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

1. Male death rates from hypertension and stroke in England and Wales in 1949-53 were highest in those socio-economic and occupational groups with the highest death rates for cirrhosis of the liver (and presumably with highest alcohol intake. 2. In prevalence data from the Busselton population in Western Australia in 1969, there was a significant association between hypertension and a history of heavy drinking. 3. Together with other data, these observations suggest that up to 30% of hypertension in affluent countries may prove to be attributable to the use of alcohol.
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PMID:Alcohol use, hypertension and coronary heart disease. 107 3

In vivo 31P-nuclear magnetic resonance (31P-NMR) spectroscopy and ion-selective electrode measurements were undertaken to determine if administration of acute doses of alcohol (ALC, 0.2-6.6 g/kg), and lethal doses of barbiturate anesthesia, exert any influence on: (1) brain cellular bioenergetics, intracellular free Mg ([Mg2+]i) and intracellular pH (pHi), and (2) serum levels of ionized Mg (IMg2+), ionized calcium (ICa2+) and K+. Approximately 20-30 min after intraperitoneal administration of ALC to anesthetized rats, brain phosphocreatine (PCr)/ATP and PCr/inorganic phosphate (P(i)) ratios dropped from 2.5 to 1.7 and from 6.6 to 2.2, respectively, P(i) rose 20-200% (depending upon ALC dose), and free ADP and creatine rose significantly. ALC induced rapid decreases in the cytosolic phosphorylation potential (CPP) and free energy of ATP hydrolysis (-delta G/delta E). Following ALC administration, brain [Mg2+]i dropped rapidly (within 4-30 min) and significantly; the greater the dose of ALC, the greater the loss in brain [Mg2+]. Correlations were found between [Mg2+]i, PCr/ATP, CPP and delta G/delta E after ALC but not in control brains. Rats that exhibited ALC-induced strokes and death (unlike barbiturate death) exhibited huge elevations in [Mg2+]i. Although ALC administration does not alter brain pHi at least (up to 70 min), ALC- and barbiturate-induced death produces rapid brain intracellular acidosis. Concomitant with ALC-induced alterations in [Mg2+]i and brain cellular bioenergetics, we noted that ALC administration results in rapid elevations in serum IMg2+ and K+ but not ICa2+. These results suggest that ALC administration and heavy or binge-drinking of ALC (1) can result in rapid alterations in brain bioenergetics, [Mg2+]i and pHi, and (2) result in rapid elevations in serum IMg2+ and K+ in rats. In addition, ALC- and barbiturate-induced deaths do not appear to produce identical alterations in brain bioenergetics and [Mg2+]i, and lastly binge or heavy drinking of ALC may result in stroke-like events and sudden death via rapid alterations in brain cellular bioenergetics.
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PMID:Alcohol intoxication results in rapid loss in free magnesium in brain and disturbances in brain bioenergetics: relation to cerebrovasospasm, alcohol-induced strokes, and barbiturate anesthesia-induced deaths. 184 45

To determine if a history of snoring is a risk factor for brain infarction, I conducted a case-control study of risk factors for ischemic stroke using 177 consecutive male patients aged 16-60 (mean 49) years with acute brain infarction. For each patient I chose an age-matched (+/- 6 years) male control. Arterial hypertension, coronary heart disease, snoring (habitually or often), and heavy drinking (greater than 300 g/wk) were risk factors in the stepwise multiple logistic regression analysis. The odds ratio of snoring for brain infarction was 2.13. By McNemar's test this association increased strongly if a history of sleep apnea, excessive daytime sleepiness, and obesity were all present with snoring (odds ratio 8.00). My study indicates that snoring may be a risk factor for ischemic stroke, possibly because of the higher prevalence of an obstructive sleep apnea syndrome among snorers than nonsnorers.
Stroke 1991 Aug
PMID:Snoring and the risk of ischemic brain infarction. 186 48

To examine the relationship between alcohol consumption and ischemic stroke risk, we used data from our case-control study of stroke risk. Eighty-nine patients admitted to the hospital with ischemic stroke documented by computed tomography of the head were matched to 178 controls. Alcohol use was defined by an estimate of customary use (heavy, moderate, light, or none). We found no consistent or significant association between any level of alcohol use and ischemic stroke risk (odds ratios: any, 1.3; heavy, 0.5; moderate, 1.5; and light, 1.5). We repeated the analysis of our study using a control group assembled according to the study criteria of another case-control study that reported a significant association in men with heavy alcohol use (odds ratio, 4.2). We demonstrated that the association in the prior study may be spurious due to methodological problems.
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PMID:Evidence against the association between alcohol use and ischemic stroke risk. 273 Feb 58

