Sleep disordered breathing (SDB) is highly prevalent, but frequently unrecognized among stroke patients. Polysomnography (PSG) is difficult to perform soon after a stroke. We evaluated the use of screening questionnaires and portable sleep testing (PST) for patients with acute stroke, subarachnoid hemorrhage, or transient ischemic attack to expedite SDB diagnosis and management. We performed a single-center retrospective analysis of a quality improvement study on SDB screening of consecutive daytime, weekday, adult admissions to a stroke unit. We excluded patients who were unable to communicate and lacked available family members. Patients were screened with the Epworth Sleepiness Scale, Berlin Questionnaire, and STOP-BANG Questionnaire and underwent overnight PST and/or outpatient PSG. The 4-item STOP Questionnaire was derived from STOP-BANG for a secondary analysis. We compared the sensitivity and specificity of the questionnaires for the diagnosis of at least mild SDB (apnea hypopnea index (AHI) ≥5) on PST and correlated AHI measurements between PST and PSG using the Spearman correlation. Out of sixty-eight patients included in the study, 54 (80%) were diagnosed with SDB. Only one (1.5%) had a previous SDB diagnosis. Thirty-three patients completed all questionnaires and a PST. The STOP-BANG questionnaire had the highest sensitivity for at least mild SDB (0.81, 95% CI (confidence interval): 0.65–0.92) but a low specificity (0.33, 95% CI 0.10, 0.65). The discrimination of all questionnaires was overall poor (C statistic range 0.502–0.640). There was a strong correlation (r = 0.71) between the AHI results estimated using PST and outpatient PSG among 28 patients. The 4-item STOP Questionnaire was the easiest to administer and had a comparable or better sensitivity than the other questionnaires. Inpatient PSTs were useful for screening in the acute setting to facilitate an early diagnosis of SDB and to establish further outpatient evaluations with sleep medicine.

Background: Cerebral microbleeds (CMB) signal cerebral small vessel disease and are associated with ischemic stroke (IS) incidence, recurrence, and complications. While illicit drug use (IDU) is associated with cerebral small vessel disease, the association between CMB and IDU is understudied. We sought to delineate differences in vascular risk factors between IDU and CMB and determine the effect of this relationship on outcomes in IS/transient ischemic attack (TIA) patients. Methods: We included 2001 consecutive IS and TIA patients (years 2009-2018) with a readable T2*gradient-echo MRI sequence. CMB rating followed standardized guidelines and CMB were grouped topographically into lobar, deep or infratentorial. IDU data (history and/or urine toxicology) was available for 1746 patients. The adverse composite outcome included pneumonia, urinary tract infection, deep venous thrombosis or death during hospitalization. Good functional outcome was defined as modified Rankin scale score < 3 and ambulatory on discharge. Univariate analysis was used to assess vascular risk factors and multivariable logistic regression was used to characterize the IDU/CMB relationship on outcomes. Results: We observed IDU in 13.8 % (n=241), and CMB in 32.9% (n=575, 53.8% lobar, 27.3% deep and 18.8% infratentorial). Patients with IDU and at least one CMB were older (53.6±10.5 vs. 56.9±11.5, p=0.04), had a lower BMI (28.1±5.9 vs. 26.6±4.4, p=0.04), and were more likely to have had a previous IS/TIA (25.1% vs. 41.9%, p=0.01). IDU trended higher for those with severe CMB (10+) compared with those without CMB and 1-9 CMB (25% [n=9] vs 14.3% [n=1171] and 12.1% [n=65] respectively; p=0.07) without individual drug deviations from this pattern. Adverse and good functional outcomes were observed in 177 and 905 total patients, respectively. No significant interaction was observed between IDU and CMB with either adverse or functional composite outcomes. Conclusion: IDU prevalence was high in our urban study population, and showed a borderline association with increasing CMB burden. Patients with CMB and IDU history were older and more likely to have had a previous IS/TIA. Further studies are required to clarify the clinical consequences related to the relationship between IDU and CMB.

