Mechanism Of Action

The cardiac plexus in man was described in detail by Mizeres.31 Cardiac fibers emanating from both vagal and sympathetic trucks form ganglionated plexus that exist in several areas including the pulmonary trunk, right and left pulmonary arteries, aortic arch, and atrial plexus. Intrinsic cardiac plexus neurons most important for SCS effects are likely found in the fat pads of the atria. Gagliardi and colleagues32 identified these spontaneously firing cardiac neurons in the epicardial fat around the pulmonary veins and right atrium. Occlusion of the aorta and increased arterial pressure induced increased neuronal firing. Foreman and colleagues33 placed spinal stimulation electrodes at T1, T2 in a canine study. During 90 percent motor threshold stimulation at 50 Hz and 0.2 millisecond trials with left anterior descending coronary ligatures placed to induce left heart ischemia, the previously increased cardiac intrinsic neuronal activity was decreased by SCS. Later, Armour et al.34 demonstrated that SCS induced persistently decreased cardiac neuronal firing for approximately 20 minutes even after the cessation of stimulation. This after-effect suggests more than just a transient coronary vasodilatation during SCS. The question of whether spinal stimulation acts via coronary blood flow increase is not clear at present.

Chauhan and colleagues35 had studied a cohort of coronary atherosclerotic disease (CAD) patients, syndrome X patients, and cardiac transplant patients with TENS. Both syndrome X and CAD patients had increased coronary flow velocity by Doppler study.

In contrast however, Norssel's group36 studied patients with a pacing-induced ischemic episode with no consistent effect on coronary blood flow velocity. Nor-epinephrine spillover through the heart, a viable measure of increased coronary flow, was unchanged in their study. However, total body norepinephrine spillover did decrease.

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