol/l).
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PMID:[Renal insufficiency and treatment of persistent cardiac insufficiency with converting enzyme inhibitor]. 273 17

Sudden cardiac death is the major cause of death in the United States today, claiming over 400,000 victims each year, or one per minute. In the majority of cases, the underlying mechanism is malignant ventricular tachyarrhythmia, with the common substrate being abnormal myocardium from ischemic heart disease or congestive cardiomyopathy.
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PMID:Automatic implantable cardioverter defibrillator: report of the first two implants in Hawaii. 277 41

The usefulness of vasodilating agents in congestive heart failure depends on their ability to diminish left ventricular afterload; this effect does not necessarily persist with long-term treatment. The present study reports the clinical response of 16 patients in heart failure; the trial was double blind with enalapril and/or placebo during 24 weeks. Diagnoses were dilated cardiomyopathy in six, rheumatic heart disease in five, ischemic heart disease in four und hypertensive heart disease in one. Two patients on enalapril died of non cardiac causes and one was withdrawn from the study due to pregnancy. In those patients treated with enalapril the NYHA functional class improved from 2.9/0.8 to 1.1/0.4 (p less than 0.001), and the effort capacity increased from 545/171 to 888/160 seconds (p less than 0.01). Left ventricular systolic function evaluated by echocardiogram and Tc 99 m ventriculogram, radiologic size of the heart and echocardiographic left ventricular diameters showed no significant changes. There were no adverse clinical effects nor laboratory abnormalities. It is concluded that in this study, enalapril produced sustained clinical improvement in patients with heart failure and it was well tolerated during long-term treatment.
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PMID:[Usefulness of enalapril in congestive heart failure]. 282 38

The increase in sympathetic nervous system activity noted in heart failure of several etiologies has beneficial effects in the short term; in the long term, though, it may be detrimental. This provides a rationale for use of beta-blocker therapy in patients with cardiac myopathies of various etiologies. Postinfarction trials in patients with ischemic heart disease have suggested that beta blockade provides a substantial mortality benefit, and beta blockers are accepted as first-line therapy for hypertrophic cardiomyopathy. The use of beta-blocking drugs for dilated cardiomyopathy (DCM), however, is currently investigational. Early trials reporting benefits in functional class, exercise capacity, and myocardial function stimulated further interest in this application of beta blockade. Recent studies comparing metoprolol with placebo or standard treatment have shown promising improvements in functional class and exercise capacity. The patients who will benefit most from beta-blocker therapy in DCM may be those with a high resting heart rate and a short duration of symptoms and, perhaps, feminine gender. Marked structural abnormality on cardiac biopsy (eg, fibrosis) may suggest a poor response to treatment. A multicenter controlled study of metoprolol in dilated cardiomyopathy is in progress. If the outcome is favorable, beta-blocker therapy in DCM may become an accepted, rather than an experimental, treatment.
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PMID:Treatment of cardiac myopathies with beta blockers. What do we know, where do we go from here? 289 53

An acquired defect or damage of a subpopulation of suppressor T lymphocytes is reported in connection with autoimmune diseases. In the present study, the role of immunity was examined in 7 patients with dilated cardiomyopathy (DCM). The frequency of lymphocyte subsets using monoclonal antibodies and natural killer (NK) cell activity was evaluated to determine whether DCM patients had lymphocyte abnormalities that would support the hypothesis that the pathological mechanism of DCM is an immune disturbance. The peripheral lymphocyte counts were significantly lower in patients with DCM and higher in patients with ischemic heart disease (IHD) than in normal controls (NC) (p less than 0.01). The percentage of T cells, B cells, OKT4 and OKT8 positive cells was not statistically different among the three groups studied here, whereas the percentage of T gamma cells was significantly reduced in DCM patients (p less than 0.05). NK cell functional activity as tested in DCM and IHD patients was frequently deficient (22.1 +/- 19.3% in DCM, 13.8 +/- 3.0% in IHD, 37.4 +/- 12.7% in NC). Our results suggest that an imbalance in cellular immune reactions partly explain the pathogenesis of DCM.
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PMID:Study on lymphocyte subsets and NK cell function in patients with dilated cardiomyopathy. 295 Feb 55

Suppressor T lymphocyte function was examined in 11 patients with idiopathic congestive cardiomyopathy and in 11 age and sex matched patients with a similar degree of heart failure resulting from ischaemic heart disease. Suppressor T lymphocyte function was also assessed in a control population of 11 normal subjects. Suppressor T lymphocyte function was reduced in both groups of patients with heart failure but not significantly, and a wide range of suppression was demonstrated in all groups. These data do not support the hypothesis that there is a defect in T lymphocyte function in patients with congestive cardiomyopathy, but they do suggest that there may be a non-specific reduction in T lymphocyte suppressor function associated with heart failure in general.
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PMID:Suppressor T lymphocyte function in patients with idiopathic congestive cardiomyopathy. 295 74

