Journal of hypertension · 2025
Aortic characteristic impedance-induced increases in forward wave but not central arterial pulse pressure beyond brachial blood pressure in coronary artery disease.
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Peterson Vernice R, Els Danelle, Sadiq Eitzaz, Naran Ravi, Monareng Taalib, Abdool-Carrim Talib, Cassimjee Ismail, Modi Girish, Norton Gavin R, Peters Ferande, Woodiwiss Angela J
Аннотация
BACKGROUND: Whether coronary artery disease (CAD) associates with proximal aortic stiffness-induced increases in central arterial forward wave pressures (Pf), but not peak central arterial pulse pressure (PPc) beyond peripheral PP, is uncertain. Therefore, we aimed to investigate the relationship between CAD and aortic characteristic impedance (Zc) and Pf beyond brachial PP and PPc.
METHODS: From central pressure (SphygmoCor), and aortic velocity and diameter measurements (echocardiography), we compared Zc ( n = 71) and central arterial pressure wave morphology ( n = 189) in patients with CAD, to 210 age- and sex-matched controls, and patients with stroke or critical limb ischemia (CLI) ( n = 287).
RESULTS: With adjustments for confounders, including mean arterial pressure and aortic root diameter, Zc was increased in patients with CAD compared to controls and patients with stroke or CLI ( P < 0.0001). The early systolic pressures generated by the product of peak aortic flow (Q) and Zc (P QxZc ), and Pf were also increased in patients with CAD compared to controls and patients with alternative arterial diseases ( P < 0.0005). Enhanced P QxZc at peak PPc, rather than increases in re-reflected wave pressures, accounted for increases in Pf. After further adjustments for brachial PP or SBP, the higher Pf values in patients with CAD were retained ( P < 0.01 to P < 0.0005). In contrast, although peak PPc was higher in patients with CAD or alternative arterial diseases compared to controls ( P < 0.05 to P < 0.0005), these differences were abolished by further adjustments for brachial BP.
CONCLUSION: Increases in stiffness-associated proximal aortic Zc in patients with CAD translate into increases in Pf, but not peak PPc, beyond brachial BP. Hence, the pulsatile load responsible for CAD is beyond brachial BP and poorly indexed by PPc.
METHODS: From central pressure (SphygmoCor), and aortic velocity and diameter measurements (echocardiography), we compared Zc ( n = 71) and central arterial pressure wave morphology ( n = 189) in patients with CAD, to 210 age- and sex-matched controls, and patients with stroke or critical limb ischemia (CLI) ( n = 287).
RESULTS: With adjustments for confounders, including mean arterial pressure and aortic root diameter, Zc was increased in patients with CAD compared to controls and patients with stroke or CLI ( P < 0.0001). The early systolic pressures generated by the product of peak aortic flow (Q) and Zc (P QxZc ), and Pf were also increased in patients with CAD compared to controls and patients with alternative arterial diseases ( P < 0.0005). Enhanced P QxZc at peak PPc, rather than increases in re-reflected wave pressures, accounted for increases in Pf. After further adjustments for brachial PP or SBP, the higher Pf values in patients with CAD were retained ( P < 0.01 to P < 0.0005). In contrast, although peak PPc was higher in patients with CAD or alternative arterial diseases compared to controls ( P < 0.05 to P < 0.0005), these differences were abolished by further adjustments for brachial BP.
CONCLUSION: Increases in stiffness-associated proximal aortic Zc in patients with CAD translate into increases in Pf, but not peak PPc, beyond brachial BP. Hence, the pulsatile load responsible for CAD is beyond brachial BP and poorly indexed by PPc.