Transmyocardial Laser Revascularization

A 66-year-old white male with end-stage ischemic cardiomyopathy was referred to our center for transmyocardial laser revascularization (PLC Eclipse Surgical Technologies) in July 1999. The patient had a long history of interventions for his coronary artery disease, including multiple percutaneous transluminal coronary angioplasties, stent placement in 1991 and 1993, and coronary artery bypass grafting in 1987 and 1992. He was evaluated for a third bypass, but we determined he was not a suitable candidate because of his diffuse small vessel distal coronary artery disease. Given the limitations of conventional therapeutic options, the patient underwent transmyocardial laser revascularization in July 1999. Thirty transmural channels were lased in the ischemic anterior and lateral walls of the left ventricle. The patient tolerated the procedure well and received anginal relief for the following 6 months; he then experienced recurrent symptoms of angina and progressive cardiac failure. Stress thallium 201 imaging at that time demonstrated increased ischemic areas in the posterior and inferior myocardium, with improved perfusion in the previously lased anterior and lateral walls. His clinical situation continued to deteriorate, and he was listed for and subsequently received a heart transplant in March 2000. At that time, his native heart was explanted and examined for evidence of angiogenesis in the lased areas of myocardium.Gross inspection of cross-sections of the explanted heart revealed visible scar tissue in the inferior and posterolateral areas, consistent with old myocardial infarctions; however, no grossly visible scar tissue was evident in the anterolateral lased wall of the left ventricle, either on the epicardial surface or within the myocardium. The hematoxylin and eosin stained, paraffin-embedded sections of the anterolateral wall of the left ventricle demonstrated residual lased channel remnants, which were Ϸ1 mm in diameter and, therefore, were not evident during gross evaluation (Figure 1). Masson trichrome stains of the same area at the same magnification revealed minimal perichannel scarring (Figure 2). Higher magnifications of the hematoxylin-and eosin-stained sections showed multiple vessels within the channel remnant and adjacent to the channel (Figure 3). Red blood cells were present within the lumen (Figure 4). These vessels showed positive immunohistochemical staining for CD31 and factor VIII antibody, thus demonstrating the presence of endothelial linings ( Figure 5). Capillary vascular density analysis performed under high-powered fields on 5 randomly chosen lased areas revealed a mean vessel count of 3989Ϯ540; the respective vascular densities of the nonlased areas of the left and right ventricle were 1565Ϯ196 and 1523Ϯ140 vessels (PϽ0.001).To our knowledge, the photomicrographs presented here represent the longest follow-up to date after transmyocardial laser revascularization. [1][2][3] This is also the first time that red blood cells have been visualized in these neovessels. From the Re...

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“…[1][2][3] This is also the first time that red blood cells have been visualized in these neovessels. From the…”

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confidence: 73%

Histological Evidence of Angiogenesis 9 Months After Transmyocardial Laser Revascularization

et al. 2001

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“…Human autopsy studies showed occluded channels as early as 2 days after surgery. 9,10 Few studies have shown an increase in myocardial perfusion after TMR. 12,22 Increased perfusion, when present, was not correlated with channel patency.…”

Section: Discussionmentioning

confidence: 99%

“…7,8 However, the majority of human and experimental studies have not been able to demonstrate histologically sustained patency of the channels created. 9,10 Objective improvement in myocardial perfusion by thallium imaging studies has also been an inconsistent finding. 5,[11][12][13] Furthermore, improvement in myocardial perfusion has been documented primarily several months after TMR, whereas the improvement in angina is observed in most patients within a few days after the procedure.…”

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confidence: 99%

Cardiac Sympathetic Denervation After Transmyocardial Laser Revascularization

et al. 1999

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Background-Transmyocardial laser revascularization (TMR) has been shown to improve refractory angina not amenable to conventional coronary interventions. However, the mechanism of action remains controversial, because improved myocardial perfusion has not been consistently demonstrated. We hypothesized that TMR relieves angina by causing myocardial sympathetic denervation. Methods and Results-PET imaging of resting and stress myocardial perfusion with [13 N]ammonia (NH 3 ) and of sympathetic innervation with [11 C]hydroxyephedrine (HED) was performed before and after TMR in 8 patients with class IV angina ineligible for CABG or PTCA. A mean of 50Ϯ11 channels were created in the left ventricle (LV) with a holmium:YAG laser. A semiautomated program was used to determine NH 3 uptake and HED retention in the LV. Perfusion and innervation defects were defined as the percentage of LV with tracer uptake or retention Ͼ2 SD below normal mean values. All patients experienced improvement in their angina by 2.4Ϯ0.5 angina classes after surgery, Pϭ0.008. Sympathetic innervation defects exceeded resting perfusion defects in all patients before TMR (34.6Ϯ27.3% for HED versus 9.4Ϯ10.8% for NH 3 , Pϭ0.008). TMR did not significantly affect resting or stress myocardial perfusion but increased the extent of sympathetic denervation in 6 of 8 patients by 27.5Ϯ15.9%, Pϭ0.03. In the remaining 2 patients, both sympathetic denervation and stress perfusion defects decreased after surgery. Conclusions-TMR causes decreased myocardial HED uptake in most patients without significant change in resting or stress myocardial perfusion, suggesting that the improvement in angina may be at least in part due to sympathetic denervation. (Circulation. 1999;100:135-140.)

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“…Human necropsy studies [7][8][9][10] have reported an increased capillary network within the laser channels. The factors responsible for stimulating angiogenesis after laser revascularisation have not been elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…However, channel patency has been seriously questioned by experimental 5 6 as well as clinical data. [7][8][9] Neovascularisation induced by the laser has been suggested as a potential mechanism. Because of its potential for percutaneous application, the holmium:yttrium-aluminium garnet (holmium-YAG) laser has emerged as a promising device for laser revascularisation.…”

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confidence: 99%

Sudden death following occlusion of the left coronary artery by a large stalky excrescense

Abrahamsen¹,

Kristensen²,

Baandrup³

2001

Heart

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Aim-To analyse the arteriolar pattern of laser induced channels and their surroundings compared with mechanical and ischaemic injury. Methods-24 pigs were randomised to a myocardial infarction group, a transmyocardial laser revascularisation group, a needle group, or a control group. In the laser revascularisation and needle groups, five channels were created either with a 1.75 mm probe holmium-YAG laser or a Tru-cut needle of the same size. Animals were killed 28 days later. ; p = 0.6 and p = 0.4, respectively). The mean arteriolar diameter was similar throughout all the regions analysed. Conclusions-Both laser and needle channels produce a similar increase in arteriolar structures, which is limited to the lesion itself. This suggests that laser injury is not more potent as an angiogenic stimulator than mechanical injury, which in turn is superior to infarction. (Heart 2001;85:697-701)

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Transmyocardial Laser Revascularization

Cited by 174 publications

References 16 publications

Histological Evidence of Angiogenesis 9 Months After Transmyocardial Laser Revascularization

Histological Evidence of Angiogenesis 9 Months After Transmyocardial Laser Revascularization

Cardiac Sympathetic Denervation After Transmyocardial Laser Revascularization

Sudden death following occlusion of the left coronary artery by a large stalky excrescense

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