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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemodynamic, contractile and energetic functions of isolated working hearts from ethanol-fed and control rats were studied to determine the time course of cardiac dysfunction development during long-term consumption of alcohol. Hearts from fasted, 24 hr withdrawn rats were studied after 2, 4, 7 and 11 months consuming ethanol as 38% of daily calories in a nutritionally-adequate liquid diet. After 2 months, the right ventricle of the alcoholic rat hearts was significantly enlarged; left ventricular weight was not significantly different from control and there was little evidence that left ventricular function was compromised. After 4 months and 7 months, there was biventricular cardiomegaly and evidence of reduced left ventricular function in the alcoholics, although altered sensitivity to the positive inotropic agent, dobutamine, was not evident in those hearts. After 11 months, cardiac output, stroke work, and peak power of the alcoholic rat hearts were significantly depressed, the responsiveness of the left ventricle to dobutamine was diminished, and both ventricles were enlarged compared to controls. Cardiac function during early withdrawal was studied in rats that had consumed alcohol for 14-16 months. Hearts from non-fasted rats at 0 hr of withdrawal exhibited diminished responsiveness to dobutamine compared to controls; at 24 hr and 72 hr of withdrawal no differences between alcoholic and control rat heart dobutamine responsiveness were observed. The data indicated that: (a) cardiomegaly, beginning with right ventricular enlargement, was an early indicator of alcohol's cardiac effects in rats; (b) left ventricular enlargement of the alcoholic rat hearts was associated with basal left ventricular dysfunction; and (c) evidence of cardiac subsensitivity to dobutamine, which is characteristic of this alcoholic rat model, depended on the nutritional status and withdrawal state of the rat at the time that the heart was excised for study.
Alcohol Alcohol 1988
PMID:The development of alcohol-induced cardiac dysfunction in the rat. 322 60

Arterial hypertension is the most important risk factor in all types of stroke. The significance of alcohol in the pathogenesis of stroke is less well defined. Chronic alcoholism leads to an elevation of blood pressure. Thus, the association between alcohol and stroke might be the blood pressure effect of alcohol. However, some studies have shown a significant influence of alcohol on the incidence of stroke--especially of intracerebral haemorrhage and subarachnoid haemorrhage--even after adjustment for blood pressure. Many possible pathomechanisms are discussed. Alcohol inhibits aggregation of thrombocytes, and chronic alcohol abuse may induce thrombocytopenia, which could lead to a haemorrhagic stroke. Alcohol withdrawal leads to rebound thrombocytosis. Acute alcohol ingestion induces a decrease in fibrinolytic activity and an increase in factor VIII activity, which enhances the thrombotic potential. Additionally, alcohol increases plasma osmolarity, erythrocyte aggregability, haematocrit and blood viscosity, and decreases deformability of erythrocytes. The effects of alcohol on cerebral blood flow are still under debate; there is a deterioration in autoregulation of cerebral blood flow anyway. In animal studies alcohol induced dose-dependent vasospasm of the cerebral blood vessels, which could be a possible pathomechanism in ischaemic, as well as in haemorrhagic stroke. Chronic alcoholism is the most common cause of secondary non-ischaemic cardiomyopathy, which can lead to cerebral embolism via rhythm disorders or intracardiac thrombus formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Does alcohol consumption promote the manifestation of strokes? Considerations on pathophysiology]. 328 8

For more than 30 years, clinical observations to link alcohol abuse and stroke have accumulated in several countries. Studies of general populations have indicated that the risk for stroke increases with increasing alcohol consumption. Studies of young victims of stroke where the classical risk factors of stroke are uncommon, have demonstrated that even occasional heavy drinking carries an increased risk for stroke. In particular, the increased occurrence of strokes during weekends, the very time of heavy alcohol consumption in non-alcoholics, supports this notion. Alcoholics seem to get their strokes at an earlier age than non-alcoholics. Paradoxically, the published evidence has implicated drinking in both ischemic and hemorrhagic strokes, which suggests that there may be more than one mechanism by which alcohol can increase the risk. Strokes seem to be precipitated during the alcohol intoxication itself rather than the following withdrawal syndrome, but the contributing mechanisms, except for bleedings caused by external violence, are unknown. Alcohol can produce fluctuations in platelet reactivity and untoward interactions with certain drugs, but it remains to be demonstrated that such effects are temporally related to the onset of ischemic and hemorrhagic strokes.
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PMID:What supports the role of alcohol as a risk factor for stroke? 331 65