Survival in severe left ventricular failure is poor but has not been widely assessed since the introduction of several new nonglycosidic, nonsympathomimetic oral inotropic agents for long-term therapy. We examined retrospectively the survival of 82 patients with severe left heart failure during long-term treatment with oral milrinone (17 patients), posicor (12 patients), enoximone (47 patients), and piroximone (6 patients). Sixty-five patients were in New York Heart Association (NYHA) functional class 4, 15 patients were in class 3, and two patients were in class 2. There were 57 patients with ischemic and 25 patients were in class 2. There were 57 patients with ischemic and 25 patients with nonischemic etiology of left heart failure. Most patients were referred for inotropic therapy after failing to respond to conventional agents, including vasodilators. However, in almost all patients, marked hemodynamic and clinical improvement occurred initially. Overall survival was 36 percent at six months, the majority of deaths occurring during the first three months. Survival in relation to etiology of heart failure showed a trend toward increased mortality in patients associated with ischemic heart disease vs non-ischemic dilated cardiomyopathy. Sudden death mortality was also higher in the ischemic group (28 percent at six months vs 5 percent at six months; p less than 0.05). There was a trend toward reduced sudden death mortality in patients on antiarrhythmic agents during inotropic therapy (p = 0.06). We conclude that overall survival in symptomatic patients with severe left ventricular failure remains very low during long-term therapy with several new oral inotropic agents. Sudden death appears higher in patients with an ischemic etiology during therapy with these agents.
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PMID:Survival in severe left ventricular failure treated with the new nonglycosidic, nonsympathomimetic oral inotropic agents. 295 76

We reviewed the clinical, hemodynamic, and pathology data of 22 patients with dilated congestive cardiomyopathy and 13 patients with ischemic heart disease who underwent heart transplantation, primarily to improve the pathological definition of left ventricular (LV) and right ventricular (RV) aberrant bands and hypertrophic trabeculations. Overall prevalence of aberrant bands was 37% in th LV and 28% in the RV. Similar values for hypertrophic trabeculations were 43% and 28%, respectively. Compared with ischemic heart disease, our patients with dilated congestive cardiomyopathy had similar ventricular size and wall thickness, but had a higher prevalence of LV aberrant bands (p = .005) and LV hypertrophic trabeculations (p = .01). Aberrant bands were associated, both in the LV and RV, with dilated cavities (p less than .05), whereas hypertrophic trabeculations were associated with more ventricular hypertrophy and smaller LV size. Following morphological and histological analysis of the aberrant bands, we propose their division into two categories: genuine or primary bands (probably congenital in origin) and secondary bands, which most probably represent trabecular structures that develop a free cavitary course following pathological changes in the ventricular wall structure and cavitary geometry. Compared with the muscular RV bands situated mostly in the distal portion of the ventricle, LV bands were usually fibrotic and had at least one point of insertion in the inflow or outflow tract. The pattern of trabecular hypertrophy was also different in the two ventricles. Ventricular arrhythmias and thrombi occurred equally in patients with and without bands or trabeculations.
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PMID:Ventricular aberrant bands and hypertrophic trabeculations. A clinical pathological correlation. 297 5

An account of human heart transplantation as seen by the histopathologists involved at the two UK transplant centres is presented. Between January 1979 and July 1984 179 patients received 186 hearts and 124 are still alive up to four years after operation. Cyclosporin A based immunosuppression has been used in the last 120 patients. Four patients developed neoplastic lesions. The commonest reason for transplantation was ischaemic heart disease (63%), followed by congestive cardiomyopathy (35%). The seven retransplants were for acute or chronic rejection. The monitoring of rejection by endomyocardial biopsies is described, and the causes of death and necropsy findings are presented.
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PMID:Heart transplant pathology: the British experience. 298 5

Coxsackie B virus infections are common and frequently asymptomatic. However in young people, they can cause primary congestive cardiomyopathy and complicate previous cardiovascular illnesses. Virus diagnosis is difficult and based mainly on the detection of significant rising or stating high neutralizing antibody titers. A clinical and epidemiological five years study investigated 3,856 sera. 30.2% of the patients had evidence of a significant antibody titer (greater than or equal to 64) to one of the group B Coxsackie viruses; this percentage reaches 34.6% in cardiology and fluctuates from year to year; Coxsackie B2 is predominant (55.9%) in cardiology; coxsackie B1 and B2 antibody responses were detected more frequently than B3, B4 and B5. Coxsackie B6 appears to be uncommon. From these, 66 patients have evidence of coxsackie B virus infections with 60.2% for Coxsackie B2; they include pericarditis (30.3%), acute and chronic congestive cardiomyopathies (19.7%). Moreover it has been suggested that Coxsackie B virus might be responsible for electrocardiographic abnormalities (9.1%), ischemic heart disease and myocardial infarction. Enzyme linked immunosorbent assay (ELISA) and radioimmunoassay with purified antigens (VP1 and VP4) did not appear better than microneutralisation for evaluation of IgM and IgG antibodies. To elucidate the mechanisms of cardiac injury it is refer to viral replication, virus specific and auto-reactive T cells cytotoxic activities.
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PMID:[Coxsackie B virus infections in cardiology. Apropos of 66 cases]. 303 66


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