Statins, Central Blood Pressure, and Blood Pressure Amplification
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It is well established that blood pressure (BP) differs markedly between peripheral (brachial) and central arteries (aorta).1 As the pressure wave travels distally from the heart, mean BP and diastolic BP decrease slightly (1 to 2 mmHg), but a gradual and significant increase of systolic BP (SBP) and pulse pressure (PP) occurs. This phenomenon is called BP amplification.1 The development of commercially available devices for the assessment of central BP has boosted this field of clinical research.1–3 Numerous studies have shown the close pathophysiological connection between central BP and cardiovascular diseases1–4 and have highlighted the ability of central BP to provide complementary data on cardiovascular risk beyond that provided by brachial BP.2–6
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In the present issue of Circulation,7 data from the Conduit Artery Function Evaluation-Lipid-Lowering Arm (CAFE-LLA, a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial [ASCOT]l8,9) on the effect of statins on central BP is presented. Before commenting on the available data, we briefly summarize the pathophysiology of PP amplification. Finally, we discuss potential strategies based on central hemodynamics that will hopefully improve cardiovascular risk assessment and reduction.
Pathophysiology of BP Amplification and Cardiovascular Diseases
As a consequence of the pulsatile nature of blood flow and of the presence of arterial stiffness/diameter gradient along the arterial tree, pressure wave reflections arise at various sites of the arterial bed.1 The backward-traveling reflected wave sums up with the forward-traveling wave, forming the actual pressure waveform (Figure 1a). Whereas in healthy young subjects the average aortic SBP is 100 to 110 mm Hg, at the same time the brachial SBP is amplified substantially and reaches 120 to 130 mm Hg.10 This difference of 10 to 30 mm Hg expresses the amplification of the SBP (Figure 1a).1,10 Because DBP is practically steady between the aorta and …