A synergistic effect of alcohol and hypertension has been suggested to increase the risk for stroke. However, the contribution of alcohol-induced hypertension to stroke morbidity and mortality may be greater than observed, because the effects of different drinking patterns have not been separately investigated. Alcohol-induced transient peaks in systolic blood pressure may predispose to stroke. Recent studies have measured time trends of blood pressure elevations in relation to alcohol consumption. They found a significant morning surge in blood pressure, which was related to alcohol intake in a dose-dependent manner and was independent of smoking. Men with a severe form of hypertension showed a 12-fold increased risk for cardiovascular disease mortality associated with heavy binge drinking. Binge drinking is a significant risk factor for stroke. Hypertensive patients should be warned about the risks of alcohol and urged to avoid binge drinking because of an increased risk for all subtypes of stroke.
A 10-year follow-up (1970-79) of a defined general population (n = 159 200) of middle-aged (born in 1911-40), urban, native Swedes, revealed that the prevalence rate of subarachnoid hemorrhage was 2.8 times higher in females than in males. This was mainly due to an accumulation of non-hypertensive aneurysmal subarachnoid bleeds in women born in the period 1932-40. The cases were significantly (P less than 0.001) overrepresented among divorced women, with relative risks of 1.89, 0.98 and 0.63 for divorced women, married women and spinsters (never married), respectively. Since high-dose estrogen-progestagen oral contraceptives have largely been used by the younger members of this study cohort, it may be speculated whether the observed substantial excess prevalence rate of subarachnoid hemorrhage with saccular aneurysm, not reported previously, represents a cohort effect unexpected after the introduction of low-dose oral contraceptives.
BACKGROUND AND PURPOSE: Nonsteroidal anti-inflammatory drugs (NSAIDs) have been associated with bleeding complications and may affect the risk of hemorrhagic stroke through inhibition of platelet cyclooxygenase-1. We performed a population-based case-control study to estimate the risk of intracerebral hemorrhage, subarachnoid hemorrhage, and ischemic stroke in users of NSAIDs. METHODS: We used a population-based patient registry to identify all patients with a first-ever stroke discharge diagnosis in the period of 1994 to 1999. All diagnoses were validated according to predefined criteria. We selected 40 000 random controls from the background population. Information on drug use for cases and controls was retrieved from a prescription registry. Odds ratios were adjusted for age, sex, calendar year, and use of other medication. To evaluate the effect of various potential confounders not recorded in the register, we performed separate analyses on data from 2 large population-based surveys with more detailed information on risk factors. RESULTS: The cases were classified as intracerebral hemorrhage (n=659), subarachnoid hemorrhage (n=208), and ischemic stroke (n=2717). The adjusted odds ratio of stroke in current NSAID users compared with never users was 1.2 (95% CI, 0.9 to 1.6) for intracerebral hemorrhage, 1.2 (95% CI, 0.7 to 2.1) for subarachnoid hemorrhage and 1.2 (95% confidence interval, 1.0 to 1.4) for ischemic stroke. The survey data indicated that additional confounder control would not have led to an increase in relative risk estimates. CONCLUSIONS: Current exposure to NSAIDs is not a risk factor for intracerebral hemorrhage or subarachnoid hemorrhage. Furthermore, NSAIDs probably offer no protection against first-ever ischemic stroke.
OBJECTIVE: Swedish snuff is a particular form of non-smoking tobacco with high nicotine content. It is unknown whether this form of tobacco is a risk factor similar to smoking for suffering subarachnoid haemorrhage (SAH). In the present study we report our finding concerning smoking and snuff as risk factors for the disease. METHOD: We analysed 120 consecutive patients with SAH regarding consumption of tobacco, in order to evaluate if snuff also is associated with an increased risk of SAH. RESULTS: The relative risk of SAH was about 2.5 times higher for smokers compared with the background population. Consumption of snuff was not associated with an increased risk. CONCLUSIONS: It seems unlikely that nicotine is solely responsible for the rupture of cerebral aneurysms. The final cause of the increased risk for suffering SAH has to be sought in other factors associated with tobacco smoking.