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)

The purpose of this study was to characterize the heart in patients with Friedreich's ataxia by two-dimensional echocardiography, systolic time intervals, and heart biopsy. Ten patients with Friedreich's ataxia (seven females and three males, age 15 +/- 7 years) were compared with 10 age-matched normal subjects (five males and five females, age 16 +/- 7 years). The mean systolic blood pressure in the patients with Friedreich's ataxia was lower (114 +/- 9 mm Hg) than that in the control subjects (122 +/- 8 mm Hg; p less than 0.05); diastolic blood pressures were the same. The heart rate in the patients with Friedreich's ataxia (102 +/- 17 beats/minute) was greater than that in the control subjects (76 +/- 12 beats/minute; p less than 0.001). The interventricular septal wall thickness was much greater in Friedreich's ataxia (13 +/- 2 versus 8 +/- 1 mm, p less than 0.001) as was the posterior wall thickness (13 +/- 3 versus 8 +/- 1 mm, p less than 0.001). The left ventricular end-diastolic diameter was smaller in Friedreich's ataxia (35 +/- 6 mm versus 47 +/- 6 mm; p less than 0.01), and the fractional change of the left ventricular minor axis with systole was greater in Friedreich's ataxia (40 +/- 9 percent versus 33 +/- 5 percent; p less than 0.05). An 11th patient with Friedreich's ataxia (age 33) had clinical heart failure, but his course was complicated by alcohol abuse. Heart biopsy in three patients with Friedreich's ataxia demonstrated myocyte hypertrophy (21.5 +/- 2.0 microns diameter; normal, 14 to 17 microns) and increased fibrosis (16 +/- 9 percent; normal, less than 5 percent). Thus, heart disease in Friedreich's ataxia is characterized by myocyte hypertrophy, interstitial fibrosis, increased left ventricular wall thickness, decreased left ventricular cavity size, sinus tachycardia, and normal systolic function. Further biochemical analysis of tissues may lead to the link of the neurologic and cardiac diseases and eventually to more effective therapy of this condition.
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PMID:Morphologic and functional characteristics of the heart in Friedreich's ataxia. 379 93

Beriberi heart disease should be considered in all patients with cardiac failure and a history of alcohol abuse or dietary deficiency. We studied the haemodynamic changes which took place immediately after intravenous administration of thiamine to a patient with high-output beriberi. Cardiac output and stroke volume fell rapidly, but not below normal levels, and systemic vascular resistance rose.
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PMID:Beriberi heart disease. A case report describing the haemodynamic features. 403 86

Clinical observations over the past two decades have pointed to the relationship between heart disease and alcohol abuse, usually without evident malnutrition or cirrhosis. While the prevalence of heart failure in the alcoholic population is now known, subclinical abnormalities of left ventricular function in noncardiac alcoholics who were normotensive have a high prevalence with or without some degree of ventricular hypertrophy by echocardiogram. This is frequently a diastolic rather than systolic abnormality. Congestive cardiomyopathy is not infrequently associated with high diastolic arterial blood pressures. Intoxication itself may contribute to blood pressure elevation. Angina pectoris in the absence of significant coronary disease is another presentation. Although the history may not be readily obtained, the major diagnostic feature in this entity is the history of ethanol ingestion in intoxicating amounts for at least 10 years, often marked by periods of spree drinking. While the course of congestive cardiomyopathy may be progressively downhill in individuals who continue to be actively alcoholic after the onset of heart failure, in one series one third of the patients became abstinent. These patients had a 4 year mortality that was persistently one-sixth of the alcoholic group. Management of heart failure is traditional in these patients. Atrial arrhythmias have been shown to occur during the early ethanol withdrawal phase in patients without other clinical evidence of heart disease. Sudden death in a segment of the alcoholic population is considered arrhythmia related and is commonly associated with cigarette use. Identification of the addicted individual is the essential element to management.
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PMID:Alcoholic cardiomyopathy. 808 32

