Effect of continuous enhanced vagal tone on atrioventricular nodal and sinoatrial nodal function in humans

A constant intravenous infusion of phenylephrine (0.74 +/- 0.41 micrograms/kg/min) was given to 10 patients to cause a continuous augmentation in reflex vagal tone. After the infusion, the diastolic blood pressure increased from 76 +/- 7 to 89 +/- 11 mm Hg (p less than 0.01). The sinus cycle length and atrial-His (AH) interval were measured, and incremental atrial pacing was performed before and during phenylephrine infusion until atrioventricular (AV) nodal block was achieved. For each patient, the AV nodal function curve (i.e., the AH interval plotted as a function of the atrial pacing cycle length) was compared during both the control state and phenylephrine infusion; the AH intervals during each condition at chosen short (AHS) and long (AHL) cycle lengths were compared. The sinus cycle length increased during phenylephrine infusion from 941 +/- 294 to 1,115 +/- 347 msec (p = 0.013). The AH interval during sinus rhythm was not significantly prolonged (77 versus 82 msec, p = NS). The shortest atrial pacing cycle length yielding 1:1 AV nodal conduction increased during phenylephrine infusion from 412 +/- 120 to 575 +/- 211 msec (p less than 0.01). Of note, the degree of sinus cycle length prolongation did not correlate with the degree of prolongation in the shortest atrial pacing cycle length yielding 1:1 AV nodal conduction. The AV nodal function curve was shifted markedly to the right and only slightly upward.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sequential dual chamber extrastimulation: A novel pacing maneuver to identify the presence of a slowly conducting concealed accessory pathway

BACKGROUND: Transient VA block can be created in the AV node (AVN) when an atrial extrastimulus is delivered at the AVN effective refractory period (ERP) due to anterograde concealed conduction. OBJECTIVE: We hypothesized that ventricular stimulation during pacing-induced AVN refractoriness could identify concealed accessory pathways (APs) that remain hidden with standard maneuvers. METHODS: Patients undergoing electrophysiological study for supraventricular tachycardia were screened for presence of an AP using standard pacing maneuvers and/or V pacing during adenosine infusion. The dual-chamber sequential extrastimulation maneuver consisted of an 8-beat drive train of simultaneous AV pacing at 600 msec, followed by an A2 delivered at AVN ERP, followed by a V2 delivered at the drive train cycle length (600 msec). Repeat drives were then performed with decrements of 10 msec for V2 until VA block was seen. Retrograde AVN and AP ERP were recorded with standard (V1, V2) and dual-chamber extrastimulation (A1/V1, A2, V2). Patients with an AP identified with standard pacing, manifest pre-excitation, or A ERP < AVN ERP were excluded. RESULTS: Fourteen patients with and 19 patients without an AP were studied. In all patients with an AP, exclusive VA conduction over the AP, without fusion, was seen with the described pacing maneuver. In patients without an AP, retrograde AV nodal ERP was extended by a mean of 138 +/- 46 msec (range 50 to 210 msec) with the A2. Anterograde concealed conduction into the AP was also seen in some patients who showed AP conduction during standard V1V2 pacing (mean retrograde extension of ERP 12 +/- 8 msec, range 0 to 20 msec). CONCLUSION: Dual-chamber sequential extrastimulation is a useful maneuver for identifying slowly conducting APs not revealed with standard pacing maneuvers because of an ERP and conduction time similar to the AVN. The maneuver uses anterograde concealed conduction to prolong AVN refractoriness much more than that of a concealed AP, thereby allowing the AP to become manifest with the V2.     

The electrophysiologic characteristics of the transplanted human heart

The electrophysiologic characteristics of the denervated human heart were assessed in 14 cardiac transplant recipients. Conduction intervals and refractory periods were measured at pacing cycle lengths of 500 msec and 400 msec. The faster pacing rate caused lengthening of the AH interval (83 +/- 23 msec to 116 +/- 41 msec, p less than 0.01) and shortening of the QT (338 +/- 27 msec to 313 +/- 22 msec, p less than 0.001) and JT (249 +/- 21 msec to 229 +/- 19 msec, p less than 0.001) intervals. There was no change in the SA, HV, or QRS durations. Wenckebach periodicity occurred at a longer cycle length in the retrograde than in the anterograde direction (409 +/- 96 msec vs 318 +/- 46 msec, p less than 0.01) and anterograde conduction was better than retrograde conduction in 13 of the 14 patients (93%). Increasing pacing cycle length resulted in shortening of the atrial effective (203 +/- 28 msec to 190 +/- 25 msec, p less than 0.001), ventricular effective (224 +/- 18 msec to 211 +/- 17 msec, p less than 0.01), and AV nodal functional (367 +/- 38 msec to 357 +/- 36 msec, NS) refractory periods. The AV nodal effective refractory period lengthened (294 +/- 31 msec to 314 +/- 52 msec, p less than 0.05). There was a close correlation between AV Wenckebach cycle length and the functional refractory period of the AV node (r = 0.853, p less than 0.001). These results are qualitatively and quantitatively similar to those reported in the innervated heart. The autonomic nervous system appears to have little influence on the resting electrophysiologic characteristics of the atrioventricular conduction system in the innervated heart.     

