VENTRICULOARTERIAL COUPLING AND LEFT-VENTRICULAR PERFORMANCE IN HYPERTENSIVE PATIENTS WITH LEFT-VENTRICULAR HYPERTROPHY

It has been shown that 1) contractile performance of hypertrophied lef t ventricle (LV) of hypertensive patients (HP) is depressed, and 2) ve ntriculoarterial (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 t he VA coupling in hypertensive patients, LV angiography coupled with s imultaneous recording of pressures with micromanometer were used to de termine end-systolic stress/volume index ratio (ESS/ESVi). the slope o f end-systolic pressure-volume relationship, i.e. end-systolic elastan ce (Ees), effective arterial elastance (Ea), external work (EW) and pr essure-volume area (PVA). Comparison of results in 30 HP and 20 contro l subjects (CS) showed that LV contractile performance assessed by Ees /100 g left ventricular myocardial mass (LVM, echocardiographic determ ination) 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 = -0.0 26 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/cm(2)/ml/m(2) in HT vs 6.72 +/- 1.36 in CS; NS) and negative ly 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/m(2)) was slightly higher in HT (0.53 +/- 0.08 vs 0.48 +/- 0.09 in CS; p < 0.05), work efficiency (EW/PVA) was simila r 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 ventricul oarterial coupling is almost normal in HP with LV hypertrophy. Thus, i t appears that LV hypertrophy might be a useful means of preservation of matching LV and arterial receptor with minimal energetical cost.