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

While conduction disturbances and arrhythmias are seen frequently in alcoholic cardiomyopathy, the specific relationship of these changes to ethyl alcohol has been unclear. To investigate the long-term effects of ethanol upon cardiac conduction, alcoholism was induced in 11 male mongrel dogs for 7 to 33 (mean 14.4) months by feeding up to 36 per cent of total daily calories as ethanol while adequate nutrition was maintained. His and left bundle branch electrograms in the intact anesthetized animals were recorded along with high-speed, high-frequency ECG's. While resting left ventricular pressures, volumes, and stroke outputs were normal, H-Q time was prolonged in the alcoholic animals drinking for longer than one year (35 +/- 3 msec., normals 26 +/- 1 msec.-P less than 0.001). QRS widening (to 80 +/- 4 msec.) was also evident after one year as compared with normals (62 +/- 2 msec.-P less than 0.001), and both H-Q and QRS alterations correlated with duration of intake. These changes were less after shorter ingestion periods, could not be reproduced in normals by acute ethanol infusion, and were not associated with ventricular hypertrophy, inflammation, or necrosis. No abnormalities of atrial conduction were noted. Morphologic correlates of the conduction abnormalities included accumulation of Alcian Blue-positive interstitial material as well as dilatation and localized swelling of the nonspecialized region of the intercalated discs in ventricular muscle and Purkinje fibers. Thus, prolonged ethanol intake in the absence of evident malnutrition resulted in demonstrable intraventricular conduction abnormalities and morphologic alterations which were related to duration of ingestion, consistent with a cumulative toxic effect of ethanol.
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PMID:Cardiac conduction abnormalities produced by chronic alcoholism. 94 75

The acute effects of ethanol (ETOH) on cardiac function in 32 normal subjects has been studied utilizing systolic time intervals. Seven (group I) 13 (group II), and 12 subjects (group III), reported an average daily consumption of less than 1 oz, 1-2 oz, and more than 2 oz of ETOH, respectively. Progressively higher control values from group I to group III in PEP, PEPI, ICT and PET/LVET were observed (PEP-I vs PEPI-III: P smaller than 0.05; PEP/LVET-I vs PEP/LVET-II and PEP/LVET-III: P smaller than 0.05). There was progressively less change in these variables following acute ETOH (P smaller than 0.02-0.05 in group I; P equals NS in group III, group II intermediate). This indicates some degree of chronic myocardial impairment in group II and especially in group III, which tends to be proportionate to the degree of chronic ETOH exposure. These data are not necessarily disparate with previous reports of little or even a salutary hemodynamic effect of ETOH in normal subjects. Thus, the relative stability of LVET post ETOH, coupled with the observed increase in heart rate, is consistent with previous reports of ETOH-induced rate-dependent increments in cardiac output with unchanging stroke volumes, in spite of the presence of acute myocardial depression. The observations reported herein demonstrate the probable incremental influence of ETOH consumption in a chain of events which may culminate in alcoholic cardiomyopathy.
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PMID:The basis for differences in ethanol-induced myocardial depression in normal subjects. 113 3

The effects of alcohol on the heart include modification of the risk of coronary artery disease, the development of alcoholic cardiomyopathy, exacerbation of conduction disorders, atrial and ventricular dysrhythmias, and an increased risk of hypertension, hemorrhagic stroke, infectious endocarditis, and fetal heart abnormalities.
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PMID:Cardiovascular effects of alcohol. 268 74

