Resting heart rate and the risk of cardiovascular disease, total cancer, and all-cause mortality - A systematic review and dose-response meta-analysis of prospective studies

Background and aim Epidemiological studies have reported increased risk of cardiovascular disease, cancer and all-cause mortality with greater resting heart rate, however, the evidence is not consistent. Differences by gender, adjustment for confounding factors, as well as the potential impact of subclinical disease are not clear. A previous meta-analysis missed a large number of studies, and data for atrial fibrillation have not been summarized before. We therefore aimed to clarify these associations in a systematic review and meta-analysis of prospective studies. Methods and results PubMed and Embase were searched up to 29 March 2017. Summary RRs and 95% confidence intervals (CIs) were calculated using random effects models. Eighty seven studies were included. The summary RR per 10 beats per minute increase in resting heart rate was 1.07 (95% CI: 1.05–1.10, I2 = 61.9%, n = 31) for coronary heart disease, 1.09 (95% CI: 1.00–1.18, I2 = 62.3%, n = 5) for sudden cardiac death, 1.18 (95% CI: 1.10–1.27, I2 = 74.5%, n = 8) for heart failure, 0.97 (95% CI: 0.92–1.02, I2 = 91.4%, n = 9) for atrial fibrillation, 1.06 (95% CI: 1.02–1.10, I2 = 59.5%, n = 16) for total stroke, 1.15 (95% CI: 1.11–1.18, I2 = 84.3%, n = 35) for cardiovascular disease, 1.14 (95% CI: 1.06–1.23, I2 = 90.2%, n = 12) for total cancer, and 1.17 (95% CI: 1.14–1.19, I2 = 94.0%, n = 48) for all-cause mortality. There was a positive dose–response relationship for all outcomes except for atrial fibrillation for which there was a J-shaped association. Conclusion This meta-analysis found an increased risk of coronary heart disease, sudden cardiac death, heart failure, atrial fibrillation, stroke, cardiovascular disease, total cancer and all-cause mortality with greater resting heart rate

[pt] ABERTURA DE CAPITAL DE UM CLUBE DE FUTEBOL: ANÁLISE DE VIABILIDADE

Physical fitness can independently lower the risk of cardiovascular disease (CVD). We explored the independent and combined associations of physical fitness, measured using the seated at rest heart rate (RHR), and the metabolic syndrome (MS), with CVD risk, as described by an elevated pulse wave velocity (PWV) in older Chinese. Data from 1,996 participants were drawn from the Guangzhou Biobank Cohort Study-Cardiovascular Disease Subcohort. Analysis of variance and logistic regression analysis were used to establish the independent and combined associations of the RHR and the MS with PWV. The RHR was independently associated with an elevated PWV (odds ratio [OR] 1.63, 95% confidence interval [CI] 1.22 to 2.18), as was the MS (OR 2.36, 95% CI 1.76 to 3.17). The participants with a high RHR, but without the MS, had an adjusted OR of 1.63 (95% CI 1.15 to 2.30) for the presence of the CVD proxy. Those with a low RHR and the MS had an adjusted OR of 2.35 (95% CI 1.66 to 3.33). The risk of an elevated PWV increased almost fourfold with both a high RHR and a diagnosis of the MS (OR 3.87, 95% CI 2.39 to 6.28, p = 0.52 for interaction). In conclusion, physical fitness, measured using the RHR, and the MS are independently associated with an elevated PWV, a surrogate marker for CVD. The strength of this association was further increased in the presence of both. These findings confirm the beneficial effects of physical fitness on attenuating the risk of CVD among older Chinese. © 2011 Elsevier Inc. All Rights Reserved.link_to_subscribed_fulltex

Psychoneuromicrobiology: Cytomegalovirus infection as a putative link between stress, aging, and immunity

Epidemiological evidence demonstrates increased morbidity and mortality in populations exposed to adverse psychosocial factors such as low socio-economic status and protracted psychological distress (Cohen and Herbert, Annu Rev Psychol 47:113-142, 1996; House et al., Science 241:540-545, 1988; Marmot, Lancet 365(9464):1099-1104, 2005; Schneiderman et al., Annu Rev Clin Psychol 1:607-628, 2005). While the data are clear, the precise mechanisms underlying these associations are yet to be determined (Antoni et al., Nat Rev Cancer 6(3):240-248, 2006; Cacioppo and Hawkley, Perspect Biol Med 46(3 Suppl):S39-52, 2003; Glaser and Kiecolt-Glaser, Nat Rev Immunol 5(3):243-251, 2005; McEwen, N Engl J Med 338(3):171-179, 1998; Uchino et al., Psychol Bull 119(3):488-531, 1996). We, and others, have argued that since increasing age is a major risk factor for a wide range of chronic diseases, the aging process itself may be an important target for such mechanistic research (Bosch et al., Brain Behav Immun 23(4):527-534, 2009; Nilsson, Med Hypotheses 47(1):39-42, 1996)