02377nas a2200205 4500008004100000022001400041245006000055210005900115260001300174490000600187520178700193100001901980700002201999700002302021700002302044700002202067700002302089700002302112856003602135 2016 eng d a2047-998000aConsumption of Caffeinated Products and Cardiac Ectopy.0 aConsumption of Caffeinated Products and Cardiac Ectopy c2016 Jan0 v53 a

BACKGROUND: Premature cardiac contractions are associated with increased morbidity and mortality. Though experts associate premature atrial contractions (PACs) and premature ventricular contractions (PVCs) with caffeine, there are no data to support this relationship in the general population. As certain caffeinated products may have cardiovascular benefits, recommendations against them may be detrimental.

METHODS AND RESULTS: We studied Cardiovascular Health Study participants with a baseline food frequency assessment, 24-hour ambulatory electrocardiography (Holter) monitoring, and without persistent atrial fibrillation. Frequencies of habitual coffee, tea, and chocolate consumption were assessed using a picture-sort food frequency survey. The main outcomes were PACs/h and PVCs/hour. Among 1388 participants (46% male, mean age 72 years), 840 (61%) consumed ≥1 caffeinated product per day. The median numbers of PACs and PVCs/h and interquartile ranges were 3 (1-12) and 1 (0-7), respectively. There were no differences in the number of PACs or PVCs/h across levels of coffee, tea, and chocolate consumption. After adjustment for potential confounders, more frequent consumption of these products was not associated with ectopy. In examining combined dietary intake of coffee, tea, and chocolate as a continuous measure, no relationships were observed after multivariable adjustment: 0.48% fewer PACs/h (95% CI -4.60 to 3.64) and 2.87% fewer PVCs/h (95% CI -8.18 to 2.43) per 1-serving/week increase in consumption.

CONCLUSIONS: In the largest study to evaluate dietary patterns and quantify cardiac ectopy using 24-hour Holter monitoring, we found no relationship between chronic consumption of caffeinated products and ectopy.

1 aDixit, Shalini1 aStein, Phyllis, K1 aDewland, Thomas, A1 aDukes, Jonathan, W1 aVittinghoff, Eric1 aHeckbert, Susan, R1 aMarcus, Gregory, M uhttps://chs-nhlbi.org/node/699202716nas a2200337 4500008004100000022001400041245006000055210005900115260001300174300001400187490000700201520176600208100002801974700001902002700002302021700002202044700001702066700002202083700002402105700001902129700002102148700002002169700002102189700002202210700002002232700002202252700002202274700002302296700002302319856003602342 2018 eng d a1556-387100aSleep characteristics that predict atrial fibrillation.0 aSleep characteristics that predict atrial fibrillation c2018 Sep a1289-12950 v153 a

BACKGROUND: The relationship between sleep disruption, independent of obstructive sleep apnea (OSA), and atrial fibrillation (AF) is unknown.

OBJECTIVE: The purpose of this study was to determine whether poor sleep itself is a risk factor for AF.

METHODS: We first performed an analysis of participants in the Health eHeart Study and validated those findings in the longitudinal Cardiovascular Health Study, including a subset of patients undergoing polysomnography. To determine whether the observed relationships readily translated to medical practice, we examined 2005-2009 data from the California Healthcare Cost and Utilization Project.

RESULTS: Among 4553 Health eHeart participants, the 526 with AF exhibited more frequent nighttime awakening (odd ratio [OR] 1.47; 95% confidence interval [CI] 1.14-1.89; P = .003). In 5703 Cardiovascular Health Study participants followed for a median 11.6 years, frequent nighttime awakening predicted a 33% greater risk of AF (hazard ratio [HR] 1.33; 95% CI 1.17-1.51; P <.001). In patients with polysomnography (N = 1127), every standard deviation percentage decrease in rapid eye movement (REM) sleep was associated with a 18% higher risk of developing AF (HR 1.18; 95% CI 1.00-1.38; P = .047). Among 14,330,651 California residents followed for a median 3.9 years, an insomnia diagnosis predicted a 36% increased risk of new AF (HR 1.36; 95% CI 1.30-1.42; P <.001).

CONCLUSION: Sleep disruption consistently predicted AF before and after adjustment for OSA and other potential confounders across several different populations. Sleep quality itself may be important in the pathogenesis of AF, potentially representing a novel target for prevention.

1 aChristensen, Matthew, A1 aDixit, Shalini1 aDewland, Thomas, A1 aWhitman, Isaac, R1 aNah, Gregory1 aVittinghoff, Eric1 aMukamal, Kenneth, J1 aRedline, Susan1 aRobbins, John, A1 aNewman, Anne, B1 aPatel, Sanjay, R1 aMagnani, Jared, W1 aPsaty, Bruce, M1 aOlgin, Jeffrey, E1 aPletcher, Mark, J1 aHeckbert, Susan, R1 aMarcus, Gregory, M uhttps://chs-nhlbi.org/node/778701867nas a2200253 4500008004100000022001400041245005500055210005400110260001600164300000900180490000600189520117000195100001901365700002101384700002201405700002201427700002301449700002801472700001301500700001701513700002401530700002301554856003601577 2019 eng d a2045-232200aAlcohol consumption and leukocyte telomere length.0 aAlcohol consumption and leukocyte telomere length c2019 Feb 05 a14040 v93 a

The relationship between alcohol consumption and mortality generally exhibits a U-shaped curve. The longevity observed with moderate alcohol consumption may be explained by other confounding factors, and, if such a relationship is present, the mechanism is not well understood. Indeed, the optimal amount of alcohol consumption for health has yet to be determined. Leukocyte telomere length is an emerging quantifiable marker of biological age and health, and a shorter telomere length is a predictor of increased mortality. Because leukocyte telomere length is a quantifiable and objectively measurable biomarker of aging, we sought to identify the amount of alcohol consumption associated with the longest telomere length and least telomere length attrition. Among over 2,000 participants from two distinct cohort studies, we found no pattern of alcohol consumption that was associated with longer telomere length or less telomere length attrition over time. Binge drinking may reduce telomere length. Using telomere length as a marker of age and health, these data fail to demonstrate any benefits of alcohol consumption, even when consumed in moderation.

1 aDixit, Shalini1 aWhooley, Mary, A1 aVittinghoff, Eric1 aRoberts, Jason, D1 aHeckbert, Susan, R1 aFitzpatrick, Annette, L1 aLin, Jue1 aLeung, Cindy1 aMukamal, Kenneth, J1 aMarcus, Gregory, M uhttps://chs-nhlbi.org/node/7971