title: Effect of an acute increase in afterload on left ventricular regional wall motion velocity in healthy subjects.
abstract: We recorded left ventricular (LV) wall motion velocities before and after angiotensin II infusion by pulsed tissue Doppler imaging in 20 healthy subjects, and evaluated the responses of systolic and diastolic LV function along the long and short axes during an acute increase in afterload. Angiotensin II was administered intravenously to obtain a 30% increase in mean blood pressure. After angiotensin II infusion, LV end-systolic dimension and end-systolic circumferential wall stress increased significantly, and the percentage of LV fractional shortening decreased significantly. Peak first systolic LV wall motion velocity (Sw1 ) along the long axis decreased markedly compared with that along the short axis, and peak second systolic LV wall motion velocity (Sw2 ) along the short axis decreased significantly compared with that along the long axis. Early diastolic LV wall motion velocities along both the long and short axes decreased significantly, whereas atrial systolic LV wall motion velocity did not change. In conclusion, an acute increase in afterload caused a significant decrease in longitudinal fiber shortening during the isovolumic contraction phase (Sw1 along the long axis), circumferential fiber shortening during the ejection phase (Sw2 along the short axis), and LV relaxation during early diastole (early diastolic LV wall motion velocities along both axes) in healthy subjects. Pulsed tissue Doppler imaging may be useful for detecting the effect of various loading conditions on LV wall motion velocities along the long and short axes.
authors.affiliation: Second Department of Internal Medicine, School of Medicine, The University of Tokushima, Tokushima, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Oki
authors.forename: K
authors.initials: K
authors.lastname: Fukuda
authors.forename: T
authors.initials: T
authors.lastname: Tabata
authors.forename: Y
authors.initials: Y
authors.lastname: Mishiro
authors.forename: H
authors.initials: H
authors.lastname: Yamada
authors.forename: M
authors.initials: M
authors.lastname: Abe
authors.forename: Y
authors.initials: Y
authors.lastname: Onose
authors.forename: T
authors.initials: T
authors.lastname: Wakatsuki
authors.forename: A
authors.initials: A
authors.lastname: Iuchi
authors.forename: S
authors.initials: S
authors.lastname: Ito
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D003971:Diastole; D004452:Echocardiography; D018619:Echocardiography, Doppler, Pulsed; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles / Q000000981:diagnostic imaging*; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D009200:Myocardial Contraction; D015588:Observer Variation; D012016:Reference Values; D013599:Systole; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D014662:Vasoconstrictor Agents; D000804:Angiotensin II