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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mortality rates are considerably higher in chronic ischemic heart disease (IHD) patients with non-insulin-dependent diabetes mellitus (NIDDM) than in those who are nondiabetics. The relationship between different types of antihyperglycemic pharmacological therapy and mortality rate in this NIDDM population is uncertain. We aimed to examine the survival in NIDDM patients with IHD using various types of oral antidiabetic treatments over a 5-year follow-up period. The study sample comprised 11,440 patients with a previous myocardial infarction and/or stable anginal syndrome, aged 45-74 years, who were screened, but not included in the Bezafibrate Infarction Prevention study. Among them, 9,045 were nondiabetics and 2,395 diabetics. The diabetic patients were divided into four groups on the basis of their therapeutic regimen at screening: diet alone (n = 990), sulfonylureas (n = 1,041), metformin (n = 78) and a combination of a sulfonylurea and metformin (n = 266). All NIDDM groups were similar with regard to age, gender, hypertension, smoking, heart failure, angina and prior myocardial infarction. Crude mortality rate was lower in the nondiabetic group (11.21 vs. 21.8%; p < 0.001). In the diabetic group, mortality was 18.5% for patients on diet alone, 22.5% for those on sulfonylureas, 25.6% for patients on metformin, and 31.6% for the combined sulfonylurea/metformin group (p < 0.01). When analyzing age-adjusted mortality rate and actuarial survival curves, the lowest mortality was found in patients on diet alone and the highest in patients on metformin (alone or in combination with sulfonylureas). After adjustment for variables connected with long-term prognosis, the use of metformin was associated with increased relative risk (RR) for all-cause mortality of 1.42 (95% CI 1.10-1.85), whereas the use of sulfonylureas alone was not [RR 1.11 (95% CI 0.90-1.36)]. NIDDM patients with IHD using metformin, alone or in combination with sulfonylureas, exhibited a significantly increased mortality. Until the results of problem-oriented prospective studies on oral control of NIDDM will be available, alternative therapeutic approaches should be investigated in these patients.
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PMID:Antihyperglycemic treatment in diabetics with coronary disease: increased metformin-associated mortality over a 5-year follow-up. 1051 15

Chronic myocardial ischemia is the leading cause of disturbances in myocardial contractility (myocardial infarction) or hemodynamic overload upon the left ventricle. The heart reactions consist in a series of adaptative mechanisms in order to maintain its pump function: Frank-Starling mechanism, myocardial hypertrophy and neurohumoral activation. In heart failure, the cardiac output is maintained by an increase of the preload which enhances the contractility (Frank-Starling law). Myocardial ischemia influences the systolic and diastolic function. The decrease of cardiac output leads to neurohumoral responses which, in the initial stages of cardiac failure are compensatory; along with the progression of the disease, they exert adverse effects. Increased activity of the sympathetic nervous system induces high cardiac rates, chronotropic incompetence. Activation of the renin-angiotensin system held to myocardial and vascular hypertrophy, vasoconstriction, fluid retention. Endothelin is the most powerful vasoconstrictor; its plasmatic concentrations correlate with the severity of the disease. Vasodilator mediators released in cardiac failure are the natriuretic peptide, nitric oxide, dopamine, prostacicline, bradikinin.
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PMID:[Heart failure due to ischemia--the adaptive mechanisms]. 1075 79

Myocardial stunning and hibernation are both clinically important causes of myocardial dysfunction and are caused by episodes of myocardial ischaemia. Stunning tends to occur acutely and may produce transient but clinically important reductions in left ventricular function in the setting of myocardial infarction, post coronary artery bypass grafting and even following episodes of effort induced angina. Hibernation refers to a chronic down-regulation of myocardial function in response to chronic myocardial ischaemia. Hibernating myocardium may be present in up to 50% of patients with significantly impaired left ventricular function and evidence of heart failure. Importantly, both these entities can be either prevented or ameliorated by preventing or lessening ischaemic burden. There is also evidence that there may be an overlap between these two entities and that hibernating myocardium may result from repeated episodes of myocardial ischaemia causing chronic stunning.
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PMID:Myocardial stunning and hibernation in clinical practice. 1122 Dec 79

The number of patients with heart failure secondary to chronic ischemic heart disease, also called ischemic cardiomyopathy, is increasing in clinical cardiology. Left ventricular dysfunction after ischemic episodes has been shown to be potentially reversible, as in the case of hibernating or stunned myocardium. Thus, the detection of viable myocardium is of critical importance for a therapeutic stratification of patients with left ventricular dysfunction. Viability assessment should prove decision support to achieve an optimal management of patients with ischemic cardiomyopathy by predicting the capacity of improvement of left ventricular function after revascularisation. Cardiac F-18-fluorodeoxyglucose-positron emission tomography (F-18-FDG-PET) imaging is considered the "gold-standard" for assessment of myocardial viability. This article reviews the fluorodeoxyglucose-positron emission tomography imaging from a clinical viewpoint.
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PMID:[F-18 fluorodeoxyglucose for diagnosis of myocardial viability: applications in clinical practice]. 1213 58

In the pre-natal period, hemangioblasts derived from the human ventral aorta give rise to cellular elements involved in both hematopoiesis and vasculogenesis, resulting in formation of the primitive capillary network. Endothelial precursors with phenotypic and functional characteristics of embryonic hemangioblasts are also present in human adult bone marrow, and can be used to induce infarct bed vasculogenesis and angiogenesis after experimental myocardial infarction. The neovascularization results in decreased apoptosis of hypertrophied myocytes in the peri-infarct region, long-term salvage and survival of viable myocardium, reduction in collagen deposition, and sustained improvement in cardiac function. Autologous angioblasts may also be useful in cellular therapy strategies aiming to regenerate myocardial tissue after established heart failure. It is likely that protocols using cardiomyocyte/mesenchymal stem cells will require balanced co-administration of angioblasts to provide vascular structures for supply of oxygen and nutrients to both the chronically ischemic, endogenous myocardium and to the newly-implanted cardiomyocytes. Future studies will need to address the timing, relative concentrations, source and route of delivery of each of these cellular populations in animal models of acute and chronic myocardial ischemia.
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PMID:Myocardial neovascularization by adult bone marrow-derived angioblasts: strategies for improvement of cardiomyocyte function. 1261 Oct 63

In the pre-natal period, hemangioblasts derived from the human ventral aorta give rise to cellular elements involved in both hematopoiesis and vasculogenesis, resulting in formation of the primitive capillary network. Endothelial precursors with phenotypic and functional characteristics of embryonic hemangioblasts are also present in human adult bone marrow, and can be used to induce infarct bed vasculogenesis and angiogenesis after experimental myocardial infarction. The neovascularization results in decreased apoptosis of hypertrophied myocytes in the peri-infarct region, long-term salvage and survival of viable myocardium, reduction in collagen deposition, and sustained improvement in cardiac function. Autologous angioblasts may also be useful in cellular therapy strategies aiming to regenerate myocardial tissue after established heart failure. It is likely that protocols using cardiomyocyte/mesenchymal stem cells will require balanced co-administration of angioblasts to provide vascular structures for supply of oxygen and nutrients to both the chronically ischemic, endogenous myocardium and to the newly-implanted cardiomyocytes. Future studies will need to address the timing, relative concentrations, source and route of delivery of each of these cellular populations in animal models of acute and chronic myocardial ischemia.
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PMID:Myocardial neovascularization by adult bone marrow-derived angioblasts: strategies for improvement of cardiomyocyte function. 1287 34

Chronic myocardial ischemia is the leading cause of impaired myocardial contractility and heart failure. To identify differentially expressed genes in human ischemic cardiomyopathy (ICM), we constructed a subtracted cDNA library using specimens of ICM compared to normal human heart. Among 100 randomly sequenced clones, seven sequences represented recently identified candidate genes for differential expression in cardiac hypertrophy. A further clone without a known hypertrophy-association coded for the adhesion molecule NCAM(CD56). RNase protection assay, immunohistochemistry, and Western blotting revealed strong overexpression of NCAM(CD56) in all hearts with ICM (n = 14) compared to normal hearts (n = 8), whereas in congestive cardiomyopathy (CCM) (n = 8), hypertrophic obstructive cardiomyopathy (n = 2), myocarditis (n = 4), and sarcoidosis (n = 2), at most slight overexpression of NCAM(CD56) was observed. NCAM(CD56) overexpression abnormally involved the whole cell membrane and the cytoplasma of cardiomyocytes only inside and adjacent to ischemia-induced cardiac scars. Normal or hypertrophic fibers at a distance from ischemic scars were devoid of NCAM overexpression. Identical alterations were observed in an experimental rat ICM model, but not in normal nor in spontaneously hypertensive rat hearts. In search of NCAM(CD56)-related transcription factors we found RUNX1(AML1) up-regulation in ICM and detected RUNX1(AML1) binding within the NCAM(CD56) promoter by electromobility shift assay. We concluded that strong overexpression of NCAM(CD56) and RUNX1(AML1) is a constant and characteristic feature of cardiomyocytes within or adjacent to scars in ICM.
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PMID:NCAM(CD56) and RUNX1(AML1) are up-regulated in human ischemic cardiomyopathy and a rat model of chronic cardiac ischemia. 1293 48

