Cardiac nociceptive reflexes after transmyocardial laser revascularization: implications for the neural hypothesis of angina relief

The mechanism by which transmyocardial laser revascularization relieves angina is not understood. One theory is that laser-induced thermal damage to cardiac nerves results in cardiac denervation. This study examined the acute effects of transmyocardial laser revascularization on reflex responses mediated by cardiac nociceptors, the left ventricular receptors with sympathetic afferent fibers that are thought to mediate anginal chest pain.

Experiments were performed in 13 chloralose-anesthetized dogs with sinoaortic denervation and vagotomy. Left ventricular receptors with sympathetic afferent fibers were activated by epicardial and intracoronary bradykinin before and 45 minutes after transmyocardial laser revascularization. Reflex responses elicited by bradykinin were quantitated by direct recording of efferent renal sympathetic nerve activity. Transmyocardial laser revascularization was performed in the open-chest model with a hand-held holmium:YAG laser (2.1-microm wavelength).

An average of 44.5 +/- 1.0 channels were created. Before transmyocardial laser revascularization, reflex increases in renal sympathetic nerve activity were elicited by both epicardial and intracoronary bradykinin. After transmyocardial laser revascularization, there was no significant attenuation in the reflex responses to either epicardial (before, 66% +/- 8%; after, 100% +/- 24%; P =.19) or intracoronary (before, 124% +/- 37%; after, 108% +/- 25%; P =.44) bradykinin.

Transmyocardial laser revascularization has no significant short-term effect on reflexes mediated by left ventricular receptors with sympathetic afferent fibers in anesthetized dogs. These results indicate that transmyocardial laser revascularization does not acutely interrupt the afferent nerves, which are believed to transmit the perception of anginal pain.