INTRODUCTION: We investigated the effect vigorous physical activity (VPA) on the risk of incident mild cognitive impairment (MCI) and probable dementia among individuals with high‐risk hypertension.METHODS: Baseline self‐reported frequency of VPA was categorized into low VPA (<1 session/week), and high VPA (≥1 session/week). We used multivariate Cox regression analysis to examine the association of VPA categories with incident MCI and probable dementia events.RESULTS: Participants in the high VPA category, compared with low VPA, experienced lower events rates (per 1000 person‐years) of MCI (13.9 vs 19.7), probable dementia (6.3 vs 9.0), and MCI/probable dementia (18.5 vs 25.8). In the multivariate Cox regression model, high VPA, compared with low VPA, was associated with lower risk of MCI, probable dementia, and MCI/probable dementia (HR [95% CI]: 0.81 [0.68–0.97], 0.80 [0.63–1.03], and 0.82 [0.70–0.96]), respectively.DISCUSSION: This study provides evidence that VPA may preserve cognitive function in high‐risk patients with hypertension.Highlights: Hypertension is associated with an increased risk of cognitive impairment Physical activity (PA) is associated with a lower risk of decline in cognition The effect of ≥1 sessions of vigorous‐intensity PA (VPA) per week was assessed This analysis included SPRINT MIND trial participants with high‐risk hypertension ≥1 VPA sessions/week was associated with lower risk of future cognitive impairment

BACKGROUND: Sarcopenia and hypertension are independently associated with worse cardiovascular disease (CVD) risk and survival. While individuals with sarcopenia may benefit from intensive blood pressure (BP) control, the increased vulnerability of this population raises concerns for potential harm. This study aimed to evaluate clinical and safety outcomes with intensive (target <120 mm Hg) versus standard (<140 mm Hg) systolic BP targets in older hypertensive adults with sarcopenia compared with nonsarcopenic counterparts in the SPRINT (Systolic Blood Pressure Intervention Trial). METHODS: Sarcopenia was defined using surrogates of the lowest sex-stratified median of the sarcopenia index (serum creatinine/cystatin C×100) for muscle wasting and gait speed ≤0.8 m/s for muscle weakness. Outcomes included CVD events, all-cause mortality, and serious adverse events. RESULTS: Of 2571 SPRINT participants with sarcopenia index and gait speed data available (aged ≥75 years), 502 (19.5%) met the criteria for sarcopenia, which was associated with higher risks of CVD events (adjusted hazard ratio, 1.49 [95% CI, 1.15–1.94]; P =0.003) and all-cause mortality (adjusted hazard ratio, 1.46 [95% CI, 1.09–1.94]; P =0.010). In participants with sarcopenia, intensive (versus standard) BP control nearly halved the risk of CVD events (adjusted hazard ratio, 0.57 [95% CI, 0.36–0.88]; P =0.012) without increasing serious adverse events. Similar risk reduction was seen for all-cause mortality in participants with sarcopenia (adjusted hazard ratio, 0.66 [95% CI, 0.41–1.08]; P =0.102), but the effect was only significant in those without chronic kidney disease. CONCLUSIONS: Older hypertensive adults with sarcopenia randomized to intensive BP control experienced a lower risk of CVD without increased adverse events compared with standard BP control. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01206062.

Background: The relationship between alcohol consumption and ectopic fat distribution, both known factors for cardiovascular disease, remains understudied. Therefore, we aimed to examine the association between alcohol consumption and ectopic adiposity in adults at risk for cardiovascular disease. Methods and Results: In this cross‐sectional analysis, we categorized alcohol intake among participants in MESA (Multi‐Ethnic Study of Atherosclerosis) as follows (drinks/day): 2 (heavy drinking), former drinking, and lifetime abstention. Binge drinking was defined as consuming ≥5 drinks on 1 occasion in the past month. Visceral, subcutaneous, and intermuscular fat area, pericardial fat volume, and hepatic fat attenuation were measured using noncontrast computed tomography. Using multivariable linear regression, we examined the associations between categories of alcohol consumption and natural log‐transformed fat in ectopic depots. We included 6756 MESA participants (62.1±10.2 years; 47.2% women), of whom 6734 and 1934 had chest computed tomography (pericardial and hepatic fat) and abdominal computed tomography (subcutaneous, intermuscular, and visceral fat), respectively. In adjusted analysis, heavy drinking, relative to lifetime abstention, was associated with a higher (relative percent difference) pericardial 15.1 [95% CI, 7.1–27.7], hepatic 3.4 [95% CI, 0.1–6.8], visceral 2.5 [95% CI, −10.4 to 17.2], and intermuscular 5.2 [95% CI, −6.6 to 18.4] fat but lower subcutaneous fat −3.5 [95% CI, −15.5 to 10.2]). The associations between alcohol consumption and ectopic adiposity exhibited a J‐shaped pattern. Binge drinking, relative to light‐to‐moderate drinking, was also associated with higher ectopic fat. Conclusions: Alcohol consumption had a J‐shaped association with ectopic adiposity. Both heavy alcohol intake and binge alcohol drinking were associated with higher ectopic fat.

