title: Pulsatile hemodynamics in congestive heart failure.
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 DeltaP (carotid) and DeltaQ (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 (62+/-16 versus 53+/-15 mm Hg, P=0.015) in CHF because of lower diastolic pressure (66+/-10 versus 73+/-9 mm Hg, P=0.003). CHF had higher Z(c) (225+/-76 versus 184+/-66 dyne. sec. cm(-5), P=0.020). CF-PWV did not differ (9.7+/-2.7 versus 9.2+/-2.0, P=0.337), whereas CR-PWV was lower in CHF (8.6+/-1.4 versus 9.4+/-1.5, P=0.038). There was no difference in TAC (1.4+/-0.5 versus 1.4+/-0.6 mL/mmHg, P=0.685), and augmentation index was lower in CHF (8+/-17 versus 21+/-13%, P=0.001). CHF subjects have elevated central pulsatile load (Z(c)), which is not apparent in global measures such as augmentation index or TAC, possibly because of contrasting changes in central and peripheral conduit vessels. This increased pulsatile load represents an important therapeutic target in CHF.
authors.affiliation: Cardiovascular Engineering Inc, Holliston, MA 01746, USA. GaryFMitchell@mindspring.com
authors.forename: G F
authors.initials: GF
authors.lastname: Mitchell
authors.forename: J C
authors.initials: JC
authors.lastname: Tardif
authors.forename: J M
authors.initials: JM
authors.lastname: Arnold
authors.forename: G
authors.initials: G
authors.lastname: Marchiori
authors.forename: T X
authors.initials: TX
authors.lastname: O'Brien
authors.forename: M E
authors.initials: ME
authors.lastname: Dunlap
authors.forename: M A
authors.initials: MA
authors.lastname: Pfeffer
mesh_terms: D001158:Arteries / Q000503:physiopathology*; D001783:Blood Flow Velocity; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D003285:Contractile Proteins; D004311:Double-Blind Method; D004548:Elasticity; D004562:Electrocardiography; D016326:Extracellular Matrix Proteins; D005260:Female; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow; D000072260:RNA Splicing Factors; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology
chemical_list: D003285:Contractile Proteins; D016326:Extracellular Matrix Proteins; D000072260:RNA Splicing Factors; C016598:microfibrillar protein