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Author Contributions: Drs Sammon and Trinh had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

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Body fat distribution contributes to obesity-related metabolic and cardiovascular disorders. Visceral fat is more detrimental than subcutaneous fat. However, the mechanisms underlying visceral fat-mediated cardiometabolic dysregulation are not completely understood. Localized increases in expression of the renin angiotensin system (RAS) in adipose tissue (AT) may be implicated. We therefore investigated mRNA and protein expression of RAS components in visceral versus subcutaneous AT using paired samples from individuals undergoing surgery (N = 20, body mass index: 45.6 ± 6.2 kg/m2, and age: 44.6 ± 9.1 years). We also examined RAS-related proteins in AT obtained from individuals on renin angiotensin aldosterone system (RAAS) targeted drugs (N = 10, body mass index: 47.2 ± 9.3 kg/m2, and age: 53.3 ± 10.1 years). Comparison of protein expression between subcutaneous and visceral AT samples showed an increase in renin (p = 0.004) and no change in angiotensinogen (p = 0.987) expression in visceral AT. Among proteins involved in angiotensin peptide generation, angiotensin converting enzyme (p = 0.02) was increased in subcutaneous AT while chymase (p = 0.001) and angiotensin converting enzyme-2 (p = 0.001) were elevated in visceral fat. Furthermore, visceral fat expression of angiotensin II type-2 receptor (p = 0.007) and angiotensin II type-1 receptor (p = 0.031) was higher, and MAS receptor (p < 0.001) was lower. Phosphorylated-p53 (p = 0.147), AT fibrosis (p = 0.138) and average adipocyte size (p = 0.846) were similar in the two depots. Nonetheless, visceral AT showed increased mRNA expression of inflammatory (TNFα, p < 0.001; IL-6, p = 0.001) and oxidative stress markers (NOX2, p = 0.038; NOX4, p < 0.001). Of note, mRNA and protein expression of RAS components did not differ between subjects taking or not taking RAAS related drugs. In summary, several RAS related proteins are differentially expressed in subcutaneous versus visceral AT. This differential expression may not alter AngII but likely increases Ang1-7 generation in visceral fat. These potential differences in active angiotensin peptides and receptor expression in the two depots suggest that localized RAS may not be involved in differences in visceral vs subcutaneous AT function in obese individuals. Our findings do not support a role for localized RAS differences in visceral fat-mediated development of cardiovascular and metabolic pathology.

COPD patients are at higher risk for VT and mortality. This may not be fully attributed to the confounding effect of systolic heart failure measured by LVEF. Further studies are needed to explore the mechanistic interactions between VT and COPD in order to determine whether antiarrhythmic strategies would apply especially to patients with severe COPD.

There is an increasing consumption of energy drinks both in the United States and worldwide. The components of these beverages are sometimes unclear but commonly include caffeine, sugars, taurine, and B-vitamins. Young people, particularly those engaged in sports, studying, and in the military are especially likely to be consumers of energy drinks. While limited data are available regarding their autonomic and hemodynamic effects, current literature suggests that energy drink consumption is accompanied by increases in blood pressure, sympathetic drive, and also in QT prolongation. There are no systematic long term studies identifying consequences of frequent energy drink consumption. However, multiple anecdotal reports implicate energy drinks in adverse cardiovascular events including atrial fibrillation, ventricular arrhythmia, myocardial infarction, and sudden death. Events such as atrial fibrillation may even occur in otherwise healthy subjects with structurally normal hearts. It is likely that these cardiovascular outcomes are triggered by the hemodynamic, autonomic, and electrocardiographic responses to energy drink consumption. What remains unclear is how concomitant use of other stimulants such as amphetamines and nicotine may interact to potentiate neural and circulatory responses and cardiovascular consequences when combined with energy drinks.

Failure to increase heart rate following administration of atropine and greatly-reduced reflex changes in cardiac rate during acutely-induced alterations in blood pressure in chronic chagasic cardiac patients are believed to be a functional disorder related to degeneration of the neuronal supply to the sino-atrial region of the heart. The fact that patients with myocardiopathies of other etiologies respond differently than the Chagas'' cases strengthens the evidence for the specific loss of autonomic control in the latter.

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