The hemodynamic effects of acute alcohol intoxication were studied at rest and during upright exercise in 28 patients with coronary artery disease by right-sided heart catheterization and radionuclide cardiography. The mean arterial blood pressure at rest was reduced by 5% and the left ventricular ejection fraction at rest decreased 2% because of end-systolic dilation during intoxication (serum ethanol 21 mmol/liter). No changes were observed in heart rate, stroke volume, pulmonary artery pressure, pulmonary artery wedge pressure or total peripheral resistance. No significant changes occurred in plasma catecholamines, and no changes occurred in any variable during mild exercise corresponding to a 30 to 40% heart rate increase. Thus, alcohol ingested in moderate doses causes slight impairment of left ventricular emptying and a reduction in the arterial blood pressure at rest in patients with coronary artery disease. A mild exercise load can be tolerated during alcohol intoxication without hemodynamic changes.
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PMID:Hemodynamic effects of alcohol at rest and during upright exercise in coronary artery disease. 333 17

Thirty male patients with ischemic heart disease and cardiomyopathy entered a controlled study of the acute effects of alcohol on cardiac function evaluated by right heart catheterization. Twenty patients, nine with angina pectoris and 11 with congestive heart failure, were studied during alcohol intoxication, and ten patients, five with angina pectoris and five with heart failure, served as a control group. The mean serum ethanol concentration in the alcohol group was 93 mg/100 ml (S.D. 17). The systemic arterial blood pressure was reduced by 6% in the alcohol group, P less than 0.05 compared with the control group. No significant changes occurred in the central venous pressure, the pulmonary artery pressure, the pulmonary capillary wedge pressure, or in cardiac output, stroke volume and total peripheral resistance. Alcohol intake in moderate doses has no measurable effect on pulmonary blood pressures or cardiac output in patients with ischemic heart disease and cardiomyopathy. Such an effect may, however, be masked by a reduction of afterload.
Alcohol Alcohol 1988
PMID:Cardiac function after alcohol ingestion in patients with ischemic heart disease and cardiomyopathy: a controlled study. 335 19

Seven healthy men, aged 21 to 30 years, were investigated by radionuclide cardiography at rest and during submaximal exercise at heavy (early) and during declining (late) alcohol intoxication. Control studies, in which alcohol was substituted by an isocaloric, isovolumic drink, were performed on a different day. The left ventricular ejection fraction at rest decreased from 59 to 56% during early intoxication (serum ethanol 35 +/- 6 mmol/l), whereas no change was observed in the ejection fraction during exercise. No significant change was recorded in stroke volume after alcohol consumption as opposed to a small increase after ingestion of the caloric drink. Plasma noradrenaline concentrations were elevated during exercise and early intoxication. During late intoxication (serum ethanol 21 +/- 5 mmol/l) the left ventricular ejection fraction at rest was increased by 7% compared with the baseline value. At rest the heart rate was increased from 68 +/- 7 to 84 +/- 15 beats/min, whereas cardiac output had reverted to the baseline value. Plasma noradrenaline at late intoxication was increased both at rest and during exercise compared with the baseline values. Apart from tachycardia and a reduction in left ventricular volumes during late intoxication no alcohol induced hemodynamic changes occurred during exercise.
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PMID:Cardiac function at rest and during exercise in early and late alcohol intoxication. 336 May 22

In 1980, 87,526 female nurses 34 to 59 years of age completed a dietary questionnaire that assessed their consumption of beer, wine, and liquor. By 1984, during 334,382 person-years of follow-up, we had documented 200 incident cases of severe coronary heart disease (164 nonfatal myocardial infarctions and 36 deaths due to coronary disease), 66 ischemic strokes, and 28 subarachnoid hemorrhages. Follow-up was 98 percent complete. As compared with nondrinkers, women who consumed 5 to 14 g of alcohol per day (three to nine drinks per week) had a relative risk of coronary disease of 0.6 (95 percent confidence interval, 0.4 to 0.9); for 15 to 24 g per day the relative risk was 0.6 (0.3 to 1.1), and for 25 g or more per day it was 0.4 (0.2 to 0.8), after adjustment for risk factors for coronary disease. Alcohol intake was also associated with a decreased risk of ischemic stroke. For 5 to 14 g of alcohol per day the relative risk was 0.3 (0.1 to 0.7), and for 15 g per day or more it was 0.5 (0.2 to 1.1). In contrast, although the number of cases of subarachnoid hemorrhage was small, alcohol intake tended to be associated with an increased risk of this disorder; for 5 to 14 g per day the relative risk was 3.7 (1.0 to 13.8). These prospective data suggest that among middle-aged women, moderate alcohol consumption decreases the risks of coronary heart disease and ischemic stroke but may increase the risk of subarachnoid hemorrhage.
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PMID:A prospective study of moderate alcohol consumption and the risk of coronary disease and stroke in women. 339 81