Alcohol-related minor accidents such as sprains and burns are common in sauna, but more serious accidents also take place--head contusions, heat stroke after passing out in sauna and drownings while swimming. The exact number of these accidents is not known, but in Finland (population 4.8 million) the consumption of alcohol has been estimated to be a contributing factor in some 20 to 25 sauna-related deaths every year. The scientific information on the interaction of sauna and alcohol on human physiology is totally lacking. Thus our discussion on the physiological and medical consequences of this interaction relies merely on presumptions. Ingestion of large amounts of alcohol while sauna bathing may affect the body's ability to maintain blood pressure. In particular, the risk of an orthostatic hypotensive reaction is increased with concomitant faintings and accidents. Alcohol intoxication and particularly the hangover phase exposes a person to cardiac arrhythmias, and sauna may further increase the arrhythmia-risk due to enhanced adrenergic activity. Sauna bathing and heavy drinking, and also sauna bathing during hangover phase undoubtedly create real health risks.
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PMID:The sauna and alcohol. 321 3

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

Alcohol might contribute to stroke in several ways: induction of cardiac arrhythmias and cardiac wall motion abnormalities which predispose to cerebral embolism, induction of hypertension, enhancement of platelet aggregation and activation of the clotting cascade, and reduction of cerebral blood flow by stimulation of cerebral vascular smooth muscle contraction or by altering cerebral metabolism. While these pathophysiological mechanisms have gained enthusiastic experimental and theoretical support, the findings are preliminary and will require further large-scale clinical and epidemiological analyses to substantiate their roles as causal factors or potentiators of stroke. Documentation of measurable platelet and coagulation cascade abnormalities reported in healthy volunteers who have ingested alcohol will need to be confirmed on a broader scale in stroke patients with recent ethanol consumption. The risk of stroke in those with alcohol-induced atrial fibrillation and cardiomyopathy must be ascertained for the general population. While the experimental evidence is exciting and provocative, epidemiological evidence also suggests a link between alcohol consumption and stroke. Regular alcohol ingestion is associated with hypertension, fatal and nonfatal intracranial hemorrhage, cerebral infarction, and increased risk of death from stroke. Recent, less stringently controlled studies suggest that alcohol consumption is a risk factor for cerebral infarction in young adults with occasional ethanol intoxication and middle-aged women and young men with occasional alcohol intoxication and regular heavy drinking. Alcohol may also be a risk factor for subarachnoid hemorrhage.
Stroke
PMID:Alcohol and stroke. 381 Jul 63

One hundred consecutive patients (67 men, 33 women) aged from 15-55 with acute ischemic brain infarction verified by computed tomography and/or angiography and/or brain scanning were studied. In 40 cases the onset of symptoms was preceded within 24 hours by ethanol intoxication. Ethanol intoxication preceding brain infarction was 4-7 times as common in men and 6-15 times as common in women as ethanol intoxication in the general Finnish population of the same age and sex. Nineteen of the patients were heavy drinkers. Heavy drinking was twice as common in men and 5 times as common in women as heavy drinking in the general Finnish population of the same age and sex. Both occasional ethanol intoxication and regular heavy drinking seem to carry an increased risk of ischemic brain infarction. The ethanol-induced risk was highest in middle-aged women and young men.
Stroke
PMID:Ethanol intoxication: a risk factor for ischemic brain infarction. 665 51

3 cases of stroke in young women of childbearing age are presented to show the severity of illness and mortality in women using oral contraceptives. All 3 patients smoked more than 15 cigarettes a day. The mortality rate from cerebrovascular disease in OC users has been estimated as 4.7 times that of nonusers. The risk of developing a thrombotic stroke is 9.5 times greater than a control group's. Cerebral infarction has a relatively low mortality rate in young women, 9%, but a nonfatal stroke can have a devastating effect on the patient and her family. While there were no deaths among the 3 cases, each was left with a varying degree of neurological deficit while still in the peak of a normal life span. The possibility of synergistic potentiation of OC-associated cerebral thrombosis by cigarette use is uncertain but studies have noted some correlation between the 2. It is not clear that reduction in estrogen dosage has reduced the risk of cardiac or cerebral disease. The first patient developed extreme symptoms after a heavy drinking session, thereby raising the question of alcohol as a precipitating factor.
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PMID:Strokes and contraceptive medication. 736 87

The association of snoring with some cardiovascular risk factors was studied cross-sectionally by a postal survey among 3750 males aged 40-59 years. In univariate analyses, snoring associated statistically significantly (P < 0.01) with hypertension, smoking, obesity, heavy alcohol use, physical inactivity, dyspnoea, hostility and morning tiredness. In a multiple logistic regression model adjusted by age, snoring associated significantly with smoking, obesity, physical inactivity, hostility and morning tiredness. When smoking was excluded from the multivariate model, alcohol use was also associated significantly with snoring. The association of snoring with smoking, and with obesity seemed to be almost independent from other studied correlates of snoring. Our results indicate that in further studies on predictive value of snoring with regard to coronary heart disease and stroke, the associations of snoring with hypertension, smoking, obesity, heavy alcohol use, physical inactivity and hostility have to be considered, as these risk characteristics may cause confounding effects.
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PMID:Snoring and cardiovascular risk factors. 782 98


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