Cardiac sympathetic denervation after transmyocardial laser revascularization

Thabet Al-Sheikh, Keith B. Allen, Susan P. Straka, David A. Heimansohn, Richard L. Fain, Gary Hutchins, Stephen Sawada, Douglas P. Zipes, Erica D. Engelstein

Research output: Contribution to journalArticle

118 Citations (Scopus)

Abstract

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 [13N]ammonia (NH3) and of sympathetic innervation with [11C]hydroxyephedrine (HED) was performed before and after TMR in 8 patients with class IV angina ineligible for CABG or PICA. A mean of 50 1/4 1 channels were created in the left ventricle (LV) with a holmium:YAG laser. A semiautomated program was used to determine NH3 uptake and HED retention in the LV. Perfusion and innervation defects were defined as the percentage of LV with tracer uptake or retention >2 SD below normal mean values. All patients experienced improvement in their angina by 2.4±0.5 angina classes after surgery, P=0.008. Sympathetic innervation defects exceeded resting perfusion defects in all patients before TMR (34.6±27.3% for HED versus 9.4±10.8% for NH3, P=0.008). TMR did not significantly affect resting or stress myocardial perfusion but increased the extent of sympathetic denervation in 6 of 8 patients by 27.5±15.9%, P=0.03. 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.

Original languageEnglish
Pages (from-to)135-140
Number of pages6
JournalCirculation
Volume100
Issue number2
StatePublished - Jul 13 1999

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Transmyocardial Laser Revascularization
Sympathectomy
Perfusion
Heart Ventricles
Solid-State Lasers
Ammonia
Reference Values

Keywords

  • Angina
  • Lasers
  • Nervous system, autonomic
  • Revascularization

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Al-Sheikh, T., Allen, K. B., Straka, S. P., Heimansohn, D. A., Fain, R. L., Hutchins, G., ... Engelstein, E. D. (1999). Cardiac sympathetic denervation after transmyocardial laser revascularization. Circulation, 100(2), 135-140.

Cardiac sympathetic denervation after transmyocardial laser revascularization. / Al-Sheikh, Thabet; Allen, Keith B.; Straka, Susan P.; Heimansohn, David A.; Fain, Richard L.; Hutchins, Gary; Sawada, Stephen; Zipes, Douglas P.; Engelstein, Erica D.

In: Circulation, Vol. 100, No. 2, 13.07.1999, p. 135-140.

Research output: Contribution to journalArticle

Al-Sheikh, T, Allen, KB, Straka, SP, Heimansohn, DA, Fain, RL, Hutchins, G, Sawada, S, Zipes, DP & Engelstein, ED 1999, 'Cardiac sympathetic denervation after transmyocardial laser revascularization', Circulation, vol. 100, no. 2, pp. 135-140.
Al-Sheikh T, Allen KB, Straka SP, Heimansohn DA, Fain RL, Hutchins G et al. Cardiac sympathetic denervation after transmyocardial laser revascularization. Circulation. 1999 Jul 13;100(2):135-140.
Al-Sheikh, Thabet ; Allen, Keith B. ; Straka, Susan P. ; Heimansohn, David A. ; Fain, Richard L. ; Hutchins, Gary ; Sawada, Stephen ; Zipes, Douglas P. ; Engelstein, Erica D. / Cardiac sympathetic denervation after transmyocardial laser revascularization. In: Circulation. 1999 ; Vol. 100, No. 2. pp. 135-140.
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abstract = "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 [13N]ammonia (NH3) and of sympathetic innervation with [11C]hydroxyephedrine (HED) was performed before and after TMR in 8 patients with class IV angina ineligible for CABG or PICA. A mean of 50 1/4 1 channels were created in the left ventricle (LV) with a holmium:YAG laser. A semiautomated program was used to determine NH3 uptake and HED retention in the LV. Perfusion and innervation defects were defined as the percentage of LV with tracer uptake or retention >2 SD below normal mean values. All patients experienced improvement in their angina by 2.4±0.5 angina classes after surgery, P=0.008. Sympathetic innervation defects exceeded resting perfusion defects in all patients before TMR (34.6±27.3{\%} for HED versus 9.4±10.8{\%} for NH3, P=0.008). TMR did not significantly affect resting or stress myocardial perfusion but increased the extent of sympathetic denervation in 6 of 8 patients by 27.5±15.9{\%}, P=0.03. 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.",
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AU - Allen, Keith B.

AU - Straka, Susan P.

AU - Heimansohn, David A.

AU - Fain, Richard L.

AU - Hutchins, Gary

AU - Sawada, Stephen

AU - Zipes, Douglas P.

AU - Engelstein, Erica D.

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N2 - 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 [13N]ammonia (NH3) and of sympathetic innervation with [11C]hydroxyephedrine (HED) was performed before and after TMR in 8 patients with class IV angina ineligible for CABG or PICA. A mean of 50 1/4 1 channels were created in the left ventricle (LV) with a holmium:YAG laser. A semiautomated program was used to determine NH3 uptake and HED retention in the LV. Perfusion and innervation defects were defined as the percentage of LV with tracer uptake or retention >2 SD below normal mean values. All patients experienced improvement in their angina by 2.4±0.5 angina classes after surgery, P=0.008. Sympathetic innervation defects exceeded resting perfusion defects in all patients before TMR (34.6±27.3% for HED versus 9.4±10.8% for NH3, P=0.008). TMR did not significantly affect resting or stress myocardial perfusion but increased the extent of sympathetic denervation in 6 of 8 patients by 27.5±15.9%, P=0.03. 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.

AB - 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 [13N]ammonia (NH3) and of sympathetic innervation with [11C]hydroxyephedrine (HED) was performed before and after TMR in 8 patients with class IV angina ineligible for CABG or PICA. A mean of 50 1/4 1 channels were created in the left ventricle (LV) with a holmium:YAG laser. A semiautomated program was used to determine NH3 uptake and HED retention in the LV. Perfusion and innervation defects were defined as the percentage of LV with tracer uptake or retention >2 SD below normal mean values. All patients experienced improvement in their angina by 2.4±0.5 angina classes after surgery, P=0.008. Sympathetic innervation defects exceeded resting perfusion defects in all patients before TMR (34.6±27.3% for HED versus 9.4±10.8% for NH3, P=0.008). TMR did not significantly affect resting or stress myocardial perfusion but increased the extent of sympathetic denervation in 6 of 8 patients by 27.5±15.9%, P=0.03. 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.

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KW - Lasers

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