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• W4310281880 abstract "Central aortic pulse pressure (PPc) does not confer risk beyond brachial PP. Nevertheless, pulsatile pressures predict cardiovascular events beyond steady pressures (mean arterial pressure). However, the specific determinants of pulsatile pressures that confer risk remain controversial. Various studies (Framingham, Multi-Ethnic Study of Atherosclerosis [MESA], and others) have shown increased risk associated with different components of PPc (forward [Pf] or backward [Pb] travelling pressure waves). Our interest in the role of Pf and Pb is derived primarily from the Framingham data which shows no impact of PPc, but an effect of Pf on cardiovascular risk beyond brachial PP and pulse wave velocity. The impact of Pf was attributed to an increase in aortic resistance to flow in a pulsatile system (aortic characteristic impedance [Zc]) and not flow (Q). However, when the Framingham data were published whether wave re-reflection of Pb contributed to the impact of Pf on risk was unknown. In addition, whether the effects of Pf on risk were only observed in the elderly (Framingham study, mean age = 66 years) was not known. We subsequently showed in a community study across the full adult age range, that Pf was associated with target organ changes (estimated glomerular filtration rate, endothelial activation markers) and arterial events (stroke, coronary artery disease [CAD] and critical limb ischaemia) even when these events were premature. Furthermore, in 3 cohorts of the International Database of Central Arterial properties for Risk Stratification (IDCARS) study, we show that Pf and not Pb is associated with cardiovascular outcomes. We showed that the effects of Pf on target organ changes and arterial events were driven by proximal aortic Zc and hence central arterial pressures generated by the product of Zc and Q (PQxZc), and not by Pb or wave re-reflection. Nevertheless, the strongest data to indicate that central arterial function enhances risk beyond brachial pressure comes from data with beta blockers, an effect which is due to heart rate (HR). However the mechanisms by which decreases in HR increase PPc were unclear. Our recent data show that a decreased HR does not increase Pf and hence PPc through increases in Q, but rather by enhancing Pf through harmonic effects on the pulse wave. Importantly, we have shown in patients with CAD that the HR effect on PP occurs in both the aorta and peripheral arteries. Hence, the pressure wave effect which determines events beyond brachial pressure is a Pf effect which is enhanced at lower HR through harmonic effects on the pulse wave." @default.
• W4310281880 created "2022-11-30" @default.
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• W4310281880 date "2022-11-25" @default.
• W4310281880 modified "2023-09-25" @default.
• W4310281880 title "Risk associated with forward and backward arterial pulse waves" @default.
• W4310281880 doi "https://doi.org/10.1097/01.mbp.0000905204.50337.69" @default.
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