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•We performed analysis of different epidemiological datasets to study racial and ethnic differences across the spectrum of cardiovascular diseases (CVDs) in the US.•We found a higher prevalence and mortality related to most CVDs and associated risk factors among non-Hispanic Black individuals compared to non-Hispanic White individuals.•The population-standardized representation of non-Hispanic Black and Hispanic trainees across adult general cardiovascular fellowship programs was lower than non-Hispanic White individuals.

Dysmetabolic states, such as type 2 diabetes (T2D), characterized by insulin resistance (IR), are associated with fatty liver, increased cardiovascular disease (CVD) risk, and decreased functional exercise capacity (FEC). Rosiglitazone (RO) improves exercise capacity and IR in T2D. However, the effects of RO on FEC and other markers of CVD risk in prediabetes are unknown. We hypothesized that insulin sensitization with RO would improve exercise capacity and markers of CVD risk in participants with impaired glucose tolerance (IGT). Exercise performance (peak oxygen consumption and oxygen uptake kinetics), IR (homeostasis model assessment of IR and quantitative insulin sensitivity check index), and surrogate cardiovascular endpoints (coronary artery calcium (CAC) volume and density and C-reactive protein (CRP)) were measured in participants with IGT after 12 and 18 months of RO or placebo (PL). RO did not significantly improve exercise capacity. Glycemic measures and IR were significantly lower in people on RO compared to PL at 18 months. CAC volume progression was not different between PL and RO groups. RO did not improve exercise capacity during an 18-month intervention despite improved IR and glycemia in people with IGT. Future studies should explore why effects on FEC with RO occur in T2D but not IGT. Understanding these questions may help in targeting therapeutic approaches in T2D and IGT.

•Bempedoic acid has been shown to reduce major adverse cardiovascular outcomes in patients unable to take statins due to statin-associated side effects.•Analysis of CLEAR Outcomes trial data reveals possible differences in baseline characteristics between the primary and secondary prevention subgroups.•Further research is needed to optimize use of bempedoic acid and clarify its impact on cardiovascular outcomes in diverse patient populations.

The cause of sellar region masses in large retrospective series is overwhelmingly pituitary adenomas (84.6%), followed by craniopharyngiomas (3.2%), cystic nonneoplastic lesions (2.8%), inflammatory lesions (1.1%), meningiomas (0.94%), metastases (0.6%), and chordomas (0.5%) (1). While other rare lesions were also identified (collectively 6.0%), single unusual entities in the above-cited series numbered <1–2 examples each out of the 4122 cases, underscoring their rarity. We searched our joint files for rare, often singular, sellar/suprasellar masses that we had encountered over the past several decades in our own specialty, tertiary care specialty pituitary center practices. Cases for this review were subjectively selected for their challenging clinical and/or histological features as well as teaching value based on the senior authors' (MBSL, BKD) collective experience with over 7000 examples. We excluded entities deemed to be already well-appreciated by neuropathologists such as mixed adenoma-gangliocytoma, posterior pituitary tumors, metastases, and hypophysitis. We identified examples that, in our judgment, were sufficiently unusual enough to warrant further reporting. Herein, we present 3 diffuse large cell B cell pituitary lymphomas confined to the sellar region with first presentation at that site, 2 sarcomas primary to sella in nonirradiated patients, and 1 case each of granulomatosis with polyangiitis and neurosarcoidosis with first presentations as a sellar/suprasellar mass. Other cases included 1 of chronic lymphocytic leukemia within a gonadotroph adenoma and 1 of ectopic nerve fascicles embedded within a somatotroph adenoma, neither of which impacted patient care. Our objective was to share these examples and review the relevant literature.

Introduction:Individuals with similar weights have substantial heterogeneity in metabolic risk, a key indicator of cardiovascular disease risk. Additionally, many persons progress from metabolically healthy to metabolically unhealthy status, or regress in metabolic risk, over time. The association of adipokines with transitions in metabolic risk status is unknown.Methods:Among ARIC Visit 2 (1990-92) participants without diabetes, we evaluated the associations of adipokines (adiponectin and leptin; in tertiles) with metabolic risk transitions from Visit 2 to Visit 4 (1996-98; a 6-year interval) among persons with and without obesity using logistic regression. We examined transitions from metabolically healthy (no metabolic syndrome [MetS]) to unhealthy status (MetS, with or without diabetes). Among those with MetS without diabetes at Visit 2, we examined adipokine associations with progression to MetS with diabetes and with regression to metabolically healthy status.Results:Among 7,560 participants, mean age was 57 with 56% female and 17% Black adults. Higher adiponectin levels were associated with about 75% lower risk of progression from metabolically healthy to unhealthy status in those with and without obesity, whereas higher leptin was associated with about 3-fold greater risk of progression (Table, Panel A). Among those with MetS at Visit 2, higher adiponectin was associated with lesser risk of progression to diabetes, and greater likelihood of regression to metabolically healthy status in those with and without obesity (Table, Panel B). Conversely, higher leptin was associated with greater risk of progression to diabetes in those with obesity.Conclusion:Adipokine levels are linked to transitions in metabolic risk status over time among persons with similar weight status. Adipokines may identify individuals at greatest risk of developing metabolic risk factors, who may benefit most from aggressive CVD prevention strategies.

