Alcohol Consumption and Risk of Stroke in Women
Although light to moderate alcohol consumption has been consistently associated with a lower risk of heart disease, the data for stroke are less certain. Some studies have suggested a lower risk of stroke among women with light to moderate alcohol intake but the dose response among women is uncertain and the data are limited. A total of 83 578 female participants of the Nurses' Health Study (NHS) who were free of diagnosed cardiovascular disease and cancer at baseline were followed from 1980 to 2006. Self-reported alcohol consumption was assessed at baseline and updated approximately every 4 years, whereas stroke data were updated at baseline and every 2 years. They observed 2171 total strokes, 1206 of which were ischemic, 363 hemorrhagic, and 602 of probable/unknown subtype. In multivariable analyses, low (>0–4.9 g/day) and moderate (5–14.9 g/day) alcohol consumption were associated with lower risk of total stroke compared with abstainers, whereas women who consumed 30 to 45 g/day did not have a greater risk of total stroke. After multivariable analyses, the associations between alcohol use and ischemic stroke were similar but not statistically significant. Low-to-moderate alcohol consumption was not associated with a greater risk of hemorrhagic stroke in this population. Although the intake of 30 to 45 g/day was suggestive of a nonsignificant increased risk of ischemic stroke, there was no association between this amount of consumption and the risk of hemorrhagic stroke. These results are consistent with the current American Heart Association guidelines for women, suggesting a modest inverse association between alcohol consumption of <1 drink/day with the risk of total, ischemic, and hemorrhagic stroke.
See p 939.
Stroke Occurrence and Patterns Are Not Influenced by the Degree of Stenosis in Cervical Artery Dissection
Cervical artery dissection is a common cause of stroke in young adults. The mural hematoma associated with the dissection may result in arterial stenosis or occlusion or distal embolization. This retrospective cohort sought to determine whether the occurrence and pattern of stroke on diffusion-weighted imaging (DWI) differed according to the degree of arterial narrowing due to the dissection. One hundred forty-seven consecutive patients with symptomatic cervical artery dissection (100 carotid and 47 vertebral dissections) were included in this study. The authors compared the presence, number, volume, and patterns of DWI lesions among patients with <70% stenosis (Group 1), ≥70 stenosis (Group 2), and occlusion (Group 3). Eighty-eight (60%) patients had a DWI lesion and 59 (40%) patients did not. The presence and number of DWI lesions were independent of lumen patency. The volume of DWI lesions was larger in the group with occlusion. There was no difference in the pattern of DWI lesions according to the degree of stenosis of the dissected artery. Multiple acute DWI lesions were found in more than half of the patients. There are several limitations of this study, including the small sample size and the use of contrast enhanced MR angiography. The results from this study support the concept of thromboembolism as a significant mechanism of stroke from cervical artery dissection. Further data are needed to determine whether anticoagulation or antithrombotic medications are superior in the prevention of thromboembolism secondary to cervical artery dissection.
See p 1150.
Ezetimibe and Regression of Carotid Atherosclerosis: Importance of Measuring Plaque Burden
Prior studies with ezetimibe have failed to show a reduction in carotid intima-media thickness. The authors of this study argue that intima-media thickness is “biologically and genetically” different from plaque, or “true atherosclerosis.” This observational study analyzes carotid plaque progression in 231 patients for 2 years before and regression for 2 years after the addition of ezetimibe. Carotid total plaque area and fasting lipids were measured in all patients. Total cholesterol and low-density lipoprotein cholesterol significantly declined both before and after the addition of ezetimibe. High-density lipoprotein cholesterol did not significantly change before but did decline significantly after the addition of ezetimibe. Despite the decrease in low-density lipoprotein before the initiation of ezetimibe, there was a significant increase in within-individual total plaque area in the 2 years before the addition of ezetimibe by 6.89±39.57 mm2 SD. After the addition of ezetimibe, despite the decrease in high-density lipoprotein, plaque area decreased by −3.05±38.18 mm2 SD. Based on these results, it appears that ezetimibe causes regression of carotid plaque burden. A further randomized clinical trial is needed to confirm and explore these findings further.
See p 1153.
- © 2012 American Heart Association, Inc.