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)

In epidemiological surveys and in large-scale therapeutic trials, the prognosis of patients with ischemic heart failure is worse than in patients with a non-ischemic etiology. Even heart transplant candidates may respond better to intensified therapy if they have non-ischemic heart failure. The term 'non-ischemic heart failure' includes various subgroups such as hypertensive heart disease, myocarditis, alcoholic cardiomyopathy and cardiac dysfunction due to rapid atrial fibrillation. Some of these causes are reversible. The therapeutic effect of essential drugs such as angiotensin-converting enzyme inhibitors, beta-blockers and diuretics does not, in general, significantly differ between ischemic and non-ischemic heart failure. However, in some trials, response to certain drugs (digoxin, tumor necrosis factor-alpha, inhibition with pentoxifylline, growth hormone and amiodarone) was found to be better in non-ischemic patients. Patients with ischemic heart failure and non-contracting ischemic viable myocardium may, on the other hand, considerably improve following revascularization. In view of prognostic and possible therapeutic differences, the etiology of heart failure should be determined routinely in all patients.
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PMID:Ischemic versus non-ischemic heart failure: should the etiology be determined? 1263 96

Alcoholic cardiomyopathy (ACM), a principal form of secondary dilated cardiomyopathy, can ensue from heavy consumption of alcohol over a long period of time. In harmful consumption, alcohol and its metabolites has a toxic effect on heart muscle cells. The clinical features include dilatation of the left ventricle, poor myocardial contractility and symptoms of heart failure. The heart and lung X-ray examination is required in all disease stages. The information gathered from this cheap and noninvasive investigation method, are very important in the diagnosis algorithm. In the ACM stages beginning, before the installation of the heart failure symptoms, it is possible to found normal dimensions of the heart, which is compatible with the alcoholic cardiomyopathy diagnosis. Specific for dilated alcoholic cardiomyopathy is the reversible character of cardiomegaly, objectified through the reduction of the cardio-thoracic index in conditions of alcohol abstinence and adequate treatment of the heart failure.
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PMID:[Cardio-thoracic index: marker of the clinical course of alcoholic dilated cardiomyopathy]. 1475 23

Chronic alcohol ingestion leads to alcoholic cardiomyopathy manifested by ventricular dysfunction and heart failure. Although accumulation of reactive oxygen species may play a role in alcohol-induced heart injury, direct impact of enhanced antioxidant defense on pathogenesis of alcoholic cardiomyopathy has not been elucidated. This study was designed to examine the effect of transgenic overexpression of the free radical scavenger metallothionein on alcohol-induced cardiac contractile dysfunction. Wild-type FVB and metallothionein mice were placed on a 4% alcohol or control diet for 12 wk. Cardiac contractile function was evaluated in cardiomyocytes including peak shortening (PS), time-to-peak shortening, time-to-90% relengthening (TR90), maximal velocity of shortening/relengthening (+/-dL/dt), intracellular Ca2+ rise (change in fura-2 fluorescent intensity [DeltaFFI]) and intracellular Ca2+ decay rate. Intracellular Ca2+ cycling proteins including sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2a), Na+-Ca2+ exchanger (NCX) and phospholamban were assessed using Western blot analysis. Alcohol intake depressed PS, +/-dL/dt, and DeltaFFI, increased baseline fura-2 fluorescence intensity (FFI), and prolonged intracellular Ca2+ decay and TR90, all of which with the exception of DeltaFFI were abrogated by metallothionein. Enhanced stimulating frequency caused lessened PS decline at 1.0 Hz from FVB ethanol group, which was not affected by metallothionein. Immunoblotting data showed reduced SERCA2a, NCX and phospholamban expression in FVB group consuming alcohol. All of these alcohol- induced changes in cardiac proteins were nullified by the metallothionein transgene. In summary, our findings suggest a beneficial role of antioxidants in alcohol-induced cardiomyocyte dysfunction.
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PMID:Cardiac overexpression of metallothionein attenuates chronic alcohol intake-induced cardiomyocyte contractile dysfunction. 1734 28

