title: Pulse pressure amplification, arterial stiffness, and peripheral wave reflection determine pulsatile flow waveform of the femoral artery.
abstract: Aortic stiffness, peripheral wave reflection, and aorta-to-peripheral pulse pressure amplification all predict cardiovascular risk. However, the pathophysiological mechanism behind it is unknown. Tonometric pressure waveforms were recorded on the radial, carotid, and femoral arteries in 138 hypertensive patients (age: 56±13 years) to estimate aorta-to-peripheral amplifications, aortic augmentation index, and aortic (carotid-femoral) pulse wave velocity. The femoral Doppler velocity waveform was recorded to calculate the reverse/forward flow index and diastolic/systolic forward flow ratio. The aorta-to-femoral and aorta-to-radial amplifications correlated inversely with the aortic augmentation index and pulse wave velocity. The femoral flow waveform was triphasic, composed of systolic forward, subsequent reverse, and diastolic forward phases in 129 patients, whereas it was biphasic and lacked a diastolic forward flow in 9 patients. Both the femoral reverse index (30±10%) and diastolic forward ratio (12±4%) correlated positively with the aorta-to-femoral amplification and inversely with the aortic augmentation index and pulse wave velocity; these correlations were independent of age, sex, diastolic pressure, and femoral artery diameter. Patients with biphasic (versus triphasic) flow were older, shorter, included more diabetics, had smaller femoral diameters, and showed greater aortic pulse wave velocity even when adjusted for all of these covariates. In conclusion, because of the inverse (peripheral-to-aortic) pressure gradient, pulse pressure amplification normally produces a substantial reversal of the femoral flow, the degree of which is determined by the aortic distensibility and peripheral wave reflection. Arteriosclerosis (increased stiffness, increased augmentation, and reduced amplification) decreases both the reverse and diastolic forward flows, potentially causing circulatory disturbance of truncal organs and lower extremities.
authors.affiliation: Department of Blood Pressure Research, Tohoku University Graduate School of Medicine, Sendai, Japan. hashimoto@med.tohoku.ac.jp
authors.forename: Junichiro
authors.initials: J
authors.lastname: Hashimoto
authors.forename: Sadayoshi
authors.initials: S
authors.lastname: Ito
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D001783:Blood Flow Velocity / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D005260:Female; D005263:Femoral Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow / Q000502:physiology*; D012044:Regression Analysis; D014463:Ultrasonography; D014655:Vascular Resistance / Q000502:physiology*