Evidence that cocaine slows cardiac conduction by an action on both AV nodal and His-Purkinje tissue in the dog

The effects of intravenous cocaine (2 mg/kg) were tested on several indices of cardiac electrical activity in sedated dogs. These included sinus rate, PR, AH, and HV intervals; AV nodal effective refractory period (AVNERP); ventricular effective refractory period; QRS duration; and the QT interval. Cocaine induced significant changes in six control animals with an intact-functioning autonomic nervous systems. After pharmacologic autonomic blockade with propranolol plus propantheline, cocaine increased the PR interval (+ 11 +/- 4.0 ms, p less than 0.05), primarily by slowing conduction at the AV nodal level. However, with constant atrial pacing at a rate above the sinus cycle length, prolongation of both the AH and the HV intervals (+ 15 +/- 2.5 and 6.7 +/- 1.7 ms, respectively) occurred. There was also a significant increase in the AVNERP (+ 29 +/- 5.9 ms, p less than 0.05). Consistent with the observed rate-dependent HV prolongation, cocaine decreased the rate of rise of phase 0 of the transmembrane action potential of Purkinje fibers. These data indicate that cocaine impairs cardiac conduction by direct actions on AV nodal and His-Purkinje cells.     

Attenuated nodal response. Apropos of 30 cases

In a population of 600 consecutive patients undergoing endocavitary electrophysiological study to assess nodal conduction, 40 had an atriohisian Wenckenbach point of over 200/mn. In 30 cases, vagal stimulation with ATP (10 to 40 mg IV) provoked an increase in atrioventricular conduction, with lengthening the AH interval by over 100 p. 100 or transient atrioventricular block. This increase allowed elimination of an accessory atriohisian pathway which could give similar high Wenckenbach points, but which do not show decremental conduction. In all our cases, the conduction passed through the artrioventricular node (AVN) whose response to rapid atrial stimulation was attenuated compared to normal. The parameter of this attenuated nodal response varied from case to case, but in general, the intervals were shorter than normal. The AH interval was less than 50 ms in 22 cases (N = 70 +/- 20 ms). The effective nodal refractory period was shorter than the functional atrial refractory period in 20 cases. The shortest atrial cycles transmitted 1/1 to the ventricles ranged from 230 to 300 ms (274 +/- 33 ms) (N = 375 +/- 40 ms). The functional structure of the AVN was studied by the lengthening of the AH interval with heart rate : 5 types were distinguished : 10 patients had progressive lengthening of AH interval greater than 100 ms (Type I) as in a normal AVN; 5 had progressive lengthening of AH interval of less than 50 ms (Type II), 5 had progressive lengthening of AH which then remained stable for a number of heart rates before lengthening again (Type III); 3 had an initial moderate lengthening of the AH interval which then became more rapid (Type IV) and 7 had no change in AH until 120/mn and then a progressive lengthening was observed (Type V). Two functional groups could also be identified depending on whether the lengthening was progressive, suggesting a single nodal pathway (Types I and II) or on whether differing increases were observed related to the atrial rate, suggesting two (Types IV and V) or even three (Type III) atrionodal or intranodal pathways with different refractory periods. Of these 30 patients, only 14 had documented supraventricular tachycardia, 13 being atrial fibrillation and the other a junctional tachycardia. Attenuated nodal behavior does not seem to be a direct cause of supraventricular arrhythmias but these arrhythmias were not tolerated as well because of the special properties of the atrioventricular node.     

