BackgroundAlthough anxiety and depression have been classified as distinct traits of affective disorders, previous studies have reported their co-occurrence in subjects with migraine. However, few reports are available on the clinical implications of this comorbidity. This study is to assess the comorbidity of anxiety and depression in subjects with migraine and its clinical implications in a population-based sample from Korea.MethodsWe selected Korean subjects aged 19–69 years by the stratified random sampling method, and evaluated them using a semi-structured interview, designed to identify headache type, anxiety, and depression. We used Goldberg Anxiety Scale questions and Patient Health Questionnnaire-9 for the diagnosis of anxiety and depression, respectively.ResultsOf the 2,762 participants who completed the interview, 147 subjects (5.4%) were classified as having a migraine during the previous year. Among these 147 subjects, 17 (11.6%) had anxiety and depression, 28 (19.0%) had anxiety alone, 9 (6.1%) had depression alone, and 93 (63.3%) had neither anxiety nor depression. Headache frequency per month was remarkably higher in subjects having migraine with anxiety and depression (median [25–75 percentile values], 8.0 [2.5–21.0]) than in those having migraine with anxiety alone (2.0 [1.0–5.0], p = 0.003), migraine with depression alone (1.0 [0.3–4.0], p = 0.001), and migraine without anxiety or depression (1.0 [0.3–3.0], p < 0.001). The migraine with anxiety alone (7.0 [6.0–8.0], p = 0.011) group and migraine with anxiety and depression (7.0 [5.0–9.0], p = 0.018) group showed higher Visual Analogue Scale scores for pain intensity compare to migraine without anxiety or depression (6.0 [5.0-7.0]) group.ConclusionsApproximately 1/3 of migraineurs with anxiety had depression and 2/3 of migraineurs with depression had anxiety. Combination of anxiety and depression was associated with an increased headache frequency. Anxiety was associated with exacerbation of headache intensity.Electronic supplementary materialThe online version of this article (doi:10.1186/s12883-014-0238-4) contains supplementary material, which is available to authorized users.
BackgroundStroke in cancer patients is not rare but is a devastating event with high mortality. However, the predictors of mortality in stroke patients with cancer have not been well addressed. D-dimer could be a useful predictor because it can reflect both thromboembolic events and advanced stages of cancer.AimIn this study, we evaluate the possibility of D-dimer as a predictor of 30-day mortality in stroke patients with active cancer.MethodsWe included 210 ischemic stroke patients with active cancer. The 30-day mortality data were collected by reviewing medical records. We also collected follow-up D-dimer levels in 106 (50%) participants to evaluate the effects of treatment response on D-dimer levels.ResultsOf the 210 participants, 30-day mortality occurred in 28 (13%) patients. Higher initial NIHSS scores, D-dimer levels, and CRP levels as well as frequent cryptogenic mechanism, systemic metastasis, multiple vascular territory lesion, hemorrhagic transformation, and larger infarct volume were related to 30-day mortality. In the multivariate analysis, D-dimer [adjusted OR (aOR) = 2.19; 95% CI, 1.46–3.28, P < 0.001] predicted 30-day mortality after adjusting for confounders. The initial NIHSS score (aOR = 1.07; 95% CI, 1.00–1.14, P = 0.043) and hemorrhagic transformation (aOR = 3.02; 95% CI, 1.10–8.29, P = 0.032) were also significant independent of D-dimer levels. In the analysis of D-dimer changes after treatment, the mortality group showed no significant decrease in D-dimer levels, despite treatment, while the survivor group showed the opposite response.ConclusionsD-dimer levels may predict 30-day mortality in acute ischemic stroke patients with active cancer.
