INCREASED FRUIT AND VEGETABLE INTAKE MAY REDUCE STROKE RISK

Consuming more than five servings of fruit and vegetables per day is associated with a reduced risk of stroke, according to a meta-analysis published in the January 28 Lancet. Feng J. He, PhD, and colleagues commented that such diet modification would not only greatly reduce stroke morbidity and mortality but also reduce other cardiovascular diseases and some cancers.

The researchers reviewed data from eight studies consisting of nine independent cohorts. Eligible studies were included if they reported relative risks and corresponding 95% confidence intervals for stroke related to frequency of fruit and vegetable intake. A combined total of 257,551 individuals, with 4,917 stroke events, were followed for an average of 13 years. Compared with participants who had fewer than three servings of fruit and vegetables per day, those with three to five servings per day had an 11% reduction in stroke risk, and those with more than five servings per day had a reduction of 26%. In addition, subgroup analyses showed that fruit and vegetables had a significant protective effect on both ischemic and hemorrhagic stroke.

Dr. He and colleagues discussed several possible mechanisms through which fruit and vegetable intake may be responsible for decreased stroke morbidity and mortality. They noted that because "raised blood pressure is the major cause of stroke, the blood pressure-lowering effect of potassium could be one of the major mechanisms contributing to a reduced risk of stroke with an increased fruit and vegtable intake." However, because "long-term intervention studies of vitamin C, vitamin E, and betacarotene have failed to show any beneficial effect on total stroke incidence or mortality," the effect of "dietary folate, fiber, and antioxidants to a reduced risk of stroke with an increased fruit and vegetable intake is only speculative," they noted.

In addition, the researchers commented, "The average fruit and vegetable intake in most developed countries is about three servings per day, and current recommendations encourage five or more servings per day. Our results provide strong support for these recommendations."

In an accompanying editorial, Lyn M. Steffen, PhD, MPH, RD, pointed out, "Low intake of fruit and vegetables is a major modifiable risk factor contributing to the burden of ill health. Because increased fruit and vegetable consumption may prevent adulthood diseases including stroke, coronary heart disease, some cancers, and other chronic disease, additional efforts are needed to promote healthy eating habits in children and adults."

He FJ, Nowson CA, MacGregor GA. Fruit and vegetable consumption and stroke: meta-analysis of cohort studies. Lancet. 2006;367:320-326.
Steffen LM. Eat your fruit and vegetables. Lancet. 2006;367:278-279.

GASTRIC STASIS OCCURS BOTH DURING AND OUTSIDE MIGRAINE

Contrary to previous belief, persons with migraine experience gastric stasis both during and outside an acute migraine attack, as reported in the January Headache. Sheena K. Aurora, MD, and colleagues suggested that those with migraine "may have an abnormal autonomic function" compared to persons without migraines.

The investigators compared 10 patients with migraine to 10 control participants matched for age and gender. Gastric scintigraphy was performed in all control participants once and in all 10 patients with migraines during the interictal period; in addition, nine studies were conducted during the ictal period migraine.

The investigators found that the time to half emptying was delayed both ictally (78%) and interictally (80%). Gastric stasis was less pronounced ictally (149.9 minutes) compared with interictally (188.8 minutes). There was a significant delay in persons with migraines compared to those without migraines, averaging 188.8 minutes and 111.8 minutes, respectively. These data were replicated in the percentage of radioactive material remaining in the stomach at two hours.

According to Dr. Aurora and colleagues, "The surprising observation in this study was that migraineurs had an abnormal gastric transit time compared to … controls even when they were not suffering from an acute attack. Also, contrary to previous belief, there was no worsening of gastric stasis during an acute attack. The stasis appears to be a feature of the disease rather than the acute event."

In addition, the investigators noted an absence of correlation between clinical symptom of nausea and gastric stasis. "Our studies suggest that nausea is caused by a central process as a part of changes occurring in the brain stem as a part of the acute migraine rather than due to gastric stasis, as the stasis is present even outside an attack and none of these patients were nauseous outside an attack," they commented.

Dr. Aurora’s group suggested that an abnormality of the hypothalamus may be a key factor in causing migraine. However, they pointed out that more studies are needed to determine what causes gastric stasis in persons with migraines, namely "establishing a relationship between gastric stasis and the disease burden, any correlation to disease phenotype, correlation to changes in the brain stem, hypothalamus and other areas, and correlation to other autonomic changes."

Aurora SK, Kori SH, Barrodale P, et al. Gastric stasis in migraine: more than just a paroxysmal abnormality during a migraine attack. Headache. 2006;46:1-7.