Purpose of Review: Statins are the first-line treatment for hypercholesterolemia and play a key role in the prevention of cardiovascular disease (CVD). Current studies report mixed effects of statins on cognitive health, including harmful, neutral, and protective outcomes. However, these ongoing controversies about the potential cognitive adverse effects of statins may compromise their use in CVD prevention. Several factors may influence how statins affect cognition, including the unique cholesterol homeostasis in the brain, the limited permeability of the blood-brain barrier to lipoproteins, and the varying lipophilicity of different statins. This review examines the evidence linking statins to cognitive function and considers the effect of different dosages and treatment durations. Recent Findings: Earlier studies suggested cognitive disturbances with statins, but recent evidence does not strongly support a link between statins and cognitive impairment. In fact, observational studies suggest potential neuroprotective benefits, though biases like selection bias, confounding and reverse causation limit definitive conclusions. Two large randomized controlled trials, STAREE and PREVENTABLE, are underway, and their results are expected to address some of these gaps in the literature. Summary: Due to insufficient evidence in the current literature, well-designed randomized controlled trials are needed for a better understanding of statins’ effects on cognition. More data is needed regarding statin type, dose intensity, and treatment duration, which may affect cognitive outcomes. Future studies are also needed to examine how statins may affect cognition in specific high-risk groups, such as individuals with mild cognitive impairment, diabetes, cardiovascular disease, or chronic kidney disease.

Background: Subclinical myocardial injury (SCMI) is associated with an increased risk of poor cardiovascular disease (CVD) outcomes. Understanding the underlying risk factors for SCMI is crucial for the prevention and management of CVD. We hypothesized that atherogenic dyslipidemia, a combination of high triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C), is associated with an increased risk of SCMI. Methods: This analysis from the third National Health and Nutrition Examination Survey (NHANES-III) included 7093 participants (age 59.3 ± 13.4 years, 52.8% women, and 49.4% White) free of CVD. Atherogenic dyslipidemia was defined as TG ≥ 150 mg/dL and HDL-C < 40 mg/dL in men or <50 mg/dL in women. A validated electrocardiographic-based cardiac infarction injury score (CIIS) ≥ 10 was considered positive for SCMI. Multivariable logistic regression analysis was used to examine the association of different combinations of TG and HDL-C groups, including atherogenic dyslipidemia with SCMI. Results: About 22.5% (n = 1594) of participants had atherogenic dyslipidemia, and 26.3% (n = 1862) had SCMI. Compared to participants with normal TG and normal HDL-C, those with atherogenic dyslipidemia had a higher prevalence of SCMI (31.2% vs. 23.9%, p-value < 0.001). In a multivariable logistic regression model, atherogenic dyslipidemia was associated with the highest odds of SCMI followed by high TG/normal HDL-C, then low HDL-C/normal TG [OR (95% CI): 131 (1.14, 1.52), 1.13 (0.97, 1.33), and 1.01 (0.86, 1.20), respectively). Conclusions: Atherogenic dyslipidemia is associated with a higher risk of SCMI, which highlights the role of nontraditional risk factors in the development of subclinical CVD.

Atherogenic dyslipidemia (AD), characterized by low high-density lipoprotein cholesterol (HDL-C) and elevated triglycerides (TG), is associated with increased cardiovascular disease (CVD) risk. This study evaluates the association between AD and CVD in hypertension treated to systolic blood pressure(SBP) targets of <120 mmHg (intensive) or < 140 mmHg (standard). We included 9361 participants from the Systolic Blood Pressure Intervention Trial (SPRINT). Based on baseline lipid profiles, low HDL-C was defined as <40 mg/dL in men or < 50 mg/dL in women, and high TG as ≥150 mg/dL. Participants were classified into four lipid categories according to these cutoffs. AD was defined as the combination of low HDL-C and high TG. We used multivariable Cox regression to evaluate the association between lipid categories and the primary SPRINT outcome, a composite of major CVD events. Over a median 3.8-year follow-up, 726 primary outcome events occurred. AD was present in 9.5 % of cases (n = 104), while 7.4 % (n = 434) occurred in those with normal HDL-C and TG. Compared to the reference group (normal HDL-C with normal TG), hazard ratios (HRs) for CVD events were 1.07 (95 % CI: 0.85-1.35) for high TG alone, 1.20 (95 % CI: 0.95-1.52) for low HDL-C alone, and 1.41 (95 % CI: 1.12-1.77) for AD. Similarly, HRs for the primary outcome associated with AD were 1.38 (95 % CI: 1.02-1.87) and 1.44 (95 % CI: 1.01-2.05) in the standard and intensive SBP-lowering arms, respectively. Among SPRINT participants, AD was associated with a higher CVD risk. Early detection of AD in hypertensive patients, even without diabetes, may prompt greater therapeutic effort to reduce long-term CVD risk.