Somers, Virend K.

Background Hyper‐ and hypokalemia are clinically silent, common in patients with renal or cardiac disease, and are life threatening. A noninvasive, unobtrusive, blood‐free method for tracking potassium would be an important clinical advance. Methods and Results Two groups of hemodialysis patients (development group, n=26; validation group, n=19) underwent high‐resolution digital ECG recordings and had 2 to 3 blood tests during dialysis. Using advanced signal processing, we developed a personalized regression model for each patient to noninvasively calculate potassium values during the second and third dialysis sessions using only the processed single‐channel ECG . In addition, by analyzing the entire development group's first‐visit data, we created a global model for all patients that was validated against subsequent sessions in the development group and in a separate validation group. This global model sought to predict potassium, based on the T wave characteristics, with no blood tests required. For the personalized model, we successfully calculated potassium values with an absolute error of 0.36±0.34 mmol/L (or 10% of the measured blood potassium). For the global model, potassium prediction was also accurate, with an absolute error of 0.44±0.47 mmol/L for the training group (or 11% of the measured blood potassium) and 0.5±0.42 for the validation set (or 12% of the measured blood potassium). Conclusions The signal‐processed ECG derived from a single lead can be used to calculate potassium values with clinically meaningful resolution using a strategy that requires no blood tests. This enables a cost‐effective, noninvasive, unobtrusive strategy for potassium assessment that can be used during remote monitoring.

Abstract Background: Differences in body fat (BF) distribution in patients with normal body mass index (BMI) with elevated alanine aminotransferase (ALT) remains poorly described. Objective: To determine the relationship between total BF, waist circumference (WC), insulin resistance (IR), and cardiometabolic risk profile in subjects with elevated ALT and normal BMI. Methods: We analyzed cross-sectional data from 4,914 US participants in the third National Health and Nutrition Examination Survey database, who were ≥20 years of age, had normal BMI, and had body composition assessed by bioimpedance. Results: Mean ± SD age was 41.4 ± 0.3 years, and 58% participants were women. BF was 20 ± 0.1% in men and 29.9 ± 0.1% in women. As total BF increased by tertiles, there was a tendency towards a higher prevalence of nonalcoholic fatty liver disease in men (6.1%, 6.5%, 9.5%, P = 0.13), but not in women (8.7%, 8.2%, 10.7%, P = 0.71). As WC increased by tertiles, there was a higher prevalence of elevated ALT in men (2.6%, 8.6%, 6.6%, P < 0.0001), but not in women. As ALT increased, men had significantly higher levels of nonhigh density lipoprotein cholesterol (HDL-C), increased apolipoprotein B, increased IR, and lower levels of C-reactive protein, whereas, women had higher levels of non-HDL-C and increased IR. Conclusion: In subjects with normal BMI, increased WC is associated with a higher prevalence of elevated ALT in men, but not in women. Higher levels of ALT correlated with a poor cardiometabolic risk profile.

Obstructive and central sleep apnea have been associated with increased risk of adverse cardiovascular events and mortality. Sympathetic dysregulation occurring as a result of the respiratory disturbance is thought to play a role in this increased risk. Sleep apnea increases the risk of arrhythmias, myocardial ischemia/infarction, stroke, and heart failure, all of which may increase mortality risk. A higher incidence of nocturnal arrhythmias, cardiac ischemia, and sudden death has been noted in subjects with sleep-disordered breathing (SDB). In this review, the association between SDB and each of these conditions is discussed, as well as the potential mechanisms underlying these risks and the effects of treatment of SDB. Particular emphasis is placed on the relationship between SDB and nocturnal atrial and ventricular arrhythmias, myocardial ischemia/infarction and sudden death.

