Hardy R I, James F W, Millard R W, Kaplan S
Children's Hospital Medical Center, Division of Cardiology, Cincinnati, Ohio.
Basic Res Cardiol. 1990 Mar-Apr;85(2):179-97. doi: 10.1007/BF01906971.
Laser-induced intramyocardial revascularization (LIR) has been used to promote direct communications between blood within the ventricular cavity and that of the existing myocardial vasculature in an attempt to increase perfusion in patients with ischemic heart disease. This study was conducted to measure the effects of LIR channels on regional myocardial flood flow (microspheres), cardiac mechanics (sonomicrometers), and myocardial tissue pressures in 18 dogs. Under baseline hemodynamic conditions (mean HR = 165.2 +/- 11.4 bpm, LVP = 123.6 +/- 22.9/4.0 +/- 1.8 mm Hg, AoP = 112.8 +/- 27.1/77.0 +/- 22.5 mm Hg), myocardial blood flow in laser-treated tissue (mean = 1.11 +/- .10 cc/min/gm before laser; .71 +/- .19 cc/min/gm after laser) was reduced as compared to blood flow in control tissue (mean = 1.12 +/- .15 cc/min/gm before laser; 1.25 +/- .22 cc/min/gm after laser). Regional myocardial systolic shortening (11.32% +/- 3.82% before laser; 7.49% +/- 2.86% after laser) was decreased by 33%. During simultaneous reversible ligation of the LAD and LCCA for 2 min, when intramyocardial channels represented the only tissue access for the injected microspheres, blood flow in laser-treated tissue was not increased above that of the control non-lasered tissue. However, regional blood flow was greater in laser-treated ischemic tissue (mean = .61 +/- .12 cc/min/gm) than in untreated ischemic areas (mean = .04 +/- .03 cc/min/gm) when left ventricular pressure (LVP) was acutely elevated (mean SLVP = 207.0 +/- 16.1 mm Hg). Using these measurements, a model is proposed to predict regional systolic pressure gradients between the left ventricular cavity and coronary intramyocardial vasculature required to permit restoration of blood flow to ischemic myocardium. We conclude that improved perfusion via laser-induced intramyocardial channels does not occur in otherwise normal myocardium exposed to acute coronary ligation and only small improvements in perfusion are noted when LVP is significantly elevated. Consideration of further clinical application of this approach is seriously cautioned awaiting additional experimental studies.
激光诱导心肌内血管重建术（LIR）已被用于促进心室腔内血液与现有心肌血管系统之间的直接沟通，试图增加缺血性心脏病患者的灌注。本研究旨在测量LIR通道对18只犬局部心肌血流量（微球）、心脏力学（超声心动图）和心肌组织压力的影响。在基线血流动力学条件下（平均心率 = 165.2±11.4次/分钟，左心室压 = 123.6±22.9/4.0±1.8毫米汞柱，主动脉压 = 112.8±27.1/77.0±22.5毫米汞柱），与对照组织中的血流相比（激光治疗前平均 = 1.12±0.15毫升/分钟/克；激光治疗后1.25±0.22毫升/分钟/克），激光治疗组织中的心肌血流量减少（激光治疗前平均 = 1.11±0.10毫升/分钟/克；激光治疗后0.71±0.19毫升/分钟/克）。局部心肌收缩期缩短率（激光治疗前11.32%±3.82%；激光治疗后7.49%±2.86%）降低了33%。在同时可逆性结扎左前降支和左颈总动脉2分钟期间，当心肌内通道是注射微球的唯一组织通路时，激光治疗组织中的血流并未增加到高于未激光治疗的对照组织。然而，当左心室压力（LVP）急性升高时（平均升高的左心室压 = 207.0±16.1毫米汞柱），激光治疗的缺血组织中的局部血流（平均 = 0.61±0.12毫升/分钟/克）高于未治疗的缺血区域（平均 = 0.04±0.03毫升/分钟/克）。利用这些测量结果，提出了一个模型来预测左心室腔与冠状动脉心肌内血管系统之间的局部收缩压梯度，以允许恢复对缺血心肌的血流。我们得出结论，在暴露于急性冠状动脉结扎的正常心肌中，通过激光诱导的心肌内通道改善灌注并未发生，并且当左心室压力显著升高时，仅观察到灌注有小的改善。在等待更多实验研究之前，严重警告考虑该方法的进一步临床应用。
