Intrinsic changes on automatism, conduction, and refractoriness by exercise in isolated rabbit heart.

We have studied the intrinsic modifications on myocardial automatism, conduction, and refractoriness produced by chronic exercise. Experiments were performed on isolated rabbit hearts. Trained animals were submitted to exercise on a treadmill. The parameters investigated were 1) R-R interval, noncorrected and corrected sinus node recovery time (SNRT) as automatism index; 2) sinoatrial conduction time; 3) Wenckebach cycle length (WCL) and retrograde WCL, as atrioventricular (A-V) and ventriculoatrial conduction index; and 4) effective and functional refractory periods of left ventricle, A-V node, and ventriculoatrial retrograde conduction system. Measurements were also performed on coronary flow, weight of the hearts, and thiobarbituric acid reagent substances and glutathione in myocardium, quadriceps femoris muscle, liver, and kidney, to analyze whether these substances related to oxidative stress were modified by training. The following parameters were larger (P < 0.05) in trained vs. untrained animals: R-R interval (365 +/- 49 vs. 286 +/- 60 ms), WCL (177 +/- 20 vs. 146 +/- 32 ms), and functional refractory period of the left ventricle (172 +/- 27 vs. 141 +/- 5 ms). Corrected SNRT was not different between groups despite the larger noncorrected SNRT obtained in trained animals. Thus training depresses sinus chronotropism, A-V nodal conduction, and increases ventricular refractoriness by intrinsic mechanisms, which do not involve changes in myocardial mass and/or coronary flow.

Modification of atrioventricular nodal electrophysiology by selective radiofrequency delivery on the anterior or posterior approaches.

An analysis was made in 14 isolated and perfused rabbit hearts of the electrophysiological effects of selective radiofrequency (RF) delivery in the anterior (group I, n = 7) or posterior zone (group II, n = 7) of the Koch triangle, with the aim of modifying atrioventricular nodal (AVN) conduction without suppressing 1:1 transmission. After opening the right atrium, RF was delivered (0.5 W) with a 1-mm diameter unipolar electrode positioned in the selected zone until a prolongation of no less than 15% was obtained in the Wenckebach cycle length (WCL). Before and after (30 min) RF, anterograde and retrograde AVN refractoriness and conduction were evaluated, stimulating from the crista terminalis (CT), the interatrial septum (IAS), and from the RV epicardium. After RF, the following percentage increments were observed in group I: AH(CT) = 36% +/- 9%, AH(IAS) = 38% +/- 11%, WCL(CT) = 28% +/- 8%, WCL(IAS) = 22% +/- 6%, functional refractory period (FRP) of the AVN(CT) = 13% +/- 11%, FRP-AVN(IAS) = 13% +/- 8%, retrograde WCL = 20% +/- 19%, and retrograde FRPVA = 13% +/- 16%. The increments observed in group II and the significances of the differences with respect to group I were: AH(CT) = 11% +/- 14% (P < 0.01), AH(IAS) = 19% +/- 32% (NS), WCL(CT) = 42% +/- 14% (P < 0.05), WCL(IAS) = 42% +/- 16% (P < 0.01), FRP-AVN(CT) = 28% +/- 28% (NS), FRP-AVN(LAS) = 21% +/- 19% (NS), retrograde WCL = 35% +/- 24% (NS), and retrograde FRP = 16% +/- 13% (NS). In both groups, the AH interval variations were not correlated with those of the rest of the parameters analyzed. Truncated nodal function curves suggestive of a dual AV nodal pathway were obtained in three experiments, though in only one of them was this observed under basal conditions. In the other two experiments, with dual AV nodal physiology only after RF (one from each group), AV nodal reentrant tachycardias were triggered with atrial extrastimulus at coupling intervals equal to or shorter than at those that cause a sudden lengthening of the AH interval, RF delivered in the anterior and posterior zones of the Koch triangle produced effects of different magnitude on the AH interval and Wenckebach cycle length. In the anterior zone the AH interval was prolonged to a greater extent, while in the posterior zone the effects were greater on the Wenckebach cycle length. No correlation existed between the variations in AH interval and Wenckebach cycle length, regardless of where RF was delivered. The evaluation of anterograde AV nodal refractoriness was similar when stimulating from the crista terminalis or from the interatrial septum. By delivering RF, it was possible to induce dual AV nodal physiology and reentrant tachycardias.

Recovery curve and concealed conduction in the His-Purkinje system of the rabbit heart: effects of radiofrequency modification of the low AV junction.

UNLABELLED: The aim of this study was to analyze the recovery curve and concealed conduction in the normal His-Purkinje system and after delivering radiofrequency current in the low AV junction, in the perfused rabbit heart. Twenty-one rabbit hearts were studied. Radiofrequency current (5 W) was delivered in the low AV junction to induce an incomplete His-Purkinje AV block (HV prolongation with 1:1 AV conduction); this was achieved in 9 experiments (Group I), while 12 experiments developed a complete block (Group II). Atrial stimulation was performed in both Groups at baseline, and in Group I after radiofrequency delivery, as follows: (1) pacing at increasing rates to determine the His-Purkinje AV block cycle length; (2) atrial extrastimulus test (A1A2) to calculate the His-Purkinje effective refractory period and the fitting of the recovery curve (H1H2 vs H2V2) to the exponential equation delta HV = a.e(-b)x(H1H2); (3) concealed conduction protocol (in 15 experiments) consisting of an atrial extrastimulus test with an interposed beat (A1-A0-A2) at a fixed A1A0 coupling interval. The baseline recovery curve fitted an exponential equation in 17 experiments (with a 93% +/- 42% maximum H2V2 increase at the shortest H1H2), but did not in 4 experiments (the maximum H2V2 increase being only 22% +/- 7%). Radiofrequency application prolonged the HV interval (25 +/- 6 ms vs 46 +/- 16 ms; P = 0.001) and His-Purkinje effective refractory period (167 +/- 28 ms vs 217 +/- 57 ms; P = 0.02). The percentage increment was greater for HV than for refractory period (99% +/- 65% vs 35% +/- 32%; P = 0.02); however, the increment of the His-Purkinje block cycle length (77% +/- 74%) only correlated with that of the refractory period (r = 0.95; P = 0.0001). The recovery curve after radiofrequency delivery fitted an exponential equation in all experiments, showing a rightward shift expressed by an increment of the constant ln a (2.7 +/- 1.9 vs 5.5 +/- 5.5; P = 0.02). Concealed conduction appeared in only three experiments at baseline. After radiofrequency, however, it was observed in all experiments, producing a rightward shift of the recovery curve and an ln a increase (2.87 +/- 1.2 vs 9.9 +/- 2.7; P = 0.0001). When Ho was conducted, the curve rightward shift and ln a increase (26 +/- 7.5; P = 0.0001) were greater. CONCLUSION: (1) His-Purkinje physiology, as in AV nodal physiology, can be described by a recovery curve that fits an exponential equation, especially if conduction becomes depressed with radiofrequency current. (2) Radiofrequency application in the low AV junction modifies His-Purkinje conduction more than refractoriness, though the refractoriness increase determines the degree of block at fast atrial rates. (3) Concealed conduction is uncommon in the normal His-Purkinje system during atrial pacing, but very frequent after modifying the low AV junction with radiofrequency current.