Transmyocardial laser treatment denervates canine myocardium

Kwong, King F.; Kanellopoulos, Georgios K.; Nickols, Joshua C.; Pogwizd, Steven M.; Saffitz, Jeffrey E.; Schuessler, Richard B.; Sundt, Thoralf M.

doi:10.1016/s0022-5223(97)70001-1

Cited by 159 publications

(81 citation statements)

References 20 publications

(2 reference statements)

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“…But only 2 published experimental studies suggest that TMR with Ho:YAG laser destroys cardiac nerve fibers. 29,30 Kwong et al 29 evaluated cardiac afferent nerve function by hemodynamic response to bradykinin application to the laser-treated areas of a canine model. Stoll et al 30 showed that TMR performed in nonischemic porcine heart causes significant HED defects consistent with sympathetic denervation.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

confidence: 99%

Cardiac Sympathetic Denervation After Transmyocardial Laser Revascularization

et al. 1999

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“…Three hypotheses have been put forward to explain the mechanism of action of TMLR: (1) the channels produced by the laser remain patent and blood flows up them from the endocardial surface during systole 7 ; (2) through neovascularization, production of laser channels stimulates angiogenesis and therefore new blood vessel formation 8 -10 ; and (3) through denervation, the laser treatment affects cardiac visceral afferent nerve fibers, causing a decreased perception of chest pain. 11 In the third case, an effect on myocardial blood flow (MBF) would not necessarily be required.…”

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confidence: 99%

Measurement of Myocardial Blood Flow With Positron Emission Tomography Before and After Transmyocardial Laser Revascularization

Rimoldi¹,

Burns²,

Rosen³

et al. 1999

Circulation

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Background-Transmyocardial laser revascularization (TMLR) has been proposed for treatment of refractory angina. It has been hypothesized that transmural left ventricular channels created by laser improve myocardial blood flow (MBF) in the treated zones. We aimed to assess the effect of TMLR on MBF and coronary vasodilator reserve (CVR). Methods and Results-We measured MBF by means of PET with 15 O-labeled water in 7 patients with refractory angina, Canadian Cardiovascular Society (CCS) class 3.6Ϯ0.5, on 3 occasions: before and at 7.5Ϯ2.8 weeks (FU-1) and 34.6Ϯ4.7 weeks (FU-2) after TMLR performed with a synchronized, high-powered CO 2 laser. In each study, MBF was measured at rest and during maximal intravenous dobutamine. CVR was computed as dobutamine divided by resting MBF. After TMLR, CCS class was 2.2Ϯ1.7 at FU-1 and 2.4Ϯ1 at FU-2 (Pϭ0.04 versus pre-TMLR). Resting MBF in both lasered and nonlasered regions was unchanged after TMLR. Dobutamine MBF at baseline was 1.45Ϯ0.52 and 1.55Ϯ0.52 mL ⅐ min Ϫ1 ⅐ g Ϫ1 in lasered and nonlasered regions, respectively (PϭNS). At FU-1, dobutamine MBF in nonlasered regions had increased significantly to 1.89Ϯ0.82 mL ⅐ min Ϫ1 ⅐ g Ϫ1 (PϽ0.05) and was higher than in lasered regions (1.51Ϯ0.61 mL ⅐ min Ϫ1 ⅐ g Ϫ1 ; PϽ0.05 versus nonlasered). At FU-2, dobutamine MBF in nonlasered regions was still higher than in lasered regions (1.56Ϯ0.54 versus 1.21Ϯ0.44 mL ⅐ min Ϫ1 ⅐ g Ϫ1 ; PϽ0.01). CVR was comparable in nonlasered and lasered regions at baseline and FU-1, whereas it was higher in nonlasered regions at FU-2 (1.86Ϯ0.67 versus 1.53Ϯ0.72 mL ⅐ min Ϫ1 ⅐ g Ϫ1 ; PϽ0.05). Conclusions-TMLR has been shown to reduce angina in severely diseased patients. The results of our study do not support the hypothesis that the symptomatic benefit of TMLR can be ascribed to improved myocardial perfusion or CVR in lasered areas.

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“…Two other mechanisms have emerged as valid alternatives for the explanation of the clinical improvement: nerve destruction 17 and neovascularisation. Destruction of sensitive nerve fibres of the ischaemic region could decrease anginal symptoms; however, this cannot explain the segmental wall motion improvement observed in both clinical and experimental settings.…”

Section: Discussionmentioning

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 treatment denervates canine myocardium

Abstract: Transmyocardial laser treatment destroys cardiac nerve fibers, which may contribute to the reduced angina pectoris seen clinically.

Cited by 159 publications

References 20 publications

Cardiac Sympathetic Denervation After Transmyocardial Laser Revascularization

Cardiac Sympathetic Denervation After Transmyocardial Laser Revascularization

Measurement of Myocardial Blood Flow With Positron Emission Tomography Before and After Transmyocardial Laser Revascularization

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

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