Disparities in associations of alcohol consumption to various cardiovascular conditions lead to separate consideration of several. These include (1) Alcoholic cardiomyopathy from chronic heavy drinking in susceptible persons. (2) Higher blood pressure (hypertension) in some heavier drinkers. (3) A relation of drinking to higher risk of hemorrhagic stroke but to lower risk of ischemic stroke. (4) Certain arrhythmias, especially among binge drinkers. (5) An inverse relation of alcohol use to coronary artery disease. A causal hypothesis of protection is strengthened by plausible mechanisms. The coronary disease data impact upon total mortality statistics, such that lighter drinkers are at slightly lower risk than abstainers of death within a given time period. (6) An inverse relation of drinking to type 2 (adult onset) diabetes mellitus in several recent studies. Because of close relations to cardiovascular disorders, diabetes is considered virtual cardiovascular "equivalent". (7) Composites of (1-6) result in a complex association between alcohol and the common heart failure syndrome. International comparisons suggest wine is more protective against coronary disease than liquor or beer. Reports of antioxidants, endothelial relaxants, and antithrombotic activity in wine (especially red) support hypothetical benefit from non-alcohol wine components. However, prospective population studies show apparent protection from beer, wine, or liquor. Thus, some suggest that favorable traits or drinking patterns of wine drinkers might explain the international comparison findings. Amount of alcohol taken is a crucial consideration in alcohol-health relations. Advice to concerned persons needs to take into account individual risk/benefit factors in drinkers or potential drinkers.
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PMID:Alcohol, cardiovascular diseases and diabetes mellitus. 1736 63

Numerous studies have used a J-shaped or U-shaped curve to describe the relationship between alcohol use and total mortality. The nadir of the curves based on recent meta-analysis suggested optimal benefit at approximately half a drink per day. Fewer than 4 drinks per day in men and fewer than 2 per day in women appeared to confer benefit. Reductions in cardiovascular death and nonfatal myocardial infarction were also associated with light to moderate alcohol intake. Although some studies suggested that wine had an advantage over other types of alcoholic beverages, other studies suggested that the type of drink was not important. Heavy drinking was associated with an increase in mortality, hypertension, alcoholic cardiomyopathy, cancer, and cerebrovascular events, including cerebrovascular hemorrhage. Paradoxically, light-to-moderate alcohol use actually reduced the development of heart failure and did not appear to exacerbate it in most patients who had underlying heart failure. Numerous mechanisms have been proposed to explain the benefit that light-to-moderate alcohol intake has on the heart, including an increase of high-density lipoprotein cholesterol, reduction in plasma viscosity and fibrinogen concentration, increase in fibrinolysis, decrease in platelet aggregation, improvement in endothelial function, reduction of inflammation, and promotion of antioxidant effects. Controversy exists on whether alcohol has a direct cardioprotective effect on ischemic myocardium. Studies from our laboratory do not support the concept that alcohol has a direct cardioprotective effect on ischemic/reperfused myocardium. Perhaps the time has come for a prospectively randomized trial to determine whether 1 drink per day (or perhaps 1 drink every other day) reduces mortality and major cardiovascular events.
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PMID:To drink or not to drink? That is the question. 1826 56

Cardiovascular complications of cirrhosis include cardiac dysfunction and abnormalities in the central, splanchnic and peripheral circulation, and haemodynamic changes caused by humoral and nervous dysregulation. Cirrhotic cardiomyopathy implies systolic and diastolic dysfunction and electrophysiological abnormalities, an entity that is different from alcoholic heart muscle disease. Being clinically latent, cirrhotic cardiomyopathy can be unmasked by physical or pharmacological strain. Consequently, caution should be exercised in the case of stressful procedures, such as large volume paracentesis without adequate plasma volume expansion, transjugular intrahepatic portosystemic shunt (TIPS) insertion, peritoneovenous shunting and surgery. Cardiac failure is an important cause of mortality after liver transplantation, but improved liver function has also been shown to reverse the cardiac abnormalities. No specific treatment can be recommended, and cardiac failure should be treated as in non-cirrhotic patients with sodium restriction, diuretics, and oxygen therapy when necessary. Special care should be taken with the use of ACE inhibitors and angiotensin antagonists in these patients. The clinical significance of cardiovascular complications and cirrhotic cardiomyopathy is an important topic for future research, and the initiation of new randomised studies of potential treatments for these complications is needed.
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PMID:Cardiovascular complications of cirrhosis. 1924 Feb 90

