BACKGROUND: Higher levels of resting heart rate (HR) have been associated with sudden cardiac death (SCD) but mechanisms are poorly understood. We hypothesized that severe left ventricular systolic dysfunction (LVSD) and HR-modulating drugs explain the HR-SCD relationship. OBJECTIVE: To evaluate the relationship between HR, severe LVSD, HR-modulating drugs, and SCD in the community by using a case-control approach. METHODS: From the ongoing Oregon Sudden Unexpected Death Study, SCD cases (n = 378) aged ≥35 years and with electrocardiogram-documented resting HR were compared to 378 age- and gender-matched control subjects with coronary artery disease (mean age 68 ± 13 years; 69% man). Associations with SCD were assessed by using multivariable logistic regression. RESULTS: Mean resting HR was significantly higher among SCD cases compared to controls (7.5 beats/min difference; P < .0001). HR was a significant determinant of SCD after adjustment for significant comorbidities and medications (odds ratio for 10 beats/min increase 1.26; 95% confidence interval 1.14-1.38; P < .0001). After considering LVSD, resting HR was slightly attenuated but remained significantly associated with SCD (P = .005). In addition to diabetes and digoxin as well as pulmonary and renal disease, LVSD was also independently associated with SCD (odds ratio 1.79; 95% confidence interval 1.11-2.87; P = .02). CONCLUSIONS: Contrary to expectations, the significant relationship between increased resting HR and SCD persisted even after adjustment for LVSD and HR-modulating drugs. These findings suggest a potential role for additional novel interventions/therapies that modulate autonomic tone.
BACKGROUND: Higher levels of resting heart rate (HR) have been associated with sudden cardiac death (SCD) but mechanisms are poorly understood. We hypothesized that severe left ventricular systolic dysfunction (LVSD) and HR-modulating drugs explain the HR-SCD relationship. OBJECTIVE: To evaluate the relationship between HR, severe LVSD, HR-modulating drugs, and SCD in the community by using a case-control approach. METHODS: From the ongoing Oregon Sudden Unexpected Death Study, SCD cases (n = 378) aged ≥35 years and with electrocardiogram-documented resting HR were compared to 378 age- and gender-matched control subjects with coronary artery disease (mean age 68 ± 13 years; 69% man). Associations with SCD were assessed by using multivariable logistic regression. RESULTS: Mean resting HR was significantly higher among SCD cases compared to controls (7.5 beats/min difference; P < .0001). HR was a significant determinant of SCD after adjustment for significant comorbidities and medications (odds ratio for 10 beats/min increase 1.26; 95% confidence interval 1.14-1.38; P < .0001). After considering LVSD, resting HR was slightly attenuated but remained significantly associated with SCD (P = .005). In addition to diabetes and digoxin as well as pulmonary and renal disease, LVSD was also independently associated with SCD (odds ratio 1.79; 95% confidence interval 1.11-2.87; P = .02). CONCLUSIONS: Contrary to expectations, the significant relationship between increased resting HR and SCD persisted even after adjustment for LVSD and HR-modulating drugs. These findings suggest a potential role for additional novel interventions/therapies that modulate autonomic tone.
Authors: A R Dyer; V Persky; J Stamler; O Paul; R B Shekelle; D M Berkson; M Lepper; J A Schoenberger; H A Lindberg Journal: Am J Epidemiol Date: 1980-12 Impact factor: 4.897
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Authors: Marten E van den Berg; Helen R Warren; Claudia P Cabrera; Niek Verweij; Borbala Mifsud; Jeffrey Haessler; Nathan A Bihlmeyer; Yi-Ping Fu; Stefan Weiss; Henry J Lin; Niels Grarup; Ruifang Li-Gao; Giorgio Pistis; Nabi Shah; Jennifer A Brody; Martina Müller-Nurasyid; Honghuang Lin; Hao Mei; Albert V Smith; Leo-Pekka Lyytikäinen; Leanne M Hall; Jessica van Setten; Stella Trompet; Bram P Prins; Aaron Isaacs; Farid Radmanesh; Jonathan Marten; Aiman Entwistle; Jan A Kors; Claudia T Silva; Alvaro Alonso; Joshua C Bis; Rudolf de Boer; Hugoline G de Haan; Renée de Mutsert; George Dedoussis; Anna F Dominiczak; Alex S F Doney; Patrick T Ellinor; Ruben N Eppinga; Stephan B Felix; Xiuqing Guo; Yanick Hagemeijer; Torben Hansen; Tamara B Harris; Susan R Heckbert; Paul L Huang; Shih-Jen Hwang; Mika Kähönen; Jørgen K Kanters; Ivana Kolcic; Lenore J Launer; Man Li; Jie Yao; Allan Linneberg; Simin Liu; Peter W Macfarlane; Massimo Mangino; Andrew D Morris; Antonella Mulas; Alison D Murray; Christopher P Nelson; Marco Orrú; Sandosh Padmanabhan; Annette Peters; David J Porteous; Neil Poulter; Bruce M Psaty; Lihong Qi; Olli T Raitakari; Fernando Rivadeneira; Carolina Roselli; Igor Rudan; Naveed Sattar; Peter Sever; Moritz F Sinner; Elsayed Z Soliman; Timothy D Spector; Alice V Stanton; Kathleen E Stirrups; Kent D Taylor; Martin D Tobin; André Uitterlinden; Ilonca Vaartjes; Arno W Hoes; Peter van der Meer; Uwe Völker; Melanie Waldenberger; Zhijun Xie; Magdalena Zoledziewska; Andrew Tinker; Ozren Polasek; Jonathan Rosand; Yalda Jamshidi; Cornelia M van Duijn; Eleftheria Zeggini; J Wouter Jukema; Folkert W Asselbergs; Nilesh J Samani; Terho Lehtimäki; Vilmundur Gudnason; James Wilson; Steven A Lubitz; Stefan Kääb; Nona Sotoodehnia; Mark J Caulfield; Colin N A Palmer; Serena Sanna; Dennis O Mook-Kanamori; Panos Deloukas; Oluf Pedersen; Jerome I Rotter; Marcus Dörr; Chris J O'Donnell; Caroline Hayward; Dan E Arking; Charles Kooperberg; Pim van der Harst; Mark Eijgelsheim; Bruno H Stricker; Patricia B Munroe Journal: Hum Mol Genet Date: 2017-06-15 Impact factor: 6.150