Low Ankle-Brachial Index is a Simple Physical Exam Sign Predicting Intracranial Atherosclerotic Stenosis in Ischemic Stroke Patients.

BACKGROUND: The investigation of ischemic stroke etiology is commonly limited to the heart and extracranial vessels. Nevertheless, the diagnosis of intracranial stenosis may carry important therapeutic implications. The aims of this study were to determine the prevalence and clinical predictors of intracranial atherosclerotic stenosis (ICAS) in a sample of patients with ischemic stroke. METHODS: Consecutive patients admitted to a university-based outpatient stroke clinic underwent CT angiography of the intracranial and extracranial brain vessels. Clinical, demographic, and laboratory characteristics were compared between patients with increasing levels of stenosis. Ankle-brachial index (ABI) was measured to quantify peripheral arterial disease, defined as an ABI less than or equal to .9. Multivariable ordinal logistic regression was constructed to predict increasing stenosis grades (none, 1%-49%-mild, 50%-69%-moderate, 70%-100%-severe). RESULTS: We studied 106 subjects, mean age 62 ± 15 years, 54% female. ICAS was present in 38 (36%) patients: 19 (50%) mild, 7 (18%) moderate, and 12 (32%) severe. Of 74 patients where ABI was measured, low ABI was found more frequently with increasing ICAS severity (26%, 42%, 67%, and 89% of patients with none, mild, moderate, and severe ICAS, respectively). In univariable analysis, higher age, presence of diabetes, abdominal obesity, and low ABI correlated with increasing stenosis grades. In multivariable analysis, only low ABI remained independently associated with increasing stenosis grades. CONCLUSIONS: The ABI is independently associated with increasing severity of ICAS, making it a potentially useful triaging tool for more invasive test selection.

Chagas disease is an independent predictor of stroke and death in a cohort of heart failure patients.

BACKGROUND AND AIMS: Chagas disease is a common cause of heart failure (HF) and death in developing countries. Although stroke is known to occur in these patients, an accurate estimate of stroke incidence is lacking. We aimed to determine the incidence of stroke and death in patients with HF, comparing Chagas and non-Chagas etiologies. METHODS: Cohort of stroke-free patients with HF (Framingham criteria) followed in a university-based outpatient clinic in Brazil. Baseline characteristics included sociodemographic, risk factor assessment, echocardiographic and electrocardiographic findings. Chagas disease was defined by appropriate serologic tests. Cause-specific Cox regression was used to search for predictors of stroke or death as separate outcomes. RESULTS: We studied 565 patients with HF between January 2003 and December 2018, mean age 54.3 ± 12.9 years, 305 (54.0%) females, 271/535 (50.7%) with Chagas disease. Chagas patients were older (55.5 vs. 53.1 years), more frequently women (60.5% vs. 47.3%), less frequently harbored coronary artery disease (14.5% vs. 34.1%) when compared to non-Chagas patients. Echocardiography showed more severe disease among non-Chagas patients [median left ventricle ejection fraction (LVEF) 37.3% vs. 47.0%]. Over a mean 42.9 (±34.4) months, we followed 404 (71.5%) patients, completing 1442 patient-years of follow-up. Stroke incidence was higher in Chagas when compared to non-Chagas patients (20.2 vs. 13.9 events per 1000 patient-years), while death rate was similar (41.6 vs. 43.1 deaths per 1000 patient-years). In the multivariable analysis for stroke outcome adjusted for LVEF and arrhythmias, cause-specific hazard ratio (CSHR) for Chagas was 2.54 (95% confidence interval 1.01-6.42, p = 0.048). Chagas disease was also associated with increased risk of death (CSHR 1.83; 95% confidence interval 1.04-3.24, p = 0.037). CONCLUSION: Chagas disease is associated with increased risk of stroke and death when compared to other etiologies of HF, independently of HF severity or cardiac arrhythmias, suggesting other factors contribute to increased stroke risk and mortality in Chagas disease. Early prevention and treatment of Chagas disease is imperative to reduce a later risk of stroke in endemic areas.

Association Between Risk of Obstructive Sleep Apnea and Cerebrovascular Reactivity in Stroke Patients.

Background Obstructive sleep apnea (OSA) is present in 60% to 70% of stroke patients. Cerebral vasoreactivity in patients with stroke and OSA has not been well studied and could identify a new pathophysiologic mechanism with potential therapeutic intervention. We aimed to determine whether risk categories for OSA are associated with cerebral vasoreactivity in stroke patients. Methods and Results In this cross-sectional study of a cohort of patients with stroke, we used clinical questionnaires (Sleep Obstructive Apnea Score Optimized for Stroke [SOS] and snoring, tiredness, observed, pressure, bmi, age, neck, gender [STOP-BANG] scores) to assess the risk of OSA and transcranial Doppler to assess cerebral vasoreactivity (breath-holding index and visual evoked flow velocity response). Of the 99 patients included, 77 (78%) had medium or high risk of OSA and 80 performed transcranial Doppler. Mean breath-holding index was 0.52±0.37, and median visual evoked flow velocity response was 10.8% (interquartile range: 8.8-14.5); 54 of 78 (69%) showed impaired anterior circulation vasoreactivity (breath-holding index <0.69) and 53 of 71 (75%) showed impaired posterior circulation vasoreactivity (visual evoked flow velocity response ≤14.0%). There was a significant negative correlation between the risk of OSA calculated by STOP-BANG and the breath-holding index (rS=-0.284, P=0.012). The following variables were associated with low anterior circulation vasoreactivity: dyslipidemia (odds ratio: 4.7; 95% CI, 1.5-14.2) and STOP-BANG score (odds ratio: 1.7 per 1-point increase; 95% CI, 1.1-1.5). Conclusions A high risk of OSA and impaired vasoreactivity exists in the population that has had stroke. Dyslipidemia and STOP-BANG sleep apnea risk categories were independently associated with impaired anterior circulation vasoreactivity.