Interaction of obesity and atrial fibrillation: an overview of pathophysiology and clinical management

Introduction: Obesity, defined as a Body Mass Index (BMI) of ≥30 kg/m2, is the most common chronic metabolic disease worldwide and its prevalence has been strongly increasing. Obesity is associated with various diseases such as cardiovascular disease, type 2 diabetes, and hypertension. Regarding heart rhythm disorders, obesity is associated with an increase in atrial fibrillation (AF), the most common arrhythmia in clinical practice. AF is associated with increased cardiovascular morbidity and mortality. Obesity, a novel risk factor, is responsible for a 50%-increased incidence of AF.

Areas covered: We will briefly discuss the obesity paradox and its mechanisms regarding cardiac and hemodynamic function changes. In the first main part of this review, we will be discussing risk assessment studies, pathophysiology, genetic predisposition, epicardial adipose tissue, and ventricular adaptation in relation to obesity and development of AF. In the second part, we will discuss treatment strategies like conservative management and the effect of bariatric and metabolic surgery.

Expert opinion: Cardiac arrhythmias, in particular, AF, in patients with obesity comprise complex pathophysiological mechanisms that remain poorly understood. In recent literature, there has been increased interest in the role of epicardial adipose tissue and structural remodeling in obese hearts.     

Differences in insulin resistance markers between children born small for gestational age or born preterm appropriate for gestational age

Aim: To evaluate the impact of prenatal or postnatal compromised environment on glucose homoeostasis in children born preterm and appropriate for gestational age or small for gestational age (SGA) at term. Method: Seventy-seven children (median 9.9 years, range 8.5–10) born at Karolinska Hospital were allocated to three groups: 21 subjects born before 30 weeks of gestational age (preterm), 26 SGA at term and 30 at term with appropriate birth weight (control). Anthropometric measurements were taken, and fasting blood samples for haemoglobin A1c, glucose, insulin, IGFBP-1, IGF-1 and lipid profile were taken. Glucose, insulin and IGFBP-1 samples were taken at 0, 30 and 120 min during an oral glucose tolerance test (OGTT). Results: Subjects born preterm or SGA were shorter and thinner compared with Controls. After adjustment for body mass index (BMI), the SGA group had higher basal insulin levels (p = 0.029), higher homoeostasis model assessment—insulin resistance (p = 0.012) and lower whole-body insulin sensitivity index (p = 0.007) than Controls. IGFBP-1 decrease during OGTT was attenuated in the Preterm group compared with the Control (p = 0.045) and SGA groups (p = 0.007). Conclusion: The higher fasting insulin level in the SGA children, adjusted for BMI, could indicate peripheral insulin resistance. Preterm born children had reduced suppression of IGFBP-1 during OGTT, suggesting hepatic insulin resistance.     

Postpartum behaviour as predictor of weight change from before pregnancy to one year postpartum

Background  

Postpartum weight retention affects many women and increases the risk of becoming overweight. The research objective was to study modifiable factors contributing to weight change at one year postpartum.     

Mast cell chymase in experimentally induced psoriasis

Mast cell chymase can have a pro‐inflammatory or an immunosuppressive function in psoriasis, but the outcome may depend on the level of chymase activity. Therefore, mast cells showing chymase activity (Chy_act) and immunoreactivity (Chy_prot) were studied during the Köbner reaction (0 days, 2 h, 1 day, 3 days and 7 days) of psoriasis induced by the tape‐stripping technique. Also, the effect of recombinant human chymase (rh‐chymase) or human LAD2 mast cells (LAD2) on the ³H‐thymidine uptake of psoriatic peripheral blood mononuclear cells (PBMC) or total T cells was studied. The Chy_act/Chy_prot ratio tended to be higher in all time‐point biopsies in the Köbner‐negative (n = 10) than ‐positive (n = 8) group (P = 0.073), although chymase activity decreased significantly at 2 h to 1 day only in the Köbner‐negative group. rh‐chymase (0.05–0.5 μg/mL) stimulated to a varying extent PBMC in eight out of nine cultures, but in all cultures 5 μg/mL rh‐chymase turned the stimulation towards inhibition. The effect of rh‐chymase on T cells varied from stimulation to inhibition, but in 11 of 15 cultures rh‐chymase, at least at 5 μg/mL, produced a change to inhibition. In co‐cultures, LAD2 inhibited PBMC in the absence of soybean trypsin inhibitor (SBTI). In the presence of SBTI, LAD2 stimulated PBMC in the majority of seven cultures. In summary, the psoriatic immunopathogenesis may be promoted at low, but controlled at high, activity status of chymase.