AimObesity is a major cardiovascular (CV) risk factor. Bariatric surgery (BSx) is an approved therapeutic alternative for class II–III obesity, but little evidence focuses on older adults. We assessed the effect of BSx on cardiometabolic variables and long‐term CV risk in older adults.MethodsWe carried out a population‐based, observational study from 1990–2009, of 40 consecutive elderly (age ≥60 years) residents of Olmsted County, MN, USA, with class II–III obesity treated with BSx at a University‐based, academic health center. Data were obtained from the Rochester Epidemiology Project. Metabolic syndrome (MetS) was defined using American Heart Association/National Heart, Lung, Blood Institute (AHA/NHLBI) criteria (increased triglycerides, low high‐density lipoprotein, increased blood pressure, increased glucose and body mass index as a modified measure of obesity instead of waist circumference). Change in CV risk factors, MetS prevalence, and impact on predicted CV risk using the Framingham risk score was ascertained at 1 year postoperatively and assessed statistically.ResultsMean age and body mass index were 64.4 ± 3.7 and 45.0 ± 6.3 kg/m2, respectively, and 28 out of 40 (70%) were women. One participant died during the 11‐month study period after BSx from respiratory complications related to BSx, and one participant died at 2 years. Percentage of excess weight loss decreased by 57.5% at 1 year. Prevalence 1 year after BSx decreased for diabetes (57.5% to 22.5%; P < 0.03), hypertension 87.5% to 73.7% (P = 0.003), dyslipidemia (80% to 42.5%; P < 0.001) and sleep apnea (62.5% to 23.7%; P < 0.001).MetS prevalence decreased from 80% to 45% (P < 0.002). Baseline risk was 14.1%, which changed at follow up at 8.2%.ConclusionsIn older adults, BSx induces considerable weight loss, improves CV risk factors, decreases MetS prevalence and is an effective treatment in this population. Geriatr Gerontol Int 2016; 16: 618–624.

The arterial baroreflex contributes importantly to the short-term regulation of blood pressure and cardiovascular variability. A number of factors (including reflex, humoral, behavioral, and environmental) may influence gain and effectiveness of the baroreflex, as well as cardiovascular variability. Many central neural structures are also involved in the regulation of the cardiovascular system and contribute to the integrity of the baroreflex. Consequently, brain injuries or ischemia may induce baroreflex impairment and deranged cardiovascular variability. Baroreflex dysfunction and deranged cardiovascular variability are also common findings in cardiovascular disease. A blunted baroreflex gain and impaired heart rate variability are predictive of poor outcome in patients with heart failure and myocardial infarction and may represent an early index of autonomic activation in left ventricular dysfunction. The mechanisms mediating these relationships are not well understood and may in part be the result of cardiac structural changes and/or altered central neural processing of baroreflex signals.

Background Epidemiologic evidence suggests a link between short sleep duration and cardiovascular risk, although the nature of any relationship and mechanisms remain unclear. Short sleep duration has also been linked to an increase in cardiovascular events. Endothelial dysfunction has itself been implicated as a mediator of heightened cardiovascular risk. We sought to determine the effect of 8 days/8 nights of partial sleep restriction on endothelial function in healthy humans. Methods and Results Sixteen healthy volunteers underwent a randomized study of usual sleep versus sleep restriction of two‐thirds normal sleep time for 8 days/8 nights in a hospital‐based clinical research unit. The main outcome was endothelial function measured by flow‐mediated brachial artery vasodilatation ( FMD ). Those randomized to sleep restriction slept 5.1 hours/night during the experimental period compared with 6.9 hours/night in the control group. Sleep restriction was associated with significant impairment in FMD (8.6±4.6% during the initial pre‐randomization acclimation phase versus 5.2±3.4% during the randomized experimental phase, P =0.01) whereas no change was seen in the control group (5.0±3.0 during the acclimation phase versus 6.73±2.9% during the experimental phase, P =0.10) for a between‐groups difference of −4.40% (95% CI −7.00 to −1.81%, P =0.003). No change was seen in non‐flow mediated vasodilatation ( NFMD ) in either group. Conclusion In healthy individuals, moderate sleep restriction causes endothelial dysfunction. Clinical Trial Registration URL : ClinicalTrials.gov. Unique identifier: NCT 01334788.