Background There is insufficient evidence on the effect of statins, particularly high‐intensity statins, in patients with acute ischemic stroke and atrial fibrillation. We investigated the impact of statins on the outcomes in these patients, including those who might be vulnerable to statin therapy and those without clinical atherosclerotic cardiovascular diseases. Methods and Results A total of 2153 patients with acute ischemic stroke and atrial fibrillation were enrolled in the present nationwide, multicenter, cohort study. The primary composite end point was the occurrence of net adverse clinical and cerebral events ( NACCE ; death from any cause, stroke, acute coronary syndrome, or major bleeding) over a 3‐year period based on statin intensity. NACCE rates were lower in patients receiving low‐ to moderate‐intensity (adjusted hazard ratio 0.64; 95% CI : 0.52‐0.78) and high‐intensity statins (hazard ratio 0.51; 95% CI 0.40‐0.66) than in those not receiving statin therapy. High‐intensity statins were associated with a lower risk for NACCE than low‐ to moderate‐intensity statins (hazard ratio 0.76; 95% CI 0.59‐0.96). Subgroup analyses showed that the differences in hazard ratio for 3‐year NACCE favored statin use across all subgroups, including older patients, those with low cholesterol levels, patients receiving anticoagulants, and patients without clinical atherosclerotic cardiovascular diseases. Magnified benefits of high‐intensity statins compared with low‐ to moderate‐intensity statins were observed in patients who underwent revascularization therapy and those under 75 years of age. Conclusions Statins, particularly high‐intensity statins, could reduce the risk for NACCE in patients with acute ischemic stroke and atrial fibrillation; this needs to be further explored in randomized controlled trials.
. Among the 4175 subjects who were registered in the Korea University Stroke Registry during the study period, 661 first-ever ischemic stroke patients with cardioembolic stroke were initially recruited. We sequentially excluded 70 patients who were lost to follow-up <30 days from discharge, 33 with incomplete data, and 23 who died during admission. Finally, data from 535 patients were analyzed ( Figure I in the online-only Data Supplement). All patients had ≥1 potential sources of cardioembolism, and AF was the most common potential source (Table I in the online-only Data Supplement). Because the main exposure of the present study was statin therapy after stroke occurrence, we classified the patients into 2 groups: the statin and nonstatin groups. The statin group was further divided into high-potency and low-potency statin groups. The high-potency statin group was defined by patients who were prescribed a dose and type of statin that was expected to reduce the initial low-density lipoprotein cholesterol level >50% (atorvastatin 40 mg, atorvastatin 80 mg, rosuvastatin 10 mg, rosuvastatin 20 mg, and simvastatin/ezetimibe 20/10 mg or 40/10 mg). 6The primary outcomes in this study were time to mortality from any cause and time to recurrent stroke. Therefore, the association between statin therapy and mortality or recurrent stroke in cardioembolic stroke was analyzed using Kaplan-Meier estimation and univariable and multivariable Cox proportional regression with subgroup analyses. In the multivariable model, variables with significant P values (<0.05) in univariable analysis, including National Institutes of Health Stroke Scale at admission and use of anticoagulants, were included with stepwise method. Finally, the effects of statins in patients with cardioembolic stroke were compared with those in patients with noncardioembolic stroke. For these analyses, we recruited 2116 subjects with noncardioembolic stroke who registered in the Korea University Stroke Registry during the study period ( Figure I in the online-only Data Supplement). All statistical analyses were performed Background and Purpose-The objective of this study was to investigate the potential benefits of statin therapy on mortality and stroke recurrence after cardioembolic stroke. Methods-In this retrospective observational study, we analyzed data from 535 patients with first-ever cardioembolic stroke.Patients were classified into nonstatin, low-potency statin, and high-potency statin groups. The primary outcomes were time to mortality and time to recurrent stroke. Results-The mean duration of follow-up was 22.2 months. The cumulative mortality rate was 7% at the end of the first year and 10% at the end of the third year. Statin therapy was independently associated with reduced mortality (hazard ratio, 0.237; 95% confidence interval, 0.080-0.703 for nonstatin versus low-potency statin; hazard ratio, 0.158; 95% confidence interval, 0.037-0.686 for nonstatin versus high-potency statin). Statin treatment did not affect the incidence of recurrent stroke i...
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