ObjectiveTo examine whether elevated resting heart rate (RHR) is an independent risk factor for mortality or a mere marker of physical fitness (VO2Max).MethodsThis was a prospective cohort study: the Copenhagen Male Study, a longitudinal study of healthy middle-aged employed men. Subjects with sinus rhythm and without known cardiovascular disease or diabetes were included. RHR was assessed from a resting ECG at study visit in 1985–1986. VO2Max was determined by the Åstrand bicycle ergometer test in 1970–1971. Subjects were classified into categories according to level of RHR. Associations with mortality were studied in multivariate Cox models adjusted for physical fitness, leisure-time physical activity and conventional cardiovascular risk factors.Results2798 subjects were followed for 16 years. 1082 deaths occurred. RHR was inversely related to physical fitness (p<0.001). Overall, increasing RHR was highly associated with mortality in a graded manner after adjusting for physical fitness, leisure-time physical activity and other cardiovascular risk factors. Compared to men with RHR ≤50, those with RHR >90 had an HR (95% CI) of 3.06 (1.97 to 4.75). With RHR as a continuous variable, risk of mortality increased with 16% (10–22) per 10 beats per minute (bpm). There was a borderline interaction with smoking (p=0.07); risk per 10 bpm increase in RHR was 20% (12–27) in smokers, and 14% (4–24) in non-smokers.ConclusionsElevated RHR is a risk factor for mortality independent of physical fitness, leisure-time physical activity and other major cardiovascular risk factors.

High triglyceride (TG) and low HDL cholesterol (HDL-C) is the characteristic dyslipidemia seen in insulin-resistant subjects. We examined the role of this dyslipidemia as a risk factor of ischemic heart disease (IHD) compared with that of high LDL cholesterol (LDL-C) in the Copenhagen Male Study. In total 2910 white men, aged 53 to 74 years, free of cardiovascular disease at baseline, were subdivided into four groups on the basis of fasting concentrations of serum TG, HDL-C, and LDL-C. "High TG-low HDL-C" was defined as belonging to both the highest third of TG and the lowest third of HDL-C; this group encompassed one fifth of the population. "High LDL-C" was defined as belonging to the highest fifth of LDL-C. A control group was defined as not belonging to either of these two groups. "Combined dyslipidemia" was defined as belonging to both dyslipidemic groups. Age-adjusted incidence of IHD during 8 years of follow-up was 11.4% in high TG-low HDL-C, 8.2% in high LDL-C, 6.6% in the control group, and 17.5% in combined dyslipidemia. Compared with the control group, relative risks of IHD (95% confidence interval), adjusted for potentially confounding factors or covariates (age, body mass index, alcohol consumption, physical activity, non-insulin-dependent diabetes, hypertension, smoking, and social class), were 1.5 (1.0-2.1), P < .05; 1.3 (0.9-2.0), P = .16; and 2.4 (1.5-4.0), P < .01, in the three dyslipidemic groups, respectively. In conclusion, the present results showed that high TG-low HDL-C, the characteristic dyslipidemia seen in insulin-resistant subjects, was at least as powerful a predictor of IHD as isolated high LDL-C. The results suggest that efforts to prevent IHD should include intervention against high TG-low HDL-C, and not just against hypercholesterolemia.

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Men with conventional risk factors for IHD have a low risk of IHD if they have low TG--high HDL-C levels.