Mann T, Goldberg S, Mudge G H, Grossman W
Circulation. 1979 Jan;59(1):14-20. doi: 10.1161/01.cir.59.1.14.
Mechanisms involved in the altered left ventricular (LV) diastolic properties during angina were studied in 26 patients with coronary artery disease. Angina was induced by rapid atrial pacing and measurements were made at rest and during angina in the immediate post-pacing period. No changes occurred in heart rate (71 +/- 3 to 73 +/- 3 beats/min, NS) or right ventricular (RV) end-diastolic pressure (10 +/- 1 to 11 +/- 1 mm Hg, NS), while significant increases occurred in LV end-diastolic pressure (17 +/- 1 to 30 +/- 1 mm Hg, p less than 0.01), aortic diastolic pressure (74 +/- 3 to 80 +/- 3 mm Hg, p less than 0.01), coronary sinus blood flow (133 +/- 15 to 212 +/- 32 ml/min, p less than 0.01), and the time constant (T) of LV pressure fall in early diastole (43 +/- 2 to 58 +/- 4 msec, p less than 0.01). Despite the rise in arterial pressure, a significant fall was observed in peak negative dP/dt (1961 +/- 106 to 1751 +/- 80 mm Hg/sec, p less than 0.01). Changes in RV end-diastolic pressure do not explain the increased LV end-diastolic pressure during angina. Increased aortic pressure and coronary blood flow may contribute, but the simultaneous fall in peak negative dP/dt and rise in T suggest that impaired ventricular relaxation is an important factor contributing to the previously demonstrated alteration in LV diastolic properties during angina pectoris.
对26例冠心病患者研究了心绞痛发作时左心室（LV）舒张特性改变所涉及的机制。通过快速心房起搏诱发心绞痛，并在静息时以及起搏后即刻心绞痛发作期间进行测量。心率（从71±3次/分钟增至73±3次/分钟，无显著性差异）或右心室（RV）舒张末期压力（从10±1毫米汞柱增至11±1毫米汞柱，无显著性差异）无变化，而左心室舒张末期压力显著升高（从17±1毫米汞柱增至30±1毫米汞柱，p<0.01），主动脉舒张压升高（从74±3毫米汞柱增至80±3毫米汞柱，p<0.01），冠状窦血流量增加（从133±15毫升/分钟增至212±32毫升/分钟，p<0.01），并且左心室舒张早期压力下降的时间常数（T）增加（从43±2毫秒增至58±4毫秒，p<0.01）。尽管动脉压升高，但负向最大dP/dt显著下降（从1961±106毫米汞柱/秒降至1751±80毫米汞柱/秒，p<0.01）。右心室舒张末期压力的变化并不能解释心绞痛发作时左心室舒张末期压力的升高。主动脉压力和冠状动脉血流量增加可能起了作用，但负向最大dP/dt同时下降以及T升高表明心室舒张功能受损是导致先前已证实在心绞痛发作时左心室舒张特性改变的一个重要因素。
