[Ventriculoarterial coupling and left ventricular performance in hypertensive patients with left ventricular hypertrophy].
It has been shown that 1) contractile performance of hypertrophied left ventricle (LV) of hypertensive patients (HP) is depressed, and 2) ventriculoarterial (VA) coupling is altered when myocardial contractile performance is reduced and when afterload is increased. To assess the relationship between contractile performance of hypertrophied LV and the VA coupling in hypertensive patients. LV angiography coupled with simultaneous recording of pressures with micromanometer were used to determine end-systolic stress/volume index ratio (ESS/ESVi), the slope of end-systolic pressure-volume relationship, i.e. end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW) and pressure-volume area (PVA). Comparison of results in 30 HP and 20 control subjects (CS) showed that LV contractile performance assessed by Ees/100 g left ventricular myocardial mass (LVM, echocardiographic determination) was depressed (HT: 4.35 +/- 1.13; CS: 5.21 +/- 1.89 mmHg/ml/100 g; p < 0.02) and was negatively correlated to the LVM (Ees = -0.026 LVM + 3.363; r = 0.581; p < 0.001), when ESS/ESVi, another estimate of LV contractile performance, was comparable in the 2 groups (6.66 +/- 1.55 g/cm2/ml/m2 in HT vs 6.72 +/- 1.36 in CS; NS) and negatively correlated with the LVM (ESS/ESVi = -0.019 LVM + 8.947; r = 0.369; p < 0.01). Ventriculoarterial coupling evaluated through Ea/Ees ratio (Ea and Ees in mmHg/ml/m2) was slightly higher in HT (0.53 +/- 0.08 vs 0.48 +/- 0.09 in CS; p < 0.05), work efficiency (EW/PVA) was similar in the 2 groups (0.78 +/- 0.04 in HP vs 0.80 +/- 0.03 in CS) and PVA, which is representative of the myocardial oxygen demand per beat, is negatively related to LVM (PVA = -0.003 MVG + 1.44; r = 0.434; p < 0.01).


CONCLUSIONS
this study shows that despite a slight depression of LV contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in HP with LV hypertrophy. Thus, it appears that LV hypertrophy might be a useful means of preservation of matching LV and arterial receptor with minimal energetical cost.
Nitenberg
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A
Service de physiologie et d'explorations fonctionnelles, INSERM U 426, hôpital Louis-Mourier, CHU Xavier-Bichat, Colombes.
Antony
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I
Loiseau
A
A
D001794:Blood Pressure; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D014655:Vascular Resistance; D016277:Ventricular Function, Left