Carotid webs exhibit a strong association with ischemic stroke, and their presence should be suspected in patients lacking other risk factors, particularly African American women.

Background and Purpose: Few studies have examined the dose-response and temporal relationships between marijuana use and ischemic stroke while controlling for important confounders, including the amount of tobacco smoking. The purpose of our study was to address these knowledge gaps. Methods: A population-based case-control study with 1090 cases and 1152 controls was used to investigate the relationship of marijuana use and early-onset ischemic stroke. Cases were first-ever ischemic stroke between the ages of 15 and 49 identified from 59 hospitals in the Baltimore-Washington region. Controls obtained by random digit dialing from the same geographic region were frequency-matched to cases by age, sex, region of residence and, except for the initial study phase, race. After excluding subjects with cocaine and other vasoactive substance use, the final study sample consisted of 751 cases and 813 controls. All participants underwent standardized interviews to characterize stroke risk factors and marijuana use. Unconditional logistic regression analysis was used to assess the relationships between marijuana use and risk of ischemic stroke, adjusting for age, sex, race, study phase, the amount of current tobacco smoking, current alcohol use, hypertension, and diabetes. Results: After adjusting for other risk factors, including the amount of current tobacco smoking, marijuana use was not associated with ischemic stroke, regardless of the timing of use in relationship to the stroke, including ever use, use within 30 days, and use within 24 hours. There was a nonsignificant trend towards increased stroke risk among those who smoked marijuana at least once a week (odds ratio, 1.9 [95% CI, 0.8–4.9]). Conclusions: These analyses do not demonstrate an association between marijuana use and an increased risk of early-onset ischemic stroke, although statistical power was limited for assessing the association among very heavy users.

No abstract

No abstract

BackgroundOutcome of patients transplanted with hepatitis C (hep-C) donor hearts has been reported to be poor. Induction therapy may confer increased risk to these patients. The outcome of hep-C in a noninduction cardiac transplant (CTx) population has not been established.MethodsWe reviewed 455 patients between 1/1994 and 3/2002. We found 18 patients who received hep-C donor hearts. 8 patients were status IA, and 10 were on our alternate CTx waiting list, which justified the use of these donor organs at that time. 5 of these patients were also hep-C positive prior to transplant (after undergoing liver biopsy demonstrating only mild disease). All patients were treated with cyclosporine/tacrolimus, and 12 also received azathioprine (AZA) while 6 received mycophenolate mofetil (MMF) without cytolytic induction therapy.ResultsThe 18 patients who received a hep-C-positive donor heart had significantly lower 1- and 5-year survival compared to CTx patients without hep-C (1-year survival 77.8% vs 81.2%, p = .028; 5-year survival 38.9% vs 71.9%, p = .007). The development of rejection and cardiac allograft vasculopathy (CAV) were not significantly increased compared to the control group. The 5 patients who were hep-C positive at the time of transplant had similar poor outcomes (5-year survival 20%). However, 4 of these 5 hep-C-positive recipients developed CAV compared to 1/13 hep-C-negative recipients. All patients were divided into those patients receiving AZA vs MMF immunosuppression, but there was no significant difference in outcomes between the use of these medications.ConclusionDonor or recipient hep-C is associated with poor outcome in CTx patients with noninduction immunosuppressive regimens. Donor hearts with hep-C should not be used. In addition, hep-C-positive recipients appear to be at higher risk for the development of CAV.