Abstract-Pulse pressure, an indirect measure of vascular stiffness and pulsatile load, predicts clinical events in congestive heart failure (CHF), suggesting that abnormal pulsatile load may contribute to CHF. This study was designed to assess more direct measures of central pulsatile load in CHF. Noninvasive hemodynamic evaluations were performed in 28 subjects with CHF and 40 controls using calibrated tonometry of the brachial, radial, femoral, and carotid arteries along with echocardiographic assessment of left ventricular outflow tract (LVOT) diameter and Doppler flow. Characteristic impedance (Z c ) was calculated as the ratio of ⌬P (carotid) and ⌬Q (LVOT flow) in early systole. Carotid-radial (CR-PWV) and carotid-femoral (CF-PWV) pulse wave velocities were calculated from tonometry. Augmentation index was assessed from the carotid waveform. Total arterial compliance (TAC) was calculated using the area method. Brachial pulse pressure was elevated (62Ϯ16 versus 53Ϯ15 mm Hg, Pϭ0.015) in CHF because of lower diastolic pressure (66Ϯ10 versus 73Ϯ9 mm Hg, Pϭ0.003). CHF had higher Z c (225Ϯ76 versus 184Ϯ66 dyne · sec · cm Ϫ5
Background. Although progressive chronic congestive heart failure (CHF) is associated with elevated systemic vascular resistance and increased impedance to ventricular outflow, the contribution of changes in large artery function has not been well documented in humans.Methods and Results. We studied 45 patients with a broad range of clinical severity of CHF and compared noninvasive measurements of brachial artery diameter, flow, and pulse wave velocity with 22 normal controls of similar age. In CHF, mean arterial pressure was lower than in
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