An impaired function of the myocardial beta-adrenergic receptor system has been reported in patients with end-stage heart failure and this impairment has been postulated to be a factor in further deterioration of cardiac contractile function. As ventricular dysfunction is often associated with prolonged alcohol abuse, we investigated whether or not chronic administration of ethanol could induce alterations in the beta-adrenergic receptor adenylate-cyclase system in rats. Male Wistar rats of 8 weeks of age received 33% ethanol in drinking water for 3 months. As compared with control rats drinking water, the ethanol-treated rats showed weight loss and an increase in the heart/body weight ratio. Chronic ethanol increased myocardial contents of norepinephrine and epinephrine, possibly resulting from sympathoadrenal activation. The beta-adrenergic receptor density (Bmax) of the myocardial membrane was significantly decreased in the ethanol-treated rats (27.7 +/- 9.9 vs 39.0 +/- 6.0 fmol/mg protein, p < 0.01), while the affinity (Kd) did not differ between the two groups. The myocardial content of cyclic-AMP was also reduced in the ethanol rats (865 +/- 59 vs 1055 +/- 83 pmol/g w.w., p < 0.01). These observations indicate that chronic ethanol administration depresses the function of the beta-adrenergic receptor adenylate-cyclase system. The decreased beta-adrenergic receptor density was partly attributed to down-regulation due to increased sympathetic stimulation. This impaired function may contribute to the cardiac contractile dysfunction observed in chronic alcoholics.
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PMID:Alterations in beta-adrenergic receptor density and cyclic-AMP level in the myocardium of rats chronically treated with alcohol. 839 53

In Spain in recent years two studies have been carried out into the prevalence of stroke. In the study made in Girona of the rural population over 64 years of age, the prevalence for stroke was 4,012 cases per 100,000 inhabitants. The figure was higher for women- 5,072 -than for men 2,675 cases. Transient Ischaemic Attacks (TIA) had a prevalence rate of 679 cases per 100,000 population of those aged over sixty-nine, being higher for men (1,161 cases) than for women (371 cases). The results from Girona differ from the findings in other Spanish regions in that the former are lower but at the same time are similar to those obtained in other western countries. The greatest risk factors for those over 69 years old were arterial hypertension, earlier episodes of TIA, diabetes, auricular fibrillation, congestive cardiac insufficiency, chronic bronchitis, myocardial infarction peripheral vascular-diseases, arteriosclerosis, heart disease with embolization and alcohol abuse.
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PMID:[Prevalence of cerebrovascular disease in Spain: a study in a rural area of Girona]. 855 97

The direct toxic effect of alcohol and its metabolite acetaldehyde has been demonstrated both in laboratory animals and in humans. Alterations in the mitochondrial ultrastructure and the dilatation of the sarcoplasmatic reticulum have been shown after an acute infusion of alcohol in the heart. These changes correlate with decreased mitochondrial function, defects in protein synthesis and the occurrence of arrhythmias. The risk of developing alcoholic cardiomyopathy is related to both the mean daily alcohol intake and the duration of drinking, but there is much individual susceptibility to the toxic effect of alcohol. Most patients, in whom alcoholic cardiomyopathy develops, have been drinking over 80 g/d for more than 5 years. The clinical diagnosis of alcoholic cardiomyopathy reflects the coexistence of global myocardial dysfunction in a heavy drinker in whom no other cause for myocardial disease was found. In studies focussing on alcoholic cardiomyopathy the surprising histologic findings in endomyocardial biopsy in about 30% of all cases was myocarditis with a lymphocytic infiltrate in association with myocyte degeneration or focal necrosis. In myocarditis, the network of microtubules and intermediate filaments is also disrupted by the inflammatory reaction which involves resident cells (myocytes, fibroblasts, endothel cells) and systemic cells (granulocytes, macrophages, monocytes, lymphocytes). Changes in the cardiac cytoskeleton and the extracellular matrix may affect contractile function, since the cytoskeleton organizes the intra- and intercellular architecture. After all, in patients with alcohol abuse and myocarditis the immune functioning appears to be compromised. Several studies suggest that heavy drinking alters both lymphocyte and granulocyte production and function. Alcohol consumption per se might harm the immune system. Furthermore, the myocardial damage due to alcohol consumption could initiate autoreactive mechanisms comparable to those in viral or idiopathic myocarditis. Patients with alcohol abuse and myocarditis have a poor prognosis: signs of biventricular failure including tachycardia, hepatomegaly, and peripheral and lung edema are observed. These symptoms are as nonspecific as are various echocardiographic and electrocardiographic changes such as atrial and ventricular arrhythmias which may be associated both with myocarditis, alcoholic cardiomyopathy and acute effects of drinking without hemodynamic alterations. For the management of patients with alcohol abuse the prevention of further alcohol intake is mandatory to reverse the myocardial damage and the unfavorable predisposition for infection. Specific treatment of myocarditis is the second important option, and treatment of heart failure by reducing the size of the dilated heart and alleviating the signs and symptoms of heart failure is a logical third step.
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PMID:[Alcohol and myocarditis]. 880 5

