title: Left ventricular mechanical efficiency in hypertensive patients with and without increased myocardial mass and with normal pump function.
abstract: Left ventricular hypertrophy (LVH) is a physiologic process of adaptation of the heart to mechanical load increase. Despite depression of left ventricular contractile performance, mechanical efficiency and ventriculoarterial coupling are preserved in hypertensive patients with LVH. To assess the differences between patients with and without LVH, left ventricular contractile performance and the ventriculoarterial coupling were compared in two groups of hypertensive patients with similar body surface area and arterial pressures, and normal pump function: 30 patients with LVH (group 1) and 23 without LVH (group 2). Left ventricular angiography coupled with simultaneous recording of pressures with a micromanometer were used to determine end-systolic stress-to-volume ratio (ESSVR), end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW), and pressure-volume area (PVA). Myocardial contractile performance, assessed by Ees normalized by myocardial mass and by ESSVR, was lower in group I than in group 2 (1.23 +/- 0.28 v 1.89 +/- 0.48 mm Hg/mL/100 g, and 3.85 +/- 0.99 v 5.13 +/- 0.56 g/cm2/mL, respectively, both P < .001). Ventriculoarterial coupling evaluated through Ea/Ees ratio, and mechanical efficiency evaluated through EW/PVA ratio, were similar in the two groups (0.53 +/- 0.08 v 0.51 +/- 0.05, and 0.78 +/- 0.03 v 0.80 +/- 0.02, respectively, NS). In conclusion, this study shows that ventriculoarterial coupling and mechanical efficiency are comparable in hypertensive patients with and without LVH. These results suggest that in hypertensive patients, the matching between left ventricular performance and arterial load and the energy transfer are preserved either through left ventricular hypertrophy with moderate depression of myocardial contractile performance or through enhancement of myocardial contractile performance in patients with normal left ventricular mass.
authors.affiliation: Service de Physiologie et d'Explorations Fonctionnelles Hôpital Louis Mourier, Colombes, France. alain.nitenberg@lmr.ap-hop-paris.fr
authors.forename: A
authors.initials: A
authors.lastname: Nitenberg
authors.forename: A
authors.initials: A
authors.lastname: Loiseau
authors.forename: I
authors.initials: I
authors.lastname: Antony
mesh_terms: D000328:Adult; D000368:Aged; D004548:Elasticity; D005260:Female; D006801:Humans; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology