Impact of arterial load and loading sequence on left ventricular tissue velocities in humans.
OBJECTIVE
The aim of this study was to examine the relationship between individual components of left ventricular (LV) afterload and tissue Doppler echocardiography (TDE) velocities in humans.


BACKGROUND
Acute increases in afterload slow diastolic relaxation as assessed invasively, yet little is known about chronic effects of load and loading sequence on LV TDE velocities.


METHODS
Forty-eight subjects underwent echo Doppler and color-coded TDE with comprehensive noninvasive vascular assessment. Arterial afterload was measured by effective arterial elastance (Ea) and systemic vascular resistance index (SVRI), and loading sequence was quantified by early- (carotid characteristic impedance [Zc]) and late-systolic loads (augmentation index [cAI]; late pressure-time integral [PTI3]). Vascular stiffness was measured by carotid-femoral pulse wave velocity (PWV) and total arterial compliance.


RESULTS
Early-diastolic velocity (E') varied inversely with Zc, SVRI, Ea, and PWV (r = -0.4 to 0.5; beta = 1.0 to 1.2; p < or = 0.004), but late-systolic load (cAI and PTI3 r = -0.6; beta = 1.6; both p < 0.0001) and arterial compliance (r = 0.6; beta = 1.4; p < 0.0001) had the strongest associations with E'. Load dependence was not altered by the presence of hypertension, and in multivariate analysis only cAI and Zc significantly predicted E', even after adjusting for age (p < 0.05). Peak systolic velocity was additionally found to be inversely related to afterload, whereas other measures of contractility were not.


CONCLUSIONS
Diastolic and systolic tissue velocities vary inversely with arterial afterload, with late-systolic load having the greatest influence on E'. These findings may partly explain the decrease in early relaxation velocity noted with aging, hypertension, and patients with heart failure. Strategies to reduce afterload, vascular stiffening, and wave reflections may prove useful to enhance early diastolic relaxation.
Borlaug
Barry A
BA
Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA. borlaug.barry@mayo.edu
Melenovsky
Vojtech
V
Redfield
Margaret M
MM
Kessler
Kristy
K
Chang
Hyuk-Jae
HJ
Abraham
Theodore P
TP
Kass
David A
DA
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016275:Atrial Function / Q000502:physiology; D001783:Blood Flow Velocity / Q000502:physiology*; D003326:Coronary Circulation / Q000502:physiology*; D003971:Diastole / Q000502:physiology*; D015150:Echocardiography, Doppler; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D008297:Male; D008365:Manometry; D008875:Middle Aged; D015999:Multivariate Analysis; D009200:Myocardial Contraction / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*