Erbel R, Schweizer P, Meyer J, Krebs W, Kempen P
Z Kardiol. 1979 Dec;68(12):809-20.
The mechanism of poststimulation potentiation (PSP) was studied in 17 patients with coronary artery disease by simultaneous pressure-dimension analysis. The left ventricular pressure (LVP) was measured by catheter-tip-micromanometer and LV diameter by M-mode echocardiography. The pressure signals were digitised and analysed on line by 400 Hz. The pressure-dimension tracings were additionally analysed half-automatically. Measurements were done during right atrial pacing at 80, 120, 140 beats/min and during the poststimulation period. 1. Right atrial pacing increased the rate of LV pressure development (dp/dt max), the rate of pressure fall (dp/dt min), the velocity of circumferential fiber shortening (VCF mn), and fiber dilatation (vcf mx) dependent on heart rate and cardiac function. 2. LV enddiastolic diameter (LVEDD) reached during the first poststimulation period the starting point independent on pacing rate and cardiac function. LV enddiastolic pressure (LVEDP) showed a slight overshoot. PSP resulted in an increase of LVP, dp/dt max, VCF mn, and the velocity of posterior wall motion, dp/dt min, VCF mx, and the velocity of posterior wall relaxation decreased, however, with the first post-stimulation beat. 3. The PSP was dependent on atrial pacing rate. The higher the pacing rate the higher the PSP. dp/dt max increased after cessation of 120/min for +29% and after 140/min for +38%. The PSP for the preload independent parameter of contractility, V-40, was, however, equal for both heart rates +25% and +28% respectively. 4. Another determinant of PSP was cardiac function. The PSP was relatively higher in patients with reduced ejection fraction than in patients with a normal ejection fraction: dp/dt max +55% and 25%, VCF mn +18% and +7% respectively. From the derived ventricular function curves, it could be shown, that atrial pacing reflected an increase in LV contractility (Bowditch effect), whereas PSP reflected an increase in LV performance by the Frank-Straub-Starling (Woodworth staircase) effect on a new left ventricular function curve, which was shifted to the left by atrial pacing.
通过同步压力-维度分析，对17例冠心病患者的刺激后增强（PSP）机制进行了研究。采用导管尖端微测压仪测量左心室压力（LVP），用M型超声心动图测量左心室直径。压力信号经数字化处理后以400Hz进行在线分析。压力-维度曲线还进行了半自动分析。测量在右心房以80、120、140次/分钟起搏时以及刺激后期间进行。1. 右心房起搏增加了左心室压力上升速率（dp/dt max）、压力下降速率（dp/dt min）、圆周纤维缩短速度（VCF mn）以及纤维扩张速度（vcf mx），其依赖于心率和心功能。2. 在第一个刺激后期间，左心室舒张末期直径（LVEDD）达到与起搏速率和心功能无关的起始点。左心室舒张末期压力（LVEDP）出现轻微的过冲。PSP导致LVP、dp/dt max、VCF mn以及后壁运动速度增加，然而，dp/dt min、VCF mx以及后壁松弛速度在第一个刺激后搏动时下降。3. PSP依赖于心房起搏速率。起搏速率越高，PSP越高。停止120次/分钟起搏后dp/dt max增加29%，停止140次/分钟起搏后增加38%。然而，对于前负荷独立的收缩性参数V-40，两种心率下的PSP分别相等，为25%和28%。4. PSP的另一个决定因素是心功能。射血分数降低的患者的PSP相对高于射血分数正常的患者：dp/dt max分别为55%和25%，VCF mn分别为18%和7%。从推导的心室功能曲线可以看出，心房起搏反映了左心室收缩性的增加（鲍迪奇效应），而PSP通过对新的左心室功能曲线的弗兰克-斯特劳布-斯塔林（伍德沃思阶梯）效应反映了左心室性能的增加，该曲线因心房起搏而向左移位。