The hemodynamic effects of an intravenous dose of 1 mg/kg of Cibenzoline, a new anti-arrhythmic agent with properties of classes I, III and IV of the Vaughan-Williams classification, were studied in 9 patients during routine cardiac catheterization. Six patients had valvular heart disease (aortic insufficiency in 5 and mitral stenosis in 1), one patient had ischemic heart disease, one patient had alcoholic cardiomyopathy and the remaining patient had coarctation of the thoracic aorta. Left ventricular pressure and right sided intracardiac pressures were recorded using a high fidelity transduced and a Swan-Ganz catheter respectively. The first derivative of the left ventricular pressure was obtained electronically and Vmax calculated by linear extrapolation to zero load of the contractile element shortening velocity--left ventricular pressure relationship. Plasma levels of Cibenzoline were measured by gas liquid chromatography. All these parameters were obtained under baseline conditions and then 5, 10, 20, 40 and 60 minutes after intravenous administration of Cibenzoline. Cardiac index fell by 20% 5 minutes after the injection of Cibenzoline, and returned to control after one hour only. This fall was primarily related to a decrease in stroke index, since heart rate remained virtually unchanged. Right and left ventricular filling pressures increased significantly from the 5th to the 40th minute. Aortic systolic pressure fell by approximately 6%, without any change in mean and diastolic aortic pressures. Peripheral and pulmonary resistances increased at 20 minutes by 33% and 45%, respectively. Left ventricular peak positive dP/dt and Vmax decreased significantly at 5 minutes and remained below the baseline value until 60 minutes by 9% and 11% respectively. Percent changes in cardiac index, dP/dt and Vmax were significantly correlated to cibenzoline plasma levels (r = 0.85, 0.79, 0.74 respectively; n = 45). Thus, doses achieving plasma levels within the reported therapeutic range (250-350 ng/ml) would be expected to result in a 8-12% decrease in cardiac output associated with 12-17% and 15-21% reduction of left ventricular dP/dt and Vmax respectively. These data indicate that cibenzoline exerts significant negative inotropic effects. Its use in the subset of patients with severely depressed ventricular function warrants caution.
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PMID:Hemodynamic effects of a new antiarrhythmic agent: cibenzoline. 406 26

Alcohol abuse is a more frequent contributor to hypertension than is generally appreciated. Although hypertension is transitory in most alcoholics and may not be evident after a short period of abstinence, it is potentially dangerous. Paroxysms of hypertension might result in target-organ damage. Hypertension may be the causal link to the increased incidence of stroke and coronary heart disease observed in problem drinkers as well as a contributor to the pathogenesis of alcoholic cardiomyopathy. Because of its transitory nature, however, alcohol-associated hypertension may, regrettably , be dismissed as inconsequential. Thus, a major potential cause of cardiovascular morbidity may go untreated.
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PMID:Alcohol use and hypertension. Clinical considerations and implications. 672 42

The complex relationship between alcohol consumption and stroke includes both benefits and risks. Regular light-to-moderate consumption of alcohol seems to decrease the risk for ischemic stroke by reducing atherothrombotic events, but the underlying mechanism is still unclear. Recent and current (but not previous) heavy drinking increases the risk for both hemorrhagic and ischemic strokes. Young and middle-aged men are stricken more often than women or elderly persons, probably because they are more often current heavy drinkers. Alcoholic cardiomyopathy is a cause of cardioembolic brain infarction. Cardiac arrhythmias caused by regular heavy drinking or binge drinking can precipitate thrombus formation and propagate already existing thrombi from the heart. The maintenance of high blood pressure by heavy drinking may promote cerebral arterial degeneration, but the effect of drinking habits on aneurysm formation is not known. Acute increases in systolic blood pressure and/or alterations in cerebral arterial tone could serve as mechanisms triggering hemorrhagic strokes during alcoholic intoxication. We lack studies to show that prevention of heavy drinking can efficiently influence the occurrence of strokes.
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PMID:Alcohol consumption and stroke: benefits and risks. 979 60

Evident disparities in relationships make it desirable to consider several disorders separately. (1) Alcoholic cardiomyopathy was perceived 150 years ago, but understanding was clouded by recognition of beriberi and of synergistic toxicity from alcohol with arsenic or cobalt. (2) A report of a link between heavy drinking and hypertension in WWI French soldiers was apparently ignored for > 50 years. Epidemiological and intervention studies have now firmly established this association, but a mechanism remains elusive. (3) The 'holiday heart syndrome', an increased risk of supraventricular tachyarrhythmias in alcoholics, has been widely known to clinicians for 25 years; data remain sparse about the total role of heavier drinking in cardiac rhythm disturbances. (4) Failure of earlier studies to distinguish types of stroke impeded understanding; it now seems probable that alcohol drinking increases risk of haemorrhagic stroke but lowers risk of ischaemic stroke. (5) Heberden reported angina relief by alcohol in 1786, and an inverse alcohol-atherosclerosis association was observed by pathologists early in this century. Recent population studies and plausible mechanisms support a protective effect of alcohol against coronary disease. International comparisons dating back to 1819 suggest beverage choice as a factor, but this issue (the 'French Paradox') remains unresolved.
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PMID:Alcohol and cardiovascular diseases: a historical overview. 994 84

