Transmyocardial laser revascularization dose response: enhanced perfusion in a porcine ischemia model as a function of channel density.

BACKGROUND: Transmyocardial laser revascularization (TMR) appears to provide symptomatic relief to patients with ischemic heart disease, but evidence that TMR enhances perfusion to ischemic myocardium remains limited. Furthermore, it is uncertain whether there exists a TMR dose-response relationship that is a function of channel number. We therefore compared restoration of blood flow as analyzed by rest and stress 99mTc-sestamibi scans and histologic grading of neovascularization after 50-channel, 25-channel, or 10-channel TMR using the excimer laser in an established model of porcine myocardial ischemia. METHODS: Yorkshire swine underwent a thoracotomy and placement of an ameroid constrictor around the proximal circumflex coronary artery. Three weeks later, the animals underwent resting and adenosine stress 99mTc-sestamibi scans for evaluation of ischemia immediately before repeat thoracotomy and TMR with either 50 channels (n = 4), 25 channels (n = 4), or 10 channels (n = 4) in the circumflex territory. The animals underwent repeat perfusion analyses 4 weeks later, after which the animals were sacrificed and the hearts were perfusion fixed for histologic evaluation of neovascularization. RESULTS: All animals survived to sacrifice. Semiquantitative analyses of the sestamibi perfusion scans 4 weeks after lasing demonstrated significant improvement (p < 0.04) in stress-induced ischemia in the 50-channel TMR animals, but not in the 25- or 10-channel TMR groups, as compared with scans obtained immediately before lasing. A computerized image analysis of perfusion scans similarly demonstrated an improvement in the area of ischemia of 42% +/- 22% in the scans obtained 4 weeks after lasing compared with scans obtained immediately before lasing in the 50-channel group (p < 0.004), but only a 12% +/- 9% improvement in the 25-channel group and an 8% +/- 4% improvement in the 10-channel group (p > 0.05). Histologic assessment of neovascularization demonstrated significantly greater number of microvessels per low-power field in the 50- versus the 25- and 10-channel groups (p < 0.001). CONCLUSIONS: In an animal model of myocardial ischemia, TMR appears to enhance myocardial perfusion. A dose-response relationship related to channel number may be of significance when evaluating the efficacy of various treatment strategies.

Carotid artery anastomosis with albumin solder and near infrared lasers: a comparative study.

BACKGROUND AND OBJECTIVE: Laser tissue-welding has been used for anastomosis of carotid arteries. During welding, thermal injury sustained by the vessel walls should be minimized to prevent thrombosis. Two different types of lasers were used and effects on tissue damage were studied in vitro and in vivo. STUDY DESIGN/MATERIALS AND METHODS: End-to-end anastomosis of dog carotid arteries (n = 10) was performed by using a human albumin solder (HAS) in conjunction with Nd:YAG or diode lasers (lambda = 1.32 microm and 1.9 microm, respectively). The arteries were evaluated for patency and evidence of histologic injury after 21 days. Another group of arteries was laser soldered in vitro to measure the intimal and adventitial temperatures by using thermocouples. RESULTS: The arteries repaired with the diode laser sustained significantly less thermal damage than those repaired with Nd:YAG laser, both in vitro and in vivo. In particular, the intimal temperature was significantly lower (P < 0.05) for the diode than for the Nd:YAG repairs (approximately 35 degrees C and approximately 50 degrees C, respectively). In the latter group, the patency rate was 75%, but thrombosis occurred in 75% of the specimens at 21 days. All diode anastomoses were patent and thrombosis developed in only 17% of the arteries. CONCLUSION: Use of the diode laser and albumin solders may provide a means to successfully repair carotid arteries with minimal thermal damage.

Cardiac angiogenesis and gene therapy: a strategy for myocardial revascularization.

Angiogenesis, the de novo formation of new vasculature, is a critical response to ischemia that provides neovascularization of ischemic tissues. In therapeutic angiogenesis, an angiogen--a mediator that induces angiogenesis--is delivered to targeted tissues, augmenting the native angiogenic process and enhancing reperfusion of ischemic tissues. Gene transfer is a novel means of providing therapeutic angiogenesis: the cDNA coding for specific angiogens, rather than the proteins themselves, is administered to the tissues in which angiogenesis is desired. This review is focused on therapeutic angiogenesis based on gene transfer strategies for the provision of myocardial revascularization.