Electrophysiologic effects of intravenous magnesium in patients with normal conduction systems and no clinical evidence of significant cardiac disease

Parenteral magnesium has been used for several decades in the empiric treatment of various arrhythmias, but the data on its electrophysiologic effects in man are limited. We evaluated the electrophysiologic effects of magnesium sulfate (MgSO4) administration in eight normomagnesemic patients with normal mononuclear cell magnesium content, who had no clinically significant heart disease and had normal baseline electrophysiologic properties. After administration of intravenous MgSO4, serum magnesium rose significantly from 1.9 +/- 0.1 to 4.4 +/- 1.7 mg/dl (p less than 0.02). During a maintenance magnesium infusion, we observed significant prolongation of the ECG PR interval (145 +/- 18 to 155 +/- 26 msec, p less than 0.05), AH interval (77 +/- 27 to 83 +/- 26 msec, p less than 0.002), antegrade atrioventricular (AV) nodal effective refractory period (278 +/- 67 to 293 +/- 67 msec, p less than 0.05), and sinoatrial conduction time (60 +/- 34 to 76 +/- 32 msec, p less than 0.02). No significant effect was observed on sinus cycle length, sinus node recovery time, intra-atrial or intraventricular conduction times, QRS duration (during both sinus rhythm and ventricular pacing), QT interval, HV interval, paced cycle length resulting in AV nodal Wenckebach block, AV nodal functional refractory period, retrograde ventriculoatrial (VA) effective refractory period, or atrial and ventricular refractory periods. These findings, in conjunction with the demonstrated ability of magnesium to block slow channels for sodium movement, may provide an explanation of the mechanism by which magnesium exerts its effect in the treatment of atrial and junctional arrhythmias.     

Postextrasystolic alterations in refractoriness of the His-Purkinje system and ventricular myocardium in man

The changes in refractoriness of the His-Purkinje system (HPS) and ventricular myocardium (VM) that are associated with the occurrence of postextrasystolic beats in man are unknown. Accordingly, using a pacing model of the cycle length changes created by a ventricular extrasystole-postextrasystole sequence, we measured retrograde HPS and VM relative and effective refractory periods (RRP and ERP) in 15 patients with the use of ventricular test extrastimuli during preextrasystolic basic control drive (method I) and after programmed extrasystolic (method II) and postextrasystolic (method III) beats. The basic cycle length (same for all three methods) ranged from 500 to 700 msec (mean 613 +/- 74 msec) and the extrasystolic coupling interval (identical for methods II and III) comprised 68 +/- 4% of the basic cycle length. In method III the postextrasystolic pause was programmed to equal the basic cycle length (i.e., noncompensatory) so that method I could serve as control for method III. RRP-HPS decreased from 331 +/- 37 msec in method I to 245 +/- 37 msec or less during the extrasystolic beat (p less than .001). A less dramatic corresponding shortening of ERP-VM and RRP-VM was observed, i.e., from 245 +/- 21 and 264 +/- 23 msec (method I) to 233 +/- 23 and 251 +/- 22 msec (method II), respectively (p less than .001). With the postextrasystolic beat, however, RRP-HPS increased to exceed the control value of method I by 23 +/- 11 msec (p less than .001). This greater-than-expected RP prolongation was also associated with significantly increased retrograde HPS conduction times (in method III vs method I) at both long and short test stimulus coupling intervals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Selective functional characteristics of rate-induced fatigue in rabbit atrioventricular node

The slowly developing rate-induced prolongation in atrioventricular nodal conduction time, termed "fatigue," was selectively studied using specifically designed stimulation protocols in isolated rabbit heart preparations. A nodal recovery curve (A2H2 versus H1A2 intervals; nodal conduction time of each premature beat plotted against corresponding recovery time) was obtained before and after a stable and nearly maximum fatigue had been reached by driving the atrium for 5 minutes at a fast rate close to the upper limit of 1:1 nodal conduction. The fatigue uniformly prolonged all A2H2 intervals (12.3 +/- 1.3 msec) and systematically increased the minimum H1A2 interval at which complete nodal block occurred (24.8 +/- 4.0 msec) (p less than 0.01, n = 6). To study the rate and time dependence of fatigue, nodal conduction times were obtained during three rapid 5-minute pacings corresponding to 50%, 75%, and 100% shortening of the pacing interval in the 1:1 nodal conduction range. The respective maximum fatigue-induced increases in conduction time were 5.4 +/- 1.8, 9.0 +/- 2.7, and 12.5 +/- 2.1 msec (p less than 0.01, n = 6). However, the pacing interval had no significant effect on the time required to reach either 50% (17.1 +/- 3.5 seconds) or 90% (92.6 +/- 15.4 seconds) of the fatigue observed after 5 minutes of fast rate. At the termination of any rapid stimulation, the fatigue effect dissipated with a time course that was inverse but symmetrical to that of its induction. These findings support the existence of an independent, slow, nodal memory process by which the conduction time changes according to past events with a long time constant.     

Differential effects of intravenous magnesium on atrioventricular node conduction in supraventricular tachycardia

Evidence from noninvasive studies suggests magnesium has a differential effect on atrioventricular nodