John J. Cai

Electrophysiological characterization of cardiac veins in humans

AbstractBackground: The coronary sinus is a complex structure with a surrounding myocardial coat and muscle bundles that course within it. The purpose of this study was to evaluate the electrical activity of the coronary sinus (CS), great cardiac vein (GCV) and related structures, such as the Vein of Marshall (VOM). Methods and Results: Data obtained from adult (n = 114) and pediatric patients (n = 16) were analyzed. The width of atrial electrograms (EGMs) within the CS at a basic pacing cycle length of 600 ms was 46 ± 7.4 ms (mean ± SD) vs. 29.7 ± 6.3 ms in the GCV (p < 0.01). With decremental pacing the width of the EGM within the CS at 300 ms increased to 66.6 ± 8.5 ms (p < 0.1 compared to CS EGM at pacing cycle length of 600 ms). The width of the EGM within the GCV increased from 29.7 ± 6.3 ms at a pacing cycle length of 600 ms to 34.6 ± 6.0 at 300 ms (p = NS). There were no significant differences in the atrial EGM width between CS and GCV in the pediatric patients. Conclusions: We conclude that atrial electrograms are wider in the CS but not in the GCV. This finding can be explained by the presence of a myocardial coat around the CS. The rate response characteristics of the atrial electrograms within the CS are consistent with a lack of tight coupling between muscle bundles and the CS musculature. Further, the absence of such differences in pediatric patients could partly explain relative differences in types of supraventricular arrhythmias seen in different age groups.

Electrophysiologic effects of civamide (zucapsaicin) on canine cardiac tissue in vivo and in vitro

The cardiac electrophysiologic effects of civamide (zucapsaicin), the cis-isomer of the alkyl vanillylamide, capsaicin, were evaluated in intact dogs and isolated Purkinje fibers. In anesthetized dogs, the mechanism of ventricular tachycardia inducible from 1 to 3 h after coronary artery occlusion was determined by activation mapping. Of 16 dogs studied, nine had ventricular tachycardia of focal endocardial origin; four, a reentrant mechanism; and three had no inducible arrhythmia. Civamide (50 microg/kg) was administered to 10 of 13 dogs that were inducible, but three dogs were used as time controls. Transmural activation times were unaltered by civamide, but mean arterial pressure decreased from 76 +/- 10 to 66 +/- 10 mm Hg (p < 0.05), and muscle refractory periods shortened from 138 +/- 3 to 132 +/- 4 ms (p < 0.05). Civamide altered inducibility in five of six dogs with ventricular tachycardia of focal endocardial origin, but those with epicardial reentrant mechanisms were not affected in three of four dogs. With microelectrode techniques in vitro, civamide (10(-5) M) shortened the action-potential duration at 50% repolarization (APD50) from 193 +/- 13 to 177 +/- 12 ms (p < 0.01) and APD90 from 260 +/- 15 to 248 +/- 13 ms (p < 0.01) in isolated Purkinje fibers (n = 10). Nifedipine prevented the effects of civamide in vitro. These results show that civamide may alter inducibility of ventricular tachycardia with focal endocardial origin and shorten APD of Purkinje fibers in vitro. The effects of civamide in vitro are prevented by preexposure of the Purkinje fibers to nifedipine, suggesting that the electrophysiologic effects of civamide may be mediated through blockade of calcium channels.

α2-Adrenergic receptor binding in canine Purkinje fibers

Autoradiograms were developed from free running strands of Purkinje fibers and from left ventricular myocardium of dog hearts exposed to [7‐methoxy‐3H]prazosin or [O‐methyl‐3H]yohimbine in the presence or absence of excessive non‐radioactive ligands. Both Purkinje fiber and ventricular myocardium showed high density, tissue‐specific binding to [3H]prazosin. In contrast, high density, tissue‐specific binding to [3H]yohimbine was present in Purkinje fibers but not in ventricular myocardium. Membrane fractions showed high affinity, saturable, and displaceable binding with [3H]yohimbine in preparations from canine cardiac Purkinje fibers but not those from canine cardiac ventricular myocardium. Scatchard analysis of the canine Purkinje membrane α 2‐adrenergic receptor binding showed a B max of 54.9 fmol/mg protein with a K d of 6.25 nM. These results confirm the electrophysiological findings that post‐junctional α 2‐adrenergic receptors are present in Purkinje fibers.