Background: Cerebral microbleeds (CMB) are associated with dementia and stroke. CMB are attributed to cerebral amyloid angiopathy (lobar CMB), and hypertensive angiopathy (deep CMB). Racial minorities (RM) have a higher prevalence and poorer control of vascular risk factors, thus CMB may differ in prevalence and distribution in RM. We determined the prevalence, burden and vascular risk factors of CMB across racial groups in patients with stroke and transient ischemic attack, and CMB influence in short term outcomes. Methods: We included 2001 consecutive (year 2009-2018) patients with a readable T2*gradient-echo MRI sequence. CMB rating followed standardized guidelines and grouped topographically into lobar, deep or infratentorial. Race was self-reported based on U.S. census procedures and categorized as White, Black or Other racial groups (ORG). Univariate analyses were done to compare vascular risk factors between CMB groups, and multivariate logistic regression analyses were used to relate CMB and short term functional (modified Ranking scale score <3 vs. higher) and adverse hospital outcomes (pneumonia, UTI, DVT, death), across racial groups. Results: We observed CMB in 679 (34%) patients. The respective distribution in lobar, deep and infratentorial regions were: Whites (n=174; 67.2%, 20.7% and 12%); Blacks (n=374; 53%, 28.4% and 18.5%); ORG (n=131; 45.5%, 25.3% and 29.3%). Blacks and ORG with CMB were younger than Whites (66 and 66 vs 70; p<0.01); and had higher prevalence of diabetes (44% and 41% vs 28%, p<0.01). Blacks had higher prevalence of previous stroke when compared with Whites (36% vs 27%, p<0.05). Patients with 10+ CMB, compared with no CMB and 1-9 CMB, had higher in-hospital pneumonia (8% vs 2.1% and 2.4% respectively; p=0.02) and were less likely to have mRS 0-2 at discharge (44.8% vs 55.3% and 48.7%; p=0.06). No difference was observed in mortality and other hospital adverse events. Conclusion: Racial minorities had higher proportion of CMB in non-lobar regions, suggesting that RM are more likely to have hypertensive angiopathy. RM with CMB were younger and differed in several risk factors compared to Whites. High CMB burden affected adversely outcomes. Further studies are needed to better characterize the clinical impact of CMB in RM.

Hypertension is highly prevalent and morbid in the chronic kidney disease population, and blood pressure (BP) targets for this population are unclear. We aimed to compare all-cause mortality outcomes with intensively targeting systolic BP to <130 mm Hg versus a standard of <140 mm Hg. Individual patient data from 4983 chronic kidney disease patients with hypertension were pooled from 4 multicenter randomized control trials—AASK (African American Study of Kidney Disease and Hypertension), ACCORD (Action to Control Cardiovascular Risk in Diabetes), MDRD (Modification of Diet in Renal Disease), and the SPRINT (Systolic Blood Pressure Intervention Trial). Patients were assigned their trial-assigned randomized intervention group—standard (n=2474) versus intensive (n=2509) BP targets. Additional analyses included excluding patients with a glomerular filtration rate ≥60 mL/min per 1.73 m 2 along with those undergoing intensive glycemic control. The primary outcome was all-cause mortality. Average achieved BP was 125.0 mm Hg in the intensive group and 136.9 mm Hg in the standard group. In the primary analysis, the all-cause mortality rate trended towards improved outcomes with intensive treatment but was not statistically significant (hazard ratio: 0.87 [0.69–1.08]; P =0.21). One hundred seventy-three of 2474 patients (1.95% per year) in the standard group and 153 of 2509 patients (1.71% per year) in the intensive group died. After excluding patients with higher glomerular filtration rate values and those undergoing intensive glycemic control, there was a statistically significant decrease in all-cause mortality rate (hazard ratio: 0.79 [0.63–1.00]; P =0.048). An intensive BP target of <130 mm Hg decreases all-cause mortality when compared with a standard target of <140 mm Hg in patients with chronic kidney disease stage 3 or greater who are not undergoing intensive glycemic therapy.

Hypertension is highly prevalent and morbid in the chronic kidney disease population, and blood pressure (BP) targets for this population are unclear. We aimed to compare all-cause mortality outcomes with intensively targeting systolic BP to <130 mm Hg versus a standard of <140 mm Hg. Individual patient data from 4983 chronic kidney disease patients with hypertension were pooled from 4 multicenter randomized control trials—AASK (African American Study of Kidney Disease and Hypertension), ACCORD (Action to Control Cardiovascular Risk in Diabetes), MDRD (Modification of Diet in Renal Disease), and the SPRINT (Systolic Blood Pressure Intervention Trial). Patients were assigned their trial-assigned randomized intervention group—standard (n=2474) versus intensive (n=2509) BP targets. Additional analyses included excluding patients with a glomerular filtration rate ≥60 mL/min per 1.73 m2 along with those undergoing intensive glycemic control. The primary outcome was all-cause mortality. Average achieved BP was 125.0 mm Hg in the intensive group and 136.9 mm Hg in the standard group. In the primary analysis, the all-cause mortality rate trended towards improved outcomes with intensive treatment but was not statistically significant (hazard ratio: 0.87 [0.69–1.08]; P=0.21). One hundred seventy-three of 2474 patients (1.95% per year) in the standard group and 153 of 2509 patients (1.71% per year) in the intensive group died. After excluding patients with higher glomerular filtration rate values and those undergoing intensive glycemic control, there was a statistically significant decrease in all-cause mortality rate (hazard ratio: 0.79 [0.63–1.00]; P=0.048). An intensive BP target of <130 mm Hg decreases all-cause mortality when compared with a standard target of <140 mm Hg in patients with chronic kidney disease stage 3 or greater who are not undergoing intensive glycemic therapy.

Background: Cortical Superficial Siderosis (cSS) detected on brain MRI affects 0.7% of the general population. In studies of predominantly White individuals, cSS is considered a sensitive marker of cerebral amyloid angiopathy (CAA) associated with increased risk of intracerebral hemorrhage. However, its prevalence and predictors in ischemic stroke (IS) —particularly in African Americans (AA)—has not been well studied. We sought to characterize the prevalence and vascular risks associated with cSS in AA with IS and transient ischemic attack (TIA). Methods: We included 2001 consecutive (year 2009-2018) IS and TIA patients, wherein 1048 patients (52%) were AA with available T2*gradient-echo MRI sequence. cSS rating was performed according to standardized guidelines. Race was determined by self-report based on U.S. census procedures, categorized as White, AA or Other racial groups (ORG). Vascular risk factors included age, diabetes, hypertension, systolic blood pressure (SBP), dyslipidemia, BMI, smoking, prior stroke, coronary artery disease; and illicit drug use (IDU). Differences in associations with cSS were assessed using univariate analyses. Results: We observed cSS in 1.15% (n=23) of AA, 0.4% (n=9) Whites and 0.6% (n=12) ORG patients. Compared to Whites with cSS, AA were younger (63 vs. 69 years), had higher proportion of men (70 vs 56%), hypertension (83 vs 78%), IDU (22 vs 11%), higher SBP (166±33 vs 162±15mmHg), and lower CAD prevalence (13 vs 33%), although differences did not reach statistical significance. Compared to AA without cSS, AA with cSS had higher proportion of men (69.6 vs 49.7%), prior stroke (39.1 vs 29.7%), IDU (21.7 vs 12.9%), and higher SBP (166±33 vs 153±37mmHg), the latter being the only statistically significant (p=0.038). The remaining vascular risk factors did not differ in patients with and without cSS, or between racial groups. Conclusion: The prevalence of cSS in AA with IS/TIA at our urban center is higher than in the general population and higher than in Whites. The vascular risk factor profile seems to differ between AA and White patients with and without cSS. Our results may be relevant in studies of cSS in AA wtih IS/TIA patients as the underlying angiopathy may not represent CAA, but require replication in larger samples.

Optimal blood pressure (BP) targets for different populations, especially diabetics, remain uncertain after conflicting data on intensive management. We assessed whether a <120 mm Hg systolic target is beneficial and whether certain patient populations differ in response. Individual patient data of 14 094 patients from 2 randomized control trials was pooled. Seven thousand forty patients were assigned to an intensive target of <120 mm Hg and 7054 patients to a standard target of <140 mm Hg in an intention-to-treat analysis. The primary outcome was a composite of myocardial infarction, other acute coronary syndromes, stroke, heart failure, and cardiovascular mortality. Interactions between treatment and baseline characteristics were assessed. Secondary outcomes included nonfatal myocardial infarction, stroke, heart failure, cardiovascular mortality, and overall mortality. Intensive management significantly lowered primary outcome rate (hazard ratio, 0.83; 95% confidence interval, 0.74–0.92; P <0.001). No significant interaction was observed between treatment effect and diabetes mellitus status ( P =0.16). Significantly reduced secondary outcomes included stroke (hazard ratio, 0.75; P =0.033) and heart failure (hazard ratio, 0.76; P =0.014). No significant interactions were observed between treatment effect and baseline age, sex, race, cardiovascular disease history, systolic BP, or diastolic BP ( P values: 0.40, 0.95, 0.54, 0.18, 0.86, and 0.67, respectively). BP targets of <120 mm Hg improved cardiovascular outcomes. Diabetic patients responded similarly to this intervention, as did those with different age, sex, cardiovascular disease history, baseline BPs, and race. The intensive group had increased risk of intervention-related adverse outcomes (3.97% versus 1.53%; P <0.001). Clinicians should consider <120 mm Hg systolic targets for a variety of patients, including diabetics.