The relationship between alcohol consumption and all-cause mortality is J-shaped in most industrialized countries. The J-shape is the result of the combination of adverse and beneficial effects of alcohol consumption. Adverse effects include several types of cancer (oropharyngeal, oesophageal, liver, laryngeal and breast cancer), other diseases of the aerodigestive tract, diseases of the heart (alcoholic cardiomyopathy, haemorrhagic stroke, arrhythmia, hypertension), addiction-related mental disorders, and accidents and injuries. Beneficial effects are for ischaemic heart disease and ischaemic stroke. The exact shape of the all-cause mortality curve in a given region depends upon the proportion of the population consuming alcohol at different levels, especially heavy consumption, and on the prevalence of the disorders named above. Thus regions with a relatively low prevalence of ischaemic cardiovascular disease show almost no benefits of consumption, and an all-cause mortality curve which is almost exponential. Females experience a minimum mortality risk at a level of alcohol intake which is lower than that associated with the minimum risk for men. Similarly, an upturn in mortality risk occurs at lower intake levels for women than for men. At present, there is no satisfactory explanation for the observation that the shape of the mortality curve varies with the consumption level of the cohort under study. Heavier-drinking cohorts tend to display their minimum risk at relatively higher levels of alcohol intake than cohorts with lower alcohol consumption.
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PMID:Alcohol and all-cause mortality: an overview. 994 96

It has been shown that certain patients with cirrhosis have asymptomatic cardiac abnormalities that have not yet been explained. Thus, cardiac troponin I, a specific marker of myocardial injury, has been measured in patients with cirrhosis without previous cardiac disease. Thirty-two consecutive patients (age 49 +/- 11) with cirrhosis and normal ECG were selected, 22 of which were alcoholic. Hemodynamic investigations were performed. Left ventricular function and mass were evaluated by echocardiography. Serum creatine kinase MB mass, myoglobin, and cardiac troponin I concentrations were measured. Cardiac troponin I concentrations were elevated in 10 patients (32%) (range 0.06-0.25 microg/L) whereas creatine kinase MB mass and myoglobin were normal in all patients. Abnormal troponin I values were not related to the severity of cirrhosis, to the degree of portal hypertension, or to other hemodynamic values. In contrast, elevated serum cardiac troponin I concentrations were related to a decreased stroke-volume index (P <. 05) and a decreased left ventricular mass (P <.05). These results show a high prevalence of slightly elevated serum cardiac troponin I in patients with cirrhosis, especially in those with alcoholic cirrhosis. Elevated troponin I is associated with subclinical left ventricular myocardial damage. These findings may be linked to a lack of left ventricular adaptation in certain patients with cirrhosis and alcoholic cardiomyopathy.
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PMID:Elevated circulating cardiac troponin I in patients with cirrhosis. 1005 61

Moderate ethanol consumption (1-3 drinks/day on 5-6 days/week) has a favourable effect on vascular disease-related mortality and morbidity [especially ischaemic heart disease (IHD)]. This cardioprotective effect may be due to significant effects on cardiovascular risk factors such as high density cholesterol (HDL) concentration (HDL protects from IHD) and an inhibition of platelet aggregation (increased platelet aggregability predicts coronary events). In contrast, alcoholics and problem drinkers have an excess of IHD-related, and possibly stroke-related, mortality. Excessive alcohol intake may raise the blood pressure. Prolonged alcohol abuse can also result in alcoholic heart muscle disease. Alcohol is the major cause of non-ischaemic cardiomyopathy in Western society. Although there is a widespread belief that red wine protects more than other alcoholic beverages, several studies do not support this interpretation.
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PMID:Beneficial effect of moderate alcohol consumption on vascular disease: myth or reality? 1091 77


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