Transmyocardial laser revascularisation in acutely ischaemic myocardium1

Abstract

Objective: Although recent experience suggests that transmyocardial laser revascularisation (TMLR) relieves angina, its mechanism of action remains undefined. We examined its functional effects and analysed its morphological features in an animal model of acute ischaemia. Methods: A total of 15 pigs were randomised to ligation of left marginal arteries (infarction group, n =5), to TMLR of the left lateral wall using a holmium:yttrium-aluminium garnet (Ho:YAG) laser (laser group, n= 5), and to both (laser-infarction group, n=5). All the animals were sacrificed 1 month after the procedure. Haemodynamics and echocardiography with segmental wall motion score were carried out at both time intervals (scale 0-3: 0, normal; 1, hypokinesia; 2, akinesia; 3, dyskinesia). Histology of the involved area was analysed. Results: Laser group showed no change of the segmental wall motion score of the involved area 30 min after the laser channels were made (score: 0 90). Infarction and laser-infarction groups both showed a persistent and definitive increase of the segmental wall motion score (at 30 min: 1.6 9 0.3 and 2 90, respectively; at 1 month: 1.8 90.2 and 1.8 90.4, respectively). These increases were all statistically significant in comparison with baseline values (PB0.5), however comparison between infarction and laser-infarction groups showed no significant difference. On macroscopic examination of the endocardial surface, no channel was opened. On histology, there were signs of neovascularisation around the channels in the laser group, whereas in the laser-infarction group the channels were embedded in the infarction scar. Conclusions: In this acute pig model, TMLR did not provide improvement of contractility of the ischaemic myocardium. To the degree that the present study pertains to the clinical setting, the results suggest that mechanisms other than blood flow through the channels should be considered, such as a laser-induced triggering of neovascularisation or neural destruction.

Solute uptake through the walls of a pulsating channel

“…Although the exact mechanism of TMLR is unknown, improved perfusion and relief of symptoms after treatment could result from patent (open) tunnels created by the laser or from laser-induced angiogenesis. While some studies have found evidence of tunnel patency and of angiogenesis (Frazier, March & Horvath 1999 and references therein; Kadipasaoglu et al 1997;Berwing et al 1997) others have failed to find such evidence (Hardy et al 1987;Landreneau et al 1991;Mueller et al 1998). Schofield et al (1999) found no evidence of improved cardiac function or myocardial perfusion, although they did find that the treatment provided relief from angina symptoms.…”

Transmyocardial Laser Revascularization: Established Procedure, Acupuncture of the Heart or Placebo Effect?

“…Whittaker et al [30,31] and others [32] found that TMLR does not increase myocardial blood flow in a region after ligature of a coronary artery, except if the channels were created 2 months before the coronary occlusion. A favorable effect of TMLR during acute myocardial infarction could also not be proven [33,34].…”

Effectiveness of percutaneous laser revascularization therapy for refractory angina

“…As with TMLR,14 the mechanisms of action during PMLR are unclear. Proposed laser mechanisms with insufficient and/or contradictory evidence include direct perfusion,15–18 microvascular angiogenesis,19–23 and cardiac afferent denervation 24–27. There is also insufficient evidence to support placebo effect13,28 and change in attitudes and expectations24 towards angina as significant factors in symptom relief.…”