Introduction: Current evidence is conflicting on whether intensive blood pressure (BP) management, specifically with targets of <130/90 mmHg, produces a mortality benefit in non-diabetic chronic kidney disease (CKD) patients. MDRD, AASK, and SPRINT are the largest randomized controlled trials available investigating intensive targets in CKD patients. The MDRD and AASK recruited exclusively CKD patients, while SPRINT had a large CKD subpopulation within its cohort. MDRD assigned patients to a standard mean arterial pressure (MAP) target of 107 mmHg vs. an intensive target of 92 mmHg (achieved BPs of 134/81 mmHg vs 126/77 mmHg, respectively). AASK assigned African American patients to a MAP of 102-107 mmHg vs. <92 mmHg (achieved BPs of 141/85 mmHg vs. 128/78 mmHg, respectively). SPRINT compared a systolic target of 140 mmHg vs. 120 mmHg (achieved BPs of 137/74 vs. 123/67 in the CKD subpopulation). Our study pools individual patient data (IPD) from these three trials. Methods: IPD for all patients in MDRD, AASK, and SPRINT were obtained and screened for non-diabetic CKD patients. The resulting 4537 patients were assigned to their original randomized intervention group – 2258 patients to the standard group and 2279 to the intensive group. The primary outcome was mortality. Statistical analysis for primary outcome was performed with Cox proportional hazards models stratified by clinical site/center. Interactions between outcome and trial enrollment were also assessed. Results: There was no statistically significant difference in mortality rate between intensive and standard BP control (HR: 0.84; 95% CI: 0.66, 1.07; p = 0.148). 126 patients (5.5%) in the intensive group and 149 patients (6.6%) in the standard group expired. No interaction was present between treatment and trial enrollment (MDRD, AASK, SPRINT) (p-value of interaction: 0.080). Conclusion: Intensive BP targets do not improve mortality for non-diabetic patients with CKD. Further investigation needs to be performed to determine if this lack of benefit is consistent across subpopulations.

Introduction: Systolic Blood Pressure Intervention Trial (SPRINT) determined that among non-diabetic patients with increased CV risk, intensive management of systolic blood pressure (SBP) to a target of 120 mmHg resulted in lower rates of CV events and all-cause mortality, as opposed to the standard goal of 140 mmHg. Current management of BP in the CKD population shows conflicting evidence on target SBP. With the use of patient-level SPRINT data, our study investigates the risks and benefits of intensive BP management in patients with CKD at baseline and is the largest study of intensive BP management in CKD patients (n=2646). Methods: The similarity between CKD patients in standard and intensive blood pressure management groups with regard to age, race, gender, estimated GFR (eGFR), and baseline SBP were assessed and no differences were found between the two groups. Differences in mortality, adverse events, and rates of achieving BP targets in intensive and standard BP management groups were examined. Cox proportional-hazards models were used for the events analysis. Multiple linear regression was used to assess the differences in achieving BP targets. Results and Discussion: We highlight three key findings. First, the average post-management SBP was higher in CKD patients than in non-CKD patients in both standard ( p = 0.017) and intensive ( p < .001) groups, controlling for age, race, gender, eGFR, and baseline SBP, possibly indicating greater difficulty in controlling BP in CKD patients . Second, intensively-treated CKD patients had increased risks for intervention-related adverse events, including events that resulted in disability, hospitalization, or harm that may have required medical or surgical intervention (p < .001). They also experienced higher rates of AKI related adverse events (p<.008). Third, intensive management showed a mortality benefit (HR: .725; 95% CI, .532 to .987), a finding that may help clarify conflicting reports in current literature. In conclusion, we present an analysis of CKD-specific SPRINT data in order to elucidate the clinical benefits and risks of intensive BP management in the CKD population.