Nitenberg A, Antony I, Loiseau A
Service de physiologie et d'explorations fonctionnelles, INSERM U 426, hôpital Louis-Mourier, CHU Xavier-Bichat, Colombes.
Arch Mal Coeur Vaiss. 1997 Aug;90(8):1025-30.
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).
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.
已表明：1）高血压患者（HP）肥厚左心室（LV）的收缩性能降低；2）当心肌收缩性能降低和后负荷增加时，心室动脉（VA）耦合发生改变。为评估高血压患者肥厚左心室的收缩性能与VA耦合之间的关系，采用左心室血管造影结合微测压同步记录压力，以确定收缩末期应力/容积指数比（ESS/ESVi）、收缩末期压力-容积关系斜率即收缩末期弹性（Ees）、有效动脉弹性（Ea）、外部功（EW）和压力-容积面积（PVA）。30例HP患者和20例对照受试者（CS）的结果比较显示，以Ees/100g左心室心肌质量（LVM，经超声心动图测定）评估的左心室收缩性能降低（HP组：4.35±1.13；CS组：5.21±1.89mmHg/ml/100g；p<0.02），且与LVM呈负相关（Ees=-0.026LVM+3.363；r=0.581；p<0.001），而两组间另一种左心室收缩性能评估指标ESS/ESVi相当（HP组6.66±1.55g/cm2/ml/m2，CS组6.72±1.36；无显著性差异），且与LVM呈负相关（ESS/ESVi=-0.019LVM+8.947；r=0.369；p<0.01）。通过Ea/Ees比值（Ea和Ees单位为mmHg/ml/m2）评估的心室动脉耦合在HP组略高（0.53±0.08，CS组0.48±0.09；p<0.05），两组的工作效率（EW/PVA）相似（HP组0.78±0.04，CS组0.80±0.03），代表每搏心肌需氧量的PVA与LVM呈负相关（PVA=-0.003MVG+1.44；r=0.434；p<0.01）。
本研究表明，尽管左心室收缩性能略有降低，但HP合并左心室肥厚患者的工作效率得以保留，心室动脉耦合几乎正常。因此，左心室肥厚似乎可能是以最小能量消耗维持左心室与动脉匹配的一种有用方式。
