title: Impaired left ventricular function in the presence of preserved ejection in chronic hypertensive conscious pigs.
abstract: Systolic function is often evaluated by measuring ejection fraction and its preservation is often assimilated with the lack of impairment of systolic left ventricular (LV) function. Considering the left ventricle as a muscular pump, we explored LV function during chronic hypertension independently of increased afterload conditions. Fourteen conscious and chronically instrumented pigs received continuous infusion of either angiotensin II (n = 8) or saline (n = 6) during 28 days. Hemodynamic recordings were regularly performed in the presence and 1 h after stopping angiotensin II infusion to evaluate intrinsic LV function. Throughout the protocol, the mean arterial pressure steadily increased by 55 ± 4 mmHg in angiotensin II-treated animals. There were no significant changes in stroke volume, LV fractional shortening or LV wall thickening, indicating the lack of alterations in LV ejection. In contrast, we observed maladaptive changes with (1) the lack of reduction in isovolumic contraction and relaxation durations with heart rate increases, (2) abnormally blunted isovolumic contraction and relaxation responses to dobutamine and (3) a linear correlation between isovolumic contraction and relaxation durations. None of these changes were observed in saline-infused animals. In conclusion, we provide evidence of impaired LV function with concomitant isovolumic contraction and relaxation abnormalities during chronic hypertension while ejection remains preserved and no sign of heart failure is present. The evaluation under unloaded conditions shows intrinsic LV abnormalities.
authors.affiliation: Faculté de Médecine, INSERM Unité U, Créteil, France.
authors.forename: Mario
authors.initials: M
authors.lastname: Rienzo
authors.forename: Alain
authors.initials: A
authors.lastname: Bizé
authors.forename: Dionyssis
authors.initials: D
authors.lastname: Pongas
authors.forename: Stéphanie
authors.initials: S
authors.lastname: Michineau
authors.forename: Jonathan
authors.initials: J
authors.lastname: Melka
authors.forename: Hon Lai
authors.initials: HL
authors.lastname: Chan
authors.forename: Lucien
authors.initials: L
authors.lastname: Sambin
authors.forename: Jin Bo
authors.initials: JB
authors.lastname: Su
authors.forename: Jean-Luc
authors.initials: JL
authors.lastname: Dubois-Randé
authors.forename: Luc
authors.initials: L
authors.lastname: Hittinger
authors.forename: Alain
authors.initials: A
authors.lastname: Berdeaux
authors.forename: Bijan
authors.initials: B
authors.lastname: Ghaleh
mesh_terms: D000804:Angiotensin II; D000818:Animals; D003971:Diastole; D005260:Female; D006439:Hemodynamics; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced; D009200:Myocardial Contraction; D013552:Swine; D016277:Ventricular Function, Left
chemical_list: D000804:Angiotensin II