Despite increasing pharmacological and mechanical treatment options, ischemic heart disease continues to be associated with considerable patient mortality and morbidity. The estimates of the direct and indirect costs associated with chronic stable angina amount to billions of dollars. Given the epidemiological and economic magnitude of the problem, the need for more effective therapies is self-evident. Based on current guidelines, the management of ischemic heart disease has progressively broadened to include risk factor modification, patient education, and pharmacological therapy. The latter includes i) classic antianginal agents such as beta-blockers, calcium antagonists, and nitrates, and ii) drugs for secondary prevention, such as aspirin, clopidogrel, statins, and angiotensin-converting enzyme inhibitors. Tailoring therapy to individual needs has become even more challenging because of the marked changes in the clinical profile of patients with chronic ischemic heart disease. Compared with the past, today's patients tend to be older, to have undergone revascularization procedures, and to frequently have associated illnesses, including heart failure and diabetes. Significant progress has been made in recent years in understanding the role of cardiac energy metabolism in the pathogenesis of myocardial ischemia. A better understanding of metabolic derangements associated with ischemia and reperfusion is translating into innovative therapeutic approaches. Optimization of cardiac energy metabolism is based on promoting cardiac glucose oxidation. This has been proved to enhance cardiac function and protect myocardial tissue against ischemia-reperfusion injury. A new class of metabolic agents, known as the 3-ketoacyl coenzyme A thiolase inhibitors (trimetazidine), is able to elicit an increase in glucose and lactate combustion secondary to partial inhibition of fatty acid oxidation, producing clinical benefits in patients with ischemic heart disease.
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PMID:["Persistent" angina: rationale for a metabolic approach]. 1507 76

It could be conjectured that the hemorheological disorders are involved in development of the ischemic heart disease. But this fact was so far insufficiently cleared up. The present studies were carried out in patients with various forms of chronic ischemic heart disease. We investigated the most significant factor of rheological disorders in the microcirculation, the erythrocyte aggregability, with a technique that provided us with the direct and quantitative data. Simultaneously we investigated in the same patients the tone of the resistance arteries of the hand with an original non-invasive technique. We found that the erythrocyte aggregability increased almost twice in the blood of investigated patients as compared to the healthy control group. The aggregability was positively correlated with severity of the disease. The most pronounced hemorheological disorders were found in the patients with the heart failure. As to the arteriolar resistance index, it was increased only in 45 percent of all the investigated patients and no significant difference between the patients with the heart failure and without it was found available. We concluded that the blood rheological disorders represent themselves a factor that plays a significant role in pathogenesis of development of the heart disease.
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PMID:Hemorheological disorders and arteriolar resistance during ischemic heart disease. 1525 72

According to the intensity and duration of invasion, superinvasion opisthorchiasis in laboratory animals and human beings involves all cardiac layers; the myocardium is mostly damaged. In its early phase, vascular inflammation of the microcirculatory bed, dystrophy, necrosis of striated muscle fibers progressing to diffuse cardiosclerosis result from abnormal immunological processes; due to reflex exposures (Botkin's syndrome), there may be persistent cardialgias that may progress to the clinical manifestations of chronic ischemic heart disease. Unpredictable dissipative clusters of metabolic Opistorchis may predispose to different forms of myocarditis progressing to focal and diffuse cardiosclerosis. In these cases, the death of patients with superinvasion opisthorchiasis results from acute or chronic heart failure. Dehelmintization in these patients fails to eliminate myocardial changes (cardiosclerosis) that further determine the clinical presentation of cardiac pathology.
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PMID:[Cardiac syndrome in opisthorchiasis]. 1548 76


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