Baur L H, Schipperheyn J J, Cats V M, van der Wall E E, Baan J, van Dijk A D, Bruschke A V
Department of Cardiology, University Hospital Leiden, The Netherlands.
Eur Heart J. 1992 Nov;13 Suppl E:52-6. doi: 10.1093/eurheartj/13.suppl_e.52.
As a rule, left ventricular relaxation is impaired in patients with coronary artery disease and congestive heart failure. In addition, the passive elastic properties in early and late diastole change when the ventricle dilates. Diastolic properties of the left ventricle were studied in 11 patients with congestive heart failure class II-IV (NYHA) before and 3 months after 10-20 mg enalapril was added to their regimen of salt restriction, a diuretic and occasionally digitalis. Haemodynamic studies were performed using radionuclide angiography and simultaneous pressure-volume measurements. Systemic vascular resistance decreased from 1479 to 1182 dynes.s.-1 cm-5 (P < 0.05) and left ventricular end-diastolic pressure from 19.2 to 15.9 mmHg (P < 0.05). Left ventricular end-diastolic volume index decreased from 130 +/- 22 to 81 +/- 22 ml (P < 0.01). Indices of early diastolic relaxation, such as peak filling rate (1.43 +/- 0.46 to 1.49 +/- 0.84 EDV/s), time to peak filling rate (460 +/- 70 to 490 +/- 70 ms), peak negative dP/dt (-903 +/- 190 to -891 +/- 190 mmHg/s) and tau, the time constant of isovolumic pressure decay (58.7 +/- 14.4 to 48.4 +/- 15.2 ms) did not change significantly. In nine patients pressure-volume loops shifted to the left in all patients but one due to reduction in end-systolic and end-diastolic volume. The steepness of the diastolic part of the pressure-volume relationship increased, indicating an increase in chamber stiffness. The stiffness constant increased about 25% towards a more normal value. The alteration in stiffness seemed to be mainly due to the change of the geometry of the ventricle and not to a major change in the visco-elastic properties of the ventricular wall. In conclusion, regression of remodelling induced by enalapril does not change diastolic function parameters in patients with chronic congestive heart failure beyond the changes caused by regression of ventricular dilation.
通常情况下，冠心病和充血性心力衰竭患者的左心室舒张功能受损。此外，心室扩张时舒张早期和晚期的被动弹性特性会发生变化。对11例II-IV级（纽约心脏协会分级）充血性心力衰竭患者在加用10 - 20毫克依那普利至限盐、利尿剂及偶尔使用洋地黄的治疗方案之前和之后3个月的左心室舒张特性进行了研究。使用放射性核素血管造影和同步压力-容积测量进行血流动力学研究。全身血管阻力从1479降至1182达因·秒·厘米⁻⁵（P < 0.05），左心室舒张末期压力从19.2降至15.9毫米汞柱（P < 0.05）。左心室舒张末期容积指数从130±22降至81±22毫升（P < 0.01）。舒张早期松弛指标，如峰值充盈率（从1.43±0.46至1.49±0.84舒张末期容积/秒）、达到峰值充盈率的时间（从460±70至490±70毫秒）、峰值负dP/dt（从-903±190至-891±190毫米汞柱/秒）以及等容压力衰减时间常数tau（从58.7±14.4至48.4±15.2毫秒）均无显著变化。在9例患者中，除1例患者外，所有患者的压力-容积环均向左移位，原因是收缩末期和舒张末期容积减小。压力-容积关系舒张部分的斜率增加，表明心室僵硬度增加。僵硬度常数增加约25%，趋向于更正常的值。僵硬度的改变似乎主要是由于心室几何形状的变化，而非心室壁粘弹性特性的重大改变。总之，依那普利诱导的重塑逆转在慢性充血性心力衰竭患者中不会改变舒张功能参数，超出心室扩张逆转所引起的变化。
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