Faculty Bibliography

BACKGROUND: Obesity, metabolic syndrome (MS) and dyslipidemia are independent risk factors for cardiovascular disease. Bariatric surgery is increasingly recognized as an effective intervention for improving each of these risk factors. There are sparse data on the long-term durability of metabolic changes associated with bariatric surgery, in particular with laparoscopic gastric banding (LGB). Our objective was to evaluate the durability of metabolic changes associated with LGB in nonmorbid obesity. METHODS: Fifty obese patients (BMI 30-40) with >/=1 obesity-related comorbidity were prospectively followed for five years. At follow-up, subjects underwent fasting blood measures, including lipid NMR spectroscopy and standard lipid profile. RESULTS: Forty-seven patients (45 female, mean age 43.8 years) completed four years follow-up (46 completed five years). Baseline BMI was 35.1 +/- 2.6. Subjects exhibited mean weight loss of 22.3 +/- 7.9 kg (22.9 +/- 7.4%) at year one and maintained this (19.8 +/- 10.2%) over five years. At baseline, 43% (20/47) of subjects met criteria for MS. This was reduced to 15% (7/47) at year one and remained reduced over five years (13%, 6/46) (p < 0.001). There were reductions in triglycerides (p < 0.001) and increases in HDL cholesterol (HDL-C, p < 0.001) and HDL particle concentration (p = 0.02), with a trend toward increased HDL particle size (p = 0.06) at year five. Changes in triglycerides and HDL-C were more prominent in patients with MS at baseline, but unassociated with weight loss or waist circumference. Changes in HDL particle size and concentration were not associated with MS status, weight loss, waist circumference, or statin use. CONCLUSIONS: LGB produces significant weight loss, resolution of MS and changes in lipid profile suggestive of beneficial HDL remodeling. These changes persist five years following LGB.

BACKGROUND:Randomized clinical trials (RCTs) investigating the impact of omega-3-fatty acid supplementation on cardiovascular events have largely shown no benefit. However, there is debate about the benign nature of the placebo in these trials. We aimed to conduct a network meta-analysis of RCTs to compare the outcomes of omega-3 fatty acid supplementation to various placebo oils. METHODS:MEDLINE and EMBASE were searched through May, 2021 to identify RCTs investigating cardiovascular outcomes with omega-3-fatty acid formulations [eicosapentaenoic acid (EPA), decosahexanoic acid (DHA), or the combination] versus placebo or standard of care controls. RESULTS:Our analysis included 17 RCTs that enrolled a total of 141,009 patients randomized to EPA (n=13,655), EPA+DHA (n=56,908), mineral oil placebo (n=5,338), corn oil placebo (n =8,876), olive oil placebo (n=41,009), and controls (no placebo oil; n=15,223). Rates of cardiovascular death [hazard ratio (HR) (95% confidence interval, CI) =0.80 (0.65-0.98); p =0.033], myocardial infarction [HR (95% CI) =0.73 (0.55-0.97); p=0.029] and stroke [HR (95% CI) =0.74 (0.58-0.94); p=0.014] were significantly lower in those receiving EPA compared to those receiving mineral oil, but were not different from rates in those receiving other oils or controls. Rates of coronary revascularization were significantly lower in those receiving EPA than in those receiving either EPA+DHA, mineral oil, corn oil, or olive oil placebo, but not controls. All-cause death was similar among all groups, but combined EPA+DHA was associated with reduced risk of cardiovascular death compared to controls [HR (95%CI): 0.83 (0.71-0.98)]. CONCLUSIONS:Our analyses demonstrate that although EPA supplementation lowers risk of coronary revascularization more than other oils, there may not be a benefit relative to standard of care. Further, EPA reduces the risk of cardiovascular events only in comparison to mineral oil and not when compared with other placebo oils or controls. In contrast, combined EPA+DHA was associated with reduced risk of cardiovascular death compared to controls.

Aspirin's clinical efficacy may be influenced by body weight and mass. Although inadequate platelet inhibition by aspirin is suggested as responsible, evidence for this in non-diabetic patients is sparse. We investigated the influence of body weight and mass on aspirin's inhibition of platelet aggregation in healthy adults without diabetes. Cohort one (NYU, n = 84) had light transmission aggregometry (LTA) of platelet-rich plasma to submaximal adenosine diphosphate (ADP) and arachidonic acid (AA) before and following 1 week of daily 81 mg non-enteric coated aspirin. Subjects in the validation cohort (Duke, n = 66) were randomized to 81 mg or 325 mg non-enteric coated aspirin for 4 weeks, immediately followed by 4 weeks of the other dose, with LTA to submaximal collagen, ADP, and AA before and after each dosage period. Body mass index (BMI) range was 18.0-57.5 kg/m² and 25% were obese. Inhibition of platelet aggregation was similar irrespective of BMI, body weight and aspirin dose. There was no correlation between platelet aggregation before or after aspirin with BMI or body weight. Our data demonstrate that aspirin produces potent inhibition of direct and indirect COX1-mediated platelet aggregation in healthy adults without diabetes regardless of body weight or mass - suggesting that other mechanisms explain lower preventive efficacy of low-dose aspirin with increasing body weight/mass.

