Introduction: Obesity is recognized as a risk factor for cardiovascular disease, expending independent adverse effects on the cardiovascular system. This relationship is complex due to several associations with cardiovascular disease risk factors/markers such as hypertension, dyslipidemia, insulin resistance/dysglycemia, or type 2 diabetes mellitus. Obesity induces a variety of cardiovascular system structural adaptations, from subclinical myocardial dysfunction to severe left ventricular systolic heart failure. Abnormalities in cardiac metabolism and subsequent cardiac energy, have been proposed as major contributors to obesity-related cardiovascular disease. Ectopic fat depots play an important role in several of the hypotheses postulated to explain the association between obesity, cardiac metabolism and cardiac dysfunction. Areas covered: In this review, we addressed with contemporary studies how obesity-associated metabolic conditions and ectopic cardiac fat accumulation, translate into cardiac energy metabolism disturbances that may lead to adverse effects on the cardiovascular system. Expert commentary: Obesity and ectopic fat accumulation has long been related to metabolic diseases and adverse cardiovascular outcomes. Recent imaging advances have just started to address the complex interplays between obesity, ectopic fat depots, cardiac metabolism and the risk of obesity-related cardiovascular disease. A better comprehension of these obesity-associated metabolic disturbances will lead to earlier detection of patients at increased risk of cardiovascular disease and to the development of novel therapeutic metabolic targets to treat a wide variety of cardiovascular diseases.

Targeting metabolic determinants of exercise performance with pharmacological agents that would mimic/potentiate the effects of exercise represents an attractive clinical alternative to counterbalance the poor exercise capacity in patients with type 2 diabetes mellitus (T2DM). We examined the effect of 1-yr treatment with the insulin sensitizer peroxisome proliferator-activated receptor (PPAR)γ agonist rosiglitazone on aerobic exercise capacity and body fat composition/distribution in men with T2DM and stable coronary artery disease (CAD). One-hundred four men (age: 64 ± 7 yr; body mass index: 30.0 ± 4.4 kg/m²) with T2DM and CAD were randomized to receive rosiglitazone or placebo for 1 yr. Aerobic exercise capacity (exercise duration) was assessed with a maximal treadmill test, and body composition/distribution were assessed by dual-energy X-ray absorptiometry/computed tomography scans. At 1 yr, patients with T2DM under PPARγ agonist treatment showed a reduction in aerobic exercise capacity compared with the control group (exercise duration change, −31 ± 8 versus 7 ± 11 s, P = 0.009). Significant increases in body fat mass (3.1 ± 0.4 kg, 12%), abdominal and mid-thigh subcutaneous adipose tissue (AT) levels, and mid-thigh skeletal muscle fat were found (all P < 0.01), whereas no effect on visceral AT levels was observed ( P > 0.05) under treatment. Subcutaneous fat mass gained under PPARγ agonist was the strongest predictor of the worsening in aerobic exercise capacity ( P > 0.0001); no association was found with skeletal muscle fat infiltration nor visceral AT. Treatment with the insulin sensitizer PPARγ agonist rosiglitazone in patients with T2DM and CAD is associated with a worsening in aerobic exercise capacity, which seems to be mainly attributable to weight gain and subcutaneous fat mass expansion.

