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Evidence from epidemiologic studies demonstrates that resting Heart Rate (HR) is an independent risk factor for Cardiovascular (CV) event. In addition, recent studies indicate that follow-up HR adds prognostic information over and above baseline HR. Elevated resting HR represents sympathetic over-activation leading to cardiometabolic deterioration and is also associated with subclinical inflammation and target organ damage. In addition, elevated resting HR might modify the local hemodynamic environment and contribute to atherosclerosis formation. A pure HR-lowering drug, Ivabradine, reduces CV event in patients with coronary artery disease and chronic heart failure. These findings indicate that elevated resting HR is not just as an epiphenomenon representing ?poor conditioning? but a therapeutic target. The potential role of HR and its modulation should be considered in the future guidance documents.