Heart failure (HF) remains a major public health issue. It is estimated that about 500,000 Americans per year are diagnosed with HF. Despite advanced medical and surgical treatments for HF, mortality after the onset of HF is still high, thereby underscoring the importance of primary prevention. Among modifiable lifestyle factors, alcohol consumption appears to play a role in the development of HF. Although excessive drinking has been known to lead to alcoholic cardiomyopathy and light-to-moderate drinking may confer some cardiovascular benefits, recent studies suggest it is not only the quantity, but also drinking patterns and genetic factors, that may influence the relation between alcohol consumption and cardiovascular disease. This article reviews current evidence on the association between alcohol consumption and HF.
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PMID:Alcohol consumption and heart failure: a systematic review. 1841 65

Although alcohol drinking increases blood pressure and heavy drinking has been associated with alcoholic cardiomyopathy, little is known about the association between light to moderate drinking and risk of heart failure (HF) in hypertensive subjects. Thus, the association between light to moderate drinking and incident HF in 5,153 hypertensive male physicians who were free of stroke, myocardial infarction, or major cancers at baseline was prospectively examined. Alcohol consumption was self-reported and classified as <1, 1 to 4, 5 to 7, and >or=8 drinks/week. HF was ascertained using follow-up questionnaires and validated using Framingham criteria. Average age was 58 years, and about 70% of subjects consumed 1 to 7 drinks/week. A total of 478 incident HF cases occurred in this cohort during follow-up. Compared with subjects consuming <1 drink/week, hazard ratios for HF were 0.89 (95% confidence interval [CI] 0.70 to 1.12), 0.72 (95% CI 0.57 to 0.91), and 0.38 (95% CI 0.20 to 0.72) for alcohol consumption of 1 to 4, 5 to 7, and >or=8 drinks/week after adjustment for age, body mass index, smoking, randomization group, use of multivitamins, vegetable consumption, breakfast cereal, exercise, and history of atrial fibrillation, respectively (p for trend <0.001). Similar results were obtained for subjects with HF with and without antecedent myocardial infarction and those without diabetes mellitus. In conclusion, our data suggested that light to moderate alcohol consumption was associated with a lower risk of HF in hypertensive male physicians.
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PMID:Alcohol consumption and heart failure in hypertensive US male physicians. 1872 18

Cardiovascular complications of liver cirrhosis include cardiac dysfunction and abnormalities in the central-, splanchnic,- and peripheral circulation. Vasodilatation prevails, but vascular beds with various degrees of reduced and increased haemodynamic resistance are the results of massive activation of powerful homeostatic, regulatory systems. Cirrhotic cardiomyopathy implies systolic and diastolic dysfunction and electrophysiological abnormalities, an entity that is different from alcoholic heart muscle disease. Being often clinical latent, cirrhotic cardiomyopathy can be unmasked by physical and pharmacological strain. Cardiac failure is an important cause of mortality after liver transplantation and stressful procedures as insertions of transjugular intrahepatic portal systemic shunt (TIPS), peritoneal venous shunting, and other types of surgery. Improvement of liver function has been shown to reverse the cardiovascular complications. The clinical significance is an important topic for future research. At present, no specific treatment can be recommended, and the cardiac failure in cirrhosis should be treated as in non-cirrhotic patients with sodium restriction, diuretics, and beta-adrenergic blocking agents. Special care should be taken with the use of ACE-inhibitors and angiotensin antagonist in these patients.
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PMID:Cardiac and systemic haemodynamic complications of liver cirrhosis. 1914 34

Cardiovascular complications of cirrhosis include cardiac dysfunction and abnormalities in the central, splanchnic and peripheral circulation, and haemodynamic changes caused by humoral and nervous dysregulation. Cirrhotic cardiomyopathy implies systolic and diastolic dysfunction and electrophysiological abnormalities, an entity that is different from alcoholic heart muscle disease. Being clinically latent, cirrhotic cardiomyopathy can be unmasked by physical or pharmacological strain. Consequently, caution should be exercised in the case of stressful procedures, such as large volume paracentesis without adequate plasma volume expansion, transjugular intrahepatic portosystemic shunt (TIPS) insertion, peritoneovenous shunting and surgery. Cardiac failure is an important cause of mortality after liver transplantation, but improved liver function has also been shown to reverse the cardiac abnormalities. No specific treatment can be recommended, and cardiac failure should be treated as in non-cirrhotic patients with sodium restriction, diuretics, and oxygen therapy when necessary. Special care should be taken with the use of ACE inhibitors and angiotensin antagonists in these patients. The clinical significance of cardiovascular complications and cirrhotic cardiomyopathy is an important topic for future research, and the initiation of new randomised studies of potential treatments for these complications is needed.
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PMID:Cardiovascular complications of cirrhosis. 1819 56


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