STENOSIS AS A PREDICTOR OF ISCHEMIC STROKE

Patients with symptomatic intracranial stenosis are at high risk of subsequent stroke, predominantly in the territory of the stenotic artery, according to findings in the January 31 Circulation. Researchers found that the risk is highest with stenosis of 70% and greater, after occurrence of recent symptoms, and in women. However, they noted that the increased risk in women was of "borderline significance."

Scott E. Kasner, MD, and colleagues analyzed data from the Warfarin versus Aspirin for Symptomatic Intracranial Disease (WASID) trial, a randomized, double-blind, multicenter study that included 569 patients with transient ischemic attack or ischemic stroke due to 50% to 99% stenosis of a major intracranial artery. Median time from qualifying event to randomization was 17 days, and mean follow-up was 1.8 years.

Subsequent ischemic stroke occurred in 106 patients, and 77 of the incidents occurred in the territory of the stenotic artery. Stroke risk in this territory was highest in patients with severe stenosis of 70% and greater, as well as in patients enrolled within 17 days after the qualifying event. Factors such as location of stenosis, type of qualifying event, and prior use of antithrombotic medications were not associated with increased risk. In addition, the researchers found that the overall rates of stroke in the territory of the stenotic artery were 11% at one year and 14% at two years, despite the use of either warfarin or aspirin and vascular risk factor modification.

"The increased risk with severe stenosis validates the findings of the retrospective WASID pilot study and parallels the findings of symptomatic extracranial carotid artery stenosis trials," the researchers commented. "Furthermore, risk increased linearly with percent stenosis, except perhaps among patients with stenosis 90% to 99%."

The researchers’ observations "suggest that potential intervention should be considered very soon after clinical presentation, unless early intervention also increases the short-term risk," they noted. "In contrast, if a patient presents for evaluation relatively late after the initial symptom, without intercurrent events, then perhaps a more conservative approach is warranted."

Due to the high risk of stroke in patients who were randomized soon after their qualifying events, the researchers stressed the importance of early identification of intracranial stenosis for prognosis and possible intervention.

Kasner SE, Chimowitz MI, Lynn MJ, et al. Predictors of ischemic stroke in the territory of a symptomatic intracranial arterial stenosis. Circulation. 2006; 113:555-563.

ANTIPLATELET USE MAY NOT INCREASE INTRACEREBRAL HEMORRHAGE RISK

Although antiplatelet agent use is relatively common following intracerebral hemorrhage, it may not be associated with a large increased risk of intracerebral hemorrhage recurrence, as reported in the January 24 Neurology. Anand Viswanathan, MD, PhD, and colleagues noted that their results "have potential implications for the treatment of intracerebral hemorrhage survivors who are also at risk for ischemic cardiovascular diseases."

The investigators gathered data from a single-center prospective cohort study in which 207 consecutive survivors of primary intracerebral hemorrhage were followed up by telephone interview and recurrent intracerebral hemorrhage and postindex antiplatelet agent use and duration were recorded. In addition, participants were later stratified according to presence of lobar (127 patients) or deep (80 patients) intracerebral hemorrhage.

Results showed that exposure to antiplatelets occurred in 46 survivors of intracerebral hemorrhage; of these, 37 patients were not taking antiplatelets at hospital discharge after the index intracerebral hemorrhage but began taking them a median of 5.4 months after index intracerebral hemorrhage. Among the 77 survivors of 127 patients with lobar intracerebral hemorrhage who underwent MRI, the number of baseline hemorrhages was not associated with the risk of exposure to antiplatelets.

Ischemic cardiovascular events occurred during follow-up in 11 participants, four of whom were taking antiplatelets. Antiplatelet agents were not associated with a reduction in ischemic cardiovascular events and were prescribed in 22% of intracerebral hemorrhage survivors, most commonly for prevention of ischemic heart disease. Antiplatelet agent use was not associated with intracerebral hemorrhage recurrence in survivors of either lobar hemorrhage or of deep hemorrhage.

"Antiplatelets may be used in selected intracerebral hemorrhage survivors without a substantial increase in the risk of recurrent intracerebral hemorrhage," the investigators pointed out. They added that the estimated risk was within the range in which aspirin was a potentially useful strategy for improving quality of life.

However, Dr. Viswanathan and colleagues cautioned that antiplatelet exposure was not randomly assigned and may have been confounded by the indication for antiplatelet use. As "these estimated risks are not based on evidence from a randomized trial and are therefore vulnerable to the possibility of confounding, it remains prudent for antiplatelets to be considered only in selected intracerebral hemorrhage survivors at high risk for thrombotic diseases." The investigators stressed that a randomized clinical trial may be required to ascertain "definitive determination of the relative risk and benefit of antiplatelet therapy in intracerebral hemorrhage survivors at risk for ischemic events."

Viswanathan A, Rakich SM, Engel C, et al. Antiplatelet use after intracerebral hemorrhage. Neurology. 2006;66:206-209.

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