We studied alcohol use before the onset of a first seizure in 308 patients with seizures and 294 controls. The risk of seizures increased with increasing current alcohol use. For unprovoked seizures (i.e., seizures occurring without an antecedent event, such as a recent stroke), the adjusted odds ratios rose from 3-fold at intakes of 51 to 100 g of ethanol per day (95 percent confidence limits, 1.3 and 6.3), to 8-fold at 101 to 200 g per day (95 percent confidence limits, 3.3 and 18.7), and to almost 20-fold at 201 to 300 g per day (95 percent confidence limits, 6.1 and 6.2). For provoked seizures, the odds ratios were lower and statistically significant only above 200 g per day (odds ratio, 10.1; 95 percent confidence limits, 2.3 and 43.8 at 201 to 300 g per day; odds ratio, 7.4; 95 percent confidence limits, 1.8 and 30.5 above 300 g per day). Among ex-drinkers (abstention greater than or equal to 1 year), no increased risk was detected. Alcohol withdrawal was not associated with the onset of seizures in this study; 16 percent of first seizures in drinkers fell outside the conventionally defined withdrawal period, and the remainder exhibited a seemingly random timing after the last drink. We conclude that the relation of seizures to alcohol use is dose dependent and appears to be causal, and that seizures can be interpreted as a disorder induced by the ingestion of alcohol, independently of alcohol withdrawal.
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PMID:Alcohol consumption and withdrawal in new-onset seizures. 341 84

The inotropic responses of chronic alcoholic and control rat hearts to phenylephrine, glucagon, ouabain, and dobutamine were studied to determine if the reported beta-adrenergic subsensitivity of alcoholic rat hearts was a specific defect. Male Long-Evans rats were maintained on nutritionally-complete liquid diets for 10 to 12 months; alcoholic rats received 38% of their calories from ethanol. Dry heart weight/body weight ratios indicated an average 15% hypertrophy of the alcoholic rat hearts. The function of isolated working hearts from these animals was studied at a constant heart rate and afterload. Ventricular function curves indicated significantly lower basal function of alcoholic rat hearts, as evident from their lower peak left ventricular relaxation rate, lower isovolumic relaxation rate, and lower peak power compared to controls. The alcoholic rat hearts had significantly lower inotropic (stroke work and peak power) responses to phenylephrine, glucagon, and dobutamine compared to controls, whereas the response of the alcoholics to ouabain was not significantly different from that of controls. Oxygen supply-to-utilization ratios decreased similarly in alcoholics and controls during treatment with the inotropic agents, as a result of increases in myocardial oxygen consumption and effects on coronary flow that were similar in both groups of animals. Thus the differences in inotropic responses observed with the alcoholic rat hearts were not primarily the result of compromised oxygen supply. Rather, the decreased stroke work response of the alcoholic hearts which occurred despite an increase in oxygen consumption suggested that the alcoholic rat hearts did not utilize oxygen as efficiently as did control hearts to perform external work. This was reflected in the significant differences between alcoholics and controls in the response of calculated external work efficiency to phenylephrine, glucagon, and dobutamine. Thus, alcohol-induced cardiac hypertrophy was associated with depressed basal left ventricular contractile function and decreased responsiveness to alpha 1-adrenergic, beta 1-adrenergic, and glucagon stimulation, but the responsiveness to ouabain was not significantly affected. These characteristics are similar to those of hearts hypertrophied by other causes.
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PMID:Alcoholic cardiomyopathy in rats: inotropic responses to phenylephrine, glucagon, ouabain, and dobutamine. 343 59

Alcohol, both alone and in concert with deficiencies or excesses of other substances, can produce cardiomyopathy. In addition, alcohol can directly affect the cardiac conduction system and produce arrhythmias. Alcohol also affects known risk factors for stroke and coronary heart disease (CHD). Alcohol increases blood pressure, which may lead to hypertension and thus increase the risk of stroke. HDL cholesterol, which is inversely related to CHD risk, increases with alcohol, and LDL cholesterol, which is positively related to CHD risk, may decrease with alcohol, a potentially dually protective effect. However, both case-control and population based studies indicate only moderate levels of consumption, defined as two drinks per day or less, may be of benefit. Preliminary data from the Lipid Research Clinics Follow-up Study suggest that the beneficial effect of moderate amounts of alcohol may be mediated in part by increased HDL cholesterol and in part by another factor, possibly reduced coagulation. Clinical and laboratory data, in addition to epidemiologic data, suggest alcohol intake above two drinks per day leads to excess cardiovascular disease (CVD), probably reflecting hypercoagulability as well as hypertension at higher levels of intake. Because alcohol can lead to excess morbidity and mortality from CVD as well as several other diseases and conditions, public health policy should continue to discourage the drinking of alcohol, especially non-moderate consumption.
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PMID:The roles of alcohol in the epidemiology of cardiovascular diseases. 347 73


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