Background: An adverse event (AE) is any undesirable medical manifestation in an individual who has received pharmacological treatment. To be considered serious (SAE), it needs to meet minimally one of the severity criteria by Health Canada. The most recent data (2006) suggested that AEs were underreported (<6%) to health authorities. In Canada, since the implementation of Vanessa’s Law (2019), hospitals are required to report SAEs; however, this law remains relatively unknown. The objectives of the study were: (i) to document the incidence of any AE and SAE over time in a ‘real’ clinical context, (ii) to quantify SAEs reported to Health Canada, and (iii) to assess whether Vanessa’s Law has led to an increase in mandatory reporting to Health Canada. Methods: We carried out a descriptive retrospective study at the Institut Universitaire de Cardiologie et de Pneumologie de Québec-Université Laval, including 500 patients hospitalized between 1 January 2018 and 31 December 2021 and randomized into 4 cohorts (125 patients/year). Descriptive and comparative analyses were performed. Results: The characteristics of the cohorts were: 43.6% women; median age: 69 years (min–max: 21–96 years), number of comorbidities: 4 (1–12). During their hospitalization, patients consumed 18 different drug products (2–56) and the median of observed SAEs/patients was 0 (0–10) (total: 302). The overall percentage of SAEs reported to Health Canada was 0%, before and following the implementation of Vanessa’s Law. Conclusion: According to 500 electronic medical records, SAEs were underreported to Health Canada, even after the implementation of Vanessa’s law.

Purpose of review: Coronary artery bypass graft (CABG) surgery remains the gold-standard treatment for multivessel and left main coronary artery disease. Despite significant improvement in cardiovascular outcomes, patients undergoing CABG remain at risk for recurrent adverse ischemic events and other cardiovascular outcomes (coronary revascularisation, stroke, cardiac death, etc.). The purpose of this review is to summarize the most recent evidence in pharmacological preventive therapies addressing the residual cardiovascular risk in patients who have undergone CABG. Recent findings: Novel cardiovascular pharmacological preventive strategies targeting inflammatory, metabolic and prothrombotic (antiplatelet and anticoagulation) pathways have been recently assessed, with promising results for secondary prevention after CABG. Summary: Secondary prevention is an essential part of postoperative care after CABG. Novel lipid-lowering and glucose-controlling agents suggest a strong and consistent benefit on native coronary artery disease and overall cardiovascular outcomes. The role and the choice of enhanced antiplatelet/anticoagulation/lipid/glucose-modulating therapies following CABG should be better defined and deserves further investigation. Additional studies are required to identify new therapeutic target addressing the specific multifactorial nature of the graft CV disease and identifying the best preventive strategies for long-term graft patency.

Introduction: Metabolic dysfunction–associated fatty liver disease (MAFLD) is highly prevalent among people living with severe obesity (body mass index [BMI] ≥ 35 kg/m ² ). However, it remains unknown how sex and adipose tissue distribution are related to MAFLD onset and progression into metabolic dysfunction–associated steatohepatitis (MASH) or advanced stages of fibrosis. Methodology: We retrospectively studied patients with severe obesity who were eligible for bariatric surgery. Demographic characteristics, biomarkers, and cardiometabolic comorbidities were reported. Anthropometric indices such as BMI, waist circumference (WC), waist‐to‐hip ratio (WHR), waist‐to‐height ratio (WHtR), neck circumference (NC), lipid accumulation product (LAP), visceral adiposity index (VAI), body adiposity index (BAI), abdominal volume index (AVI), and body roundness index (BRI) were measured or calculated. MAFLD, MASH, and stages of fibrosis (F1‐F4) were established from perioperative liver biopsies. Standardized univariate and multivariate logistic regression analyses were used to examine the association between demographic variables, anthropometric indices, cardiometabolic conditions, and the risk of MASH or severe fibrosis (F2‐F4). Results: A total of 2091 participants with severe obesity were included in the analyses; BMI 47.9 ± 7.3 kg/m ² , age 46.2 ± 11.2 years, and 68.4% females. Overall, MAFLD prevalence was 79.5%, with 44.5% having MASH and 24.4% having severe fibrosis (Stage 2 or higher). No anthropometric indices of adiposity were associated with MASH or fibrosis severity. In this population, female sex was a risk factor for severe fibrosis (OR: 1.27, 95% CI 1.01–1.59, p < 0.05). Conclusions: MAFLD and MASH are highly prevalent in individuals living with severe obesity, but no anthropometric indices or laboratory tests are good predictors of MAFLD or MASH in this population. When MAFLD is diagnosed, our results suggest that females with severe obesity might be at higher risk of advanced stages of fibrosis.