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      Modifiable Predictors of Ventricular Ectopy in the Community

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          Premature ventricular contractions (PVCs) predict heart failure and death. Data regarding modifiable risk factors for PVCs are scarce.

          Methods and Results

          We studied 1424 Cardiovascular Health Study participants randomly assigned to 24‐hour Holter monitoring. Demographics, comorbidities, habits, and echocardiographic measurements were examined as predictors of PVC frequency and, among 845 participants, change in PVC frequency 5 years later. Participants exhibited a median of 0.6 (interquartile range, 0.1–7.1) PVCs per hour. Of the more directly modifiable characteristics and after multivariable adjustment, every SD increase in systolic blood pressure was associated with 9% more PVCs (95% confidence interval [CI], 2%–17%; P=0.01), regularly performing no or low‐intensity exercise compared with more physical activity was associated with ≈15% more PVCs (95% CI, 3–25%; P=0.02), and those with a history of smoking exhibited an average of 18% more PVCs (95% CI, 3–36%; P=0.02) than did never smokers. After 5 years, PVC frequency increased from a median of 0.5 (IQR, 0.1–4.7) to 1.2 (IQR, 0.1–13.8) per hour ( P<0.0001). Directly modifiable predictors of 5‐year increase in PVCs, described as the odds per each quintile increase in PVCs, included increased diastolic blood pressure (odds ratio per SD increase, 1.16; 95% CI, 1.02–1.31; P=0.02) and a history of smoking (OR, 1.31; 95% CI, 1.02–1.68; P=0.04).


          Enhancing physical activity, smoking cessation, and aggressive control of blood pressure may represent fruitful strategies to mitigate PVC frequency and PVC‐associated adverse outcomes.

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          Most cited references 31

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          Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings.

          To determine the accuracy of echocardiographic left ventricular (LV) dimension and mass measurements for detection and quantification of LV hypertrophy, results of blindly read antemortem echocardiograms were compared with LV mass measurements made at necropsy in 55 patients. LV mass was calculated using M-mode LV measurements by Penn and American Society of Echocardiography (ASE) conventions and cube function and volume correction formulas in 52 patients. Penn-cube LV mass correlated closely with necropsy LV mass (r = 0.92, p less than 0.001) and overestimated it by only 6%; sensitivity in 18 patients with LV hypertrophy (necropsy LV mass more than 215 g) was 100% (18 of 18 patients) and specificity was 86% (29 of 34 patients). ASE-cube LV mass correlated similarly to necropsy LV mass (r = 0.90, p less than 0.001), but systematically overestimated it (by a mean of 25%); the overestimation could be corrected by the equation: LV mass = 0.80 (ASE-cube LV mass) + 0.6 g. Use of ASE measurements in the volume correction formula systematically underestimated necropsy LV mass (by a mean of 30%). In a subset of 9 patients, 3 of whom had technically inadequate M-mode echocardiograms, 2-dimensional echocardiographic (echo) LV mass by 2 methods was also significantly related to necropsy LV mass (r = 0.68, p less than 0.05 and r = 0.82, p less than 0.01). Among other indexes of LV anatomy, only measurement of myocardial cross-sectional area was acceptably accurate for quantitation of LV mass (r = 0.80, p less than 0.001) or diagnosis of LV hypertrophy (sensitivity = 72%, specificity = 94%).(ABSTRACT TRUNCATED AT 250 WORDS)
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            Cigarette smoking increases sympathetic outflow in humans.

            It is generally accepted that smoking increases blood pressure and inhibits muscle sympathetic nerve activity (SNA). The decrease in muscle SNA with cigarette smoking might be secondary to baroreflex responses to the pressor effect of smoking, thus obscuring a sympathetic excitatory effect of smoking. We tested the hypothesis that smoking increases sympathetic outflow. We examined the effects of sham smoking, cigarette smoking, and cigarette smoking in combination with nitroprusside on muscle (baroreflex-dependent) SNA in 10 healthy habitual smokers. The 3 sessions were performed in random order, each study on a separate day. In an additional study, we also investigated the effects of sham smoking and cigarette smoking on skin (baroreflex-independent) SNA in 9 subjects. Compared with sham smoking, cigarette smoking alone increased blood pressure and decreased muscle SNA. When the blood pressure increase in response to smoking was blunted by nitroprusside infusion, there was a striking increase in muscle SNA. Muscle SNA increased up to 3-fold the levels seen before smoking (P<0.001), accompanied by an increase in heart rate of up to 37+/-4 bpm. Cigarette smoking also induced a 102+/-22% increase in skin SNA (P=0.03). These data provide the first direct evidence that cigarette smoking increases sympathetic outflow.
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              Physical Activity and Risk of Coronary Heart Disease and Stroke in Older Adults: The Cardiovascular Health Study.

              Although guidelines suggest that older adults engage in regular physical activity (PA) to reduce cardiovascular disease (CVD), surprisingly few studies have evaluated this relationship, especially in those >75 years. In addition, with advancing age the ability to perform some types of PA might decrease, making light-moderate exercise such as walking especially important to meet recommendations.

                Author and article information

                J Am Heart Assoc
                J Am Heart Assoc
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                16 November 2018
                20 November 2018
                : 7
                : 22 ( doiID: 10.1002/jah3.2018.7.issue-22 )
                [ 1 ] Division of Cardiology, Electrophysiology Section University of California San Francisco CA
                [ 2 ] Department of Epidemiology and Biostatistics University of California San Francisco CA
                [ 3 ] Knight Cardiovascular Institute Oregon Health & Science University Portland OR
                [ 4 ] Cardiovascular Health Research Unit and Department of Epidemiology University of Washington Seattle WA
                [ 5 ] HRV Lab School of Medicine Washington University Saint Louis MO
                Author notes
                [* ] Correspondence to: Gregory M. Marcus, MD, MAS, Division of Cardiology, University of California San Francisco, 505 Parnassus Avenue, M‐1180B, Box 0124, San Francisco, CA 94143‐0124. E‐mail: greg.marcus@
                © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                Page count
                Figures: 2, Tables: 4, Pages: 11, Words: 7727
                Funded by: Finnish Heart Foundation
                Funded by: Instrumentarium Science Foundation
                Funded by: Onni ja Hilja Tuovinen Foundation
                Funded by: Orion Research Foundation
                Funded by: Paavo Nurmi Foundation
                Funded by: National Heart, Lung, and Blood Institute
                Award ID: HHSN268201200036C
                Award ID: HHSN268200800007C
                Award ID: HHSN268201800001C
                Award ID: N01HC55222
                Award ID: N01HC85079
                Award ID: N01HC85080
                Award ID: N01HC85081
                Award ID: N01HC85082
                Award ID: N01HC85083
                Award ID: N01HC85086
                Award ID: R01 HL062181
                Award ID: U01HL080295
                Award ID: U01HL130114
                Funded by: National Institute of Neurological Disorders and Stroke
                Funded by: National Institute on Aging
                Award ID: R01AG023629
                Original Research
                Original Research
                Arrhythmia and Electrophysiology
                Custom metadata
                20 November 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.5.3 mode:remove_FC converted:20.11.2018


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