Abstract-Elevated heart rate (HR) and pulse pressure (PP) have a cumulative effect on cardiovascular risk, with the exception of HR Ն100 bpm. How an increase in HR may influence the PP level has never been investigated. In 11 patients with pacemaker monitoring, aortic (pulse-wave analysis) and digital (photoplethysmographic device) blood pressure were measured at 3 different levels of HR, together with determinations of carotid dimensions (echo tracking technique), wave reflections (pulse-wave analysis), and aortic pulse-wave velocity. Increased HR is associated with the following: (1) a significant increase of digital systolic, diastolic, and mean blood pressure; (2) a significant reduction of digital and carotid PP, with a more pronounced reduction of the carotid than of the digital PP, resulting in a significant PP amplification; and (3) a reduction in the time required for the backward pressure wave to return toward the heart, without any change of arterial stiffness. Increased HR significantly enhances PP amplification, leading to an increase of peripheral blood pressure without comparable change in central blood pressure. These results are important to consider for a better understanding of cardiovascular risk and the mechanism of white-coat hypertension. Key Words: pacemaker Ⅲ arteries, stiffness Ⅲ heart rate Ⅲ hypertension, white coat E pidemiological studies have shown that heart rate (HR) is a significant risk factor for cardiovascular (CV) and non-CV death (see review 1 ). Nevertheless, the predictive role of HR on CV risk has been observed in the overall population but primarily in subjects with hypertension. 1,2 This observation suggests that HR and brachial arterial blood pressure act synergistically in the development of CV complications, a finding widely accepted for systolic blood pressure (SBP) and diastolic blood pressure (DBP). 2,3 Regarding the synergistic effect of brachial pulse pressure (PP) and HR on CV risk, Thomas at al 3 have observed that a cumulative effect is indeed observed, but only within certain limits. The synergistic effect was lost in men when the PP was Ͼ63 mm Hg and the HR was Ͼ100 bpm. 3 This finding is not unexpected, because for a given cardiac output, increased HR results in a parallel decrease in stroke volume, which is one of the main hemodynamic factors influencing PP.In terms of hemodynamic mechanisms, PP is a very complex parameter. PP is determined not only by the ejection pattern of the left ventricle but also by aortic stiffness and the amplitude and timing of wave reflections. The PP propagates along the arterial tree, with higher PP values in peripheral (brachial, radial, and digital) arteries than in central (aortic and carotid) arteries. The relationship between central and peripheral PP is determined by transfer functions, which are known to be highly frequency dependent. 4 O'Rourke 5 has shown that left ventricular ejection time (LVET) is negatively related to aortic to brachial amplification, a finding implying that PP amplification is likely to increase...