Low serum concentrations of potassium and magnesium are proarrhythmic factors that are well established. Atrial and ventricular fibrillation are facilitated at low serum levels of these electrolytes. Loss of potassium and magnesium might be caused by diuretic therapy, gastrointestinal loss, drugs, and alcohol abuse. However, serum levels are not representative of total body content of potassium and magnesium, hence, adjuvant therapy might be indicated also in the presence of normal serum levels. This is especially true during the initial phase of antiarrhythmic therapy, which is accompanied by proarrhythmia in a significant number of cases. Patients with heart failure should routinely receive adjuvant electrolyte substitution, if renal function is not impaired. In the experimental model magnesium successfully prevented early afterdepolarizations caused by hypokalemia and antiarrhythmic drugs. In the clinical setting high dose magnesium abolished torsade-de-pointes tachycardias caused by antiarrhythmic drugs. Unfortunately, controlled studies are not available for low dose electrolyte therapy adjuvant to antiarrhythmic drug medication.
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PMID:[Medicamentous anti-arrhythmia therapy. Is oral adjuvant therapy with electrolytes of value?]. 933 95

In 2,000 consecutive stroke patients collected in a prospective hospital-based stroke registry over a 10-year period, we assessed whether stroke in men and women was different in respect to vascular risk factors, clinical features and natural history. The frequency of the different variable in men and women was analyzed by means of univariate analysis and logistic regression models. Women accounted for 48% of the study population (n = 967) and were older than men (mean age 75 vs. 69 years, p < 0.001). In the age group of 85 years or older, stroke was more frequent in women than in men (69.8 vs. 30.2%, p < 0.001). Women showed a higher frequency of cardioembolic infarction and a lower occurrence of lacunar infarction and stroke of undetermined cause than men. In-hospital mortality (17.4 vs. 13.3%) and length of hospital stay (19.6 vs. 16.7 days) was significantly higher (p < 0.001) in women than in men. In the model based on demographic variables and cardiovascular risk factors, obesity, heart failure, atrial fibrillation and age were significant predictors of stroke in women, while intermittent claudication, ischemic heart disease, chronic obstructive pulmonary disease, cigarette smoking and alcohol abuse were predictors in male sex. Hypertension and limb weakness were predictors for stroke in women, and absence of neurological deficit at hospital discharge, lacunar syndrome and ataxia were predictors in men in the models based on all variables. Women differ from men in the distribution of risk factors and stroke subtype, stroke severity and outcome. Differences in stroke pathology and/or differences in functional anatomy or plasticity of the brain between sexes may account for these findings.
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PMID:Acute cerebrovascular disease in women. 1138 56