The onset of the coronavirus 2019 (COVID-19) pandemic prompted unique public health measures including stay-at-home (SAH) orders that provoked altered dietary and exercise patterns and may have affected medication access and use. Although these impacts have the potential to influence lipid levels, little is known of the consequences of COVID-19 SAH on objective atherosclerotic cardiovascular disease (ASCVD) risk factors. We performed a patient-level analysis of the primary measure of atherogenic lipid-associated risk, nonHDL-C during the 2020 SAH period and the same time period in 2019, in patients within a large health system in New York City. We found that women and racial and ethnic minority group members were more likely to exhibit substantial worsening of atherogenic lipid profile (≥38 mg/dL increase in nonHDL-C) during this period. Our results suggest that the pandemic and subsequent public health measures may have produced unintended negative consequences on already at-risk groups.

BACKGROUND AND AIMS/OBJECTIVE:Obesity is an independent risk factor for atherosclerotic cardiovascular disease (CVD), and platelet hyperactivation in obesity may contribute to this association. Olive oil consumption is associated with lower cardiovascular disease (CVD) risk in the general population. However, little is known for individuals with obesity. We investigated whether olive oil intake is associated with platelet activation in obesity. METHODS AND RESULTS/RESULTS:. Olive oil intake was stratified into <1 time/week (n = 21), 1-3 times/week (n = 18), ≥4 times/week (n = 24). Strata did not differ by age, BMI or platelet count. Unstimulated P-selectin expression did not differ by olive oil consumption. Subjects with more frequent olive oil intake exhibited lower P-selectin expression on submaximal thrombin exposure. CONCLUSIONS:More frequent olive oil intake is associated with reduced thrombin-induced platelet activation in obesity.

High levels of lipoprotein(a) [Lp(a)], an apoB100-containing lipoprotein, are an independent and causal risk factor for atherosclerotic cardiovascular diseases through mechanisms associated with increased atherogenesis, inflammation, and thrombosis. Lp(a) is predominantly a monogenic cardiovascular risk determinant, with ≈70% to ≥90% of interindividual heterogeneity in levels being genetically determined. The 2 major protein components of Lp(a) particles are apoB100 and apolipoprotein(a). Lp(a) remains a risk factor for cardiovascular disease development even in the setting of effective reduction of plasma low-density lipoprotein cholesterol and apoB100. Despite its demonstrated contribution to atherosclerotic cardiovascular disease burden, we presently lack standardization and harmonization of assays, universal guidelines for diagnosing and providing risk assessment, and targeted treatments to lower Lp(a). There is a clinical need to understand the genetic and biological basis for variation in Lp(a) levels and its relationship to disease in different ancestry groups. This scientific statement capitalizes on the expertise of a diverse basic science and clinical workgroup to highlight the history, biology, pathophysiology, and emerging clinical evidence in the Lp(a) field. Herein, we address key knowledge gaps and future directions required to mitigate the atherosclerotic cardiovascular disease risk attributable to elevated Lp(a) levels.

The aims were to implement physical activity (PA) screening as part of the electronic kiosk check-in process in an adult preventive cardiology clinic and assess factors related to patients' self-reported PA. The 3-question physical activity vital sign (PAVS) was embedded in the Epic electronic medical record and included how many days, minutes and intensity (light, moderate, vigorous) of PA patients conducted on average. This is a data analysis of PAVS data over a 60-day period. We conducted multivariable logistic regression to identify factors associated with not meeting current PA recommendations. Over 60 days, a total of 1322 patients checked into the clinic using the kiosk and 72% (n = 951) completed the PAVS at the kiosk. The majority of those patients were male (58%) and White (71%) with a mean age of 64 ± 15 years. Of the 951 patients completing the PAVS, 10% reported no PA, 55% reported some PA, and 35% reported achieving at least 150 min moderate or 75 min vigorous PA/week. In the logistic model, females (AOR = 1.4, 95%CI: 1.002-1.8, p = .049) vs. males, being Black (AOR = 2.0, 95%CI: 1.04-3.7, p = .038) or 'Other' race (AOR = 1.5, 95%CI: 1.02-2.3, p = .035) vs. White, unknown or other types of relationships (AOR = 0.0.26, 95%CI: 0.10-0.68, p = .006) vs. being married/partnered, and those who were retired (AOR = 1.9, 95% CI: 1.4-2.8, p < .001) or unemployed (AOR = 2.2, 95%CI: 1.3-3.7, p = .002) vs. full-time workers were associated with not achieving recommended levels of PA. The PAVS is a feasible electronic tool for quickly assessing PA and may prompt providers to counsel on this CVD risk factor.

PURPOSE OF REVIEW/OBJECTIVE:This study aims to discuss the mechanisms by which GLP-1 agonists and bariatric surgery improve cardiovascular outcomes in severely obese patients. RECENT FINDINGS/RESULTS:Recent studies have demonstrated that both GLP-1 agonist use and bariatric surgery reduce adverse cardiovascular outcomes. Improvements in traditional atherosclerosis risk factors in association with weight loss likely contribute, but weight loss-independent mechanisms are also suggested to have roles. We review the clinical and preclinical evidence base for cardiovascular benefit of LP-1 agonists and bariatric surgery beyond traditional risk factors, including improvements in endothelial function, direct impacts on atherosclerotic plaques, and anti-inflammatory effects.