Background:Chronic obesity is a major risk factor for hypertension, and obesity-associated hypertension is often difficult to control. Adipokines have vascular effects, but the degree to which they mediate the association between chronic obesity and hypertension is unknown.Methods:We conducted a cross-sectional analysis of 10,842 ARIC participants who attended Visit 3 (1993-95) with self-reported BMI at age 25 and measured BMI at visits 1 to 3 (each 3 years apart). We calculated cumulative excess BMI years by centering BMI at 25 kg/m2at each time point and multiplying the mean BMI by the duration in years from age 25 to Visit 3. We categorized cumulative excess BMI years by quartiles. Plasma adipokines (leptin, adiponectin) were measured at Visit 3. Prevalent hypertension at Visit 3 was defined as blood pressure ≥130/80mmHg or hypertension medication use. We used linear regression to assess associations between cumulative BMI quartiles and adipokines (log transformed). We used logistic regression to assess the association of cumulative BMI with prevalent hypertension and the extent to which adipokines mediate this relationship.Results:Higher quartiles of cumulative excess BMI years were associated with lower adiponectin and higher leptin levels (both p<0.001). Higher cumulative excess BMI years was strongly associated with hypertension (OR 2.52 [95% CI 2.21, 2.87], for top vs bottom quartile). Adiponectin partially mediated the association of cumulative excess BMI years with hypertension by 7% (OR for top quartile decreased from 2.52 to 2.41), leptin mediated the association by 18% (OR decreased from 2.52 to 2.24), and the combination of adiponectin and leptin mediated the association by 22% (OR decreased from 2.52 to 2.18) (Table).Conclusion:Adipokines may partially mediate the association of long-term excess adiposity with hypertension. Targeting adipokines may have therapeutic value in managing hypertension in those with chronic obesity.

Introduction:Adipokines have metabolic effects and laboratory studies also suggest direct effects of adipokines on the myocardium. However, there are no population-based studies examining heart failure (HF) risk with multiple adipokines in concert.Methods:We conducted a prospective analysis of ARIC Visit 2 (1990-92) participants without HF. Adipokines were categorized into quartiles. “Abnormal” adipokine levels were defined as the top quartile for leptin, resistin, and visfatin, and the bottom quartile for adiponectin and apelin. We compared the prevalence of adipokine abnormalities across body mass index (BMI) categories: normal weight (BMI 18.5-<25 kg/m2), overweight (BMI 25-<30 kg/m2), obesity (BMI 30-<35 kg/m2) and severe obesity (BMI ≥35 kg/m2). We used Cox regression to examine associations for each adipokine and the number of abnormal adipokines with incident HF.Results:Among 10,725 participants (mean age 58, 55% female, 22% Black), higher prevalences of multiple (≥2) adipokine abnormalities were seen with higher BMI (56% of those with severe obesity vs 15% of normal weight). After adjusting for confounders (Table), higher adiponectin and apelin were associated with lower HF risk (Q4 vs. Q1 HR: 0.70, 95%CI: 0.62-0.79; HR: 0.87, 95%CI: 0.78-0.97), and higher leptin and resistin with higher HF risk (Q4 vs. Q1 HR: 2.06, 95%CI: 1.78-2.38; HR: 1.31, 95%CI: 1.17-1.46). Visfatin was not associated with HF. Results were similar when stratified by obesity (BMI ≥30 kg/m2). For leptin and adiponectin, HF associations were attenuated by adjusting for metabolic risk factors, but not for apelin and resistin (Table). Having more adipokine abnormalities was linked to progressively higher HF risk (For 4 vs 0 abnormalities HR: 2.92, 95% CI: 1.95-4.30).Conclusions:Adipokines are linked to HF risk, with some associations mediated by metabolic risk factors and others independent of metabolic risk. Adipokines may be a key mechanistic link between adipose tissue and HF.

With the concept of patient-centered care in mind, this chapter outlines the current diabetes medications available for glucose lowering and the characteristics of each of these medications that need to be considered in shared decision-making for durable and effective therapy. Important patient characteristics such as weight, risk for hypoglycemia, cost, social determinants of health, and medical literacy need to be considered. The evidence-base informing the use of antihyperglycemic agents has changed dramatically due to 2008 Food and Drug Administration guidance for cardiovascular safety and cardiorenal protection with antihyperglycemic agents. New evidence supports an approach to diabetes management that addresses pre-existing cardiorenal disease.