Some evidence suggests that light to moderate alcohol consumption protects against cardiovascular diseases. However, this cardioprotective effect of alcohol consumption in adults is absent at the population level. Approximately 20 to 30% of patients admitted to a hospital are alcohol abusers. In medical practice, it is essential that patients' levels of consumption are known because of the many adverse effects that might result in the course of routine care. Ethanol damage to the heart is evident if alcohol consumption exceeds 90 to 100 g/d. Heavy ethanol consumption leads to increased risk for sudden cardiac death and cardiac arrhythmias. In patients with coronary heart disease, alcohol use was associated with increased mortality. An early response to drinking was an increased ventricular wall thickness to diameter ratio, possibly proceeding with continuous drinking to alcoholic cardiomyopathy, which had a worse outcome compared with idiopathic dilative cardiomyopathy if drinking was not stopped or at least reduced (< 60 g/d). In the ICU, patients with chronic alcoholism have more cardiac complications postoperatively. These complications probably are caused by biventricular dysfunction, particularly with the occurrence of severe infections or septic shock, events that are three to four times more frequent among chronic alcoholics than occasional drinkers or nondrinkers. To prevent further complications from drinking and for long-term management of drinking, patients with alcohol abuse and heart failure should be treated in brief intervention and follow-up programs. Prognosis is good even in patients with New York Heart Association class IV heart failure caused by cardiomyopathy if complete abstinence is accomplished. Noncompliance to smoking and alcohol restrictions, which are amenable to change, dramatically increases the risk for hospital readmissions among patients with heart failure.
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PMID:Effects of alcohol on the heart. 1180 30

Patients who drink too much have more complications after surgery. The aim of this thesis was to evaluate the evidence, possible mechanisms, and prevention of the increased postoperative morbidity in alcohol abusers, defined by a consumption of at least five drinks per day. The literature could be criticised for several methodological flaws. Nevertheless, the results are in agreement showing moderate to strong evidence of increased postoperative morbidity after surgical procedures on alcohol abusers. There is weak to moderate evidence of increased postoperative mortality, hospital stay, and re-operation. The personal and economic consequences are tremendous. The incidence of alcohol abusers undergoing surgery was 7% to 49%, according to gender and diagnosis. They have been identified by a self-reported alcohol intake, which implies the possibility of underestimation. Alcohol markers could be used for a more precise identification of alcohol abuse. However, the inability of the questionnaires to detect short-term changes in intake and abuse without dependence, the inconsistent predictive values of the biological markers, and the lack of evidence of an association to postoperative morbidity reduces their usefulness. A detailed alcohol history is therefore recommended. The pathophysiology may include alcohol-induced organ dysfunctions. We demonstrated that subclinical cardiac insufficiency, immune incompetence, and haemostatic imbalance were already present preoperatively. A relation between the various lesions remains to be investigated. The surgical stress response was greater in alcohol abusers, which may further compromise the already dysfunctioning organs, thus leading to the documented increase in postoperative morbidity. Withdrawal from alcohol reverses organic dysfunction in non-surgical patients. Haemostasis normalises after one to four weeks, cardiac function after one month, immune function after two months, and response to external stress after three months. Accordingly, our small randomised investigation has shown that one month of abstinence before surgery improves several organic dysfunctions and reduces postoperative morbidity. We have demonstrated that prevention before surgery is possible. The study has methodological flaws, so further studies are required before final recommendations can be given. However, in the meantime clinical guidelines for alcohol abusers undergoing surgery should include up-to-date patient information and four weeks of abstinence before surgery, in accordance with the evidence-based association, the potential prevention attained by preoperative abstinence, and the best clinical practice. Implementation should be monitored in the clinical databases. In future, all patients admitted to surgery should be offered a health promoting dialogue with the surgeon, anaesthesiologist, general practitioner, or other health professionals, which focuses on alcohol among other risk factors in relation to the operative treatment, diagnosis and prognosis. A beneficial effect attainable from this multi-modal prevention and fast track surgery should be investigated among the alcohol abusers.
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PMID:Alcohol abuse and postoperative morbidity. 1281 38


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