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.

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; <0.001). No significant interaction was observed between treatment effect and diabetes mellitus status (=0.16). Significantly reduced secondary outcomes included stroke (hazard ratio, 0.75; =0.033) and heart failure (hazard ratio, 0.76;=0.014). No significant interactions were observed between treatment effect and baseline age, sex, race, cardiovascular disease history, systolic BP, or diastolic BP ( 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%; <0.001). Clinicians should consider <120 mm Hg systolic targets for a variety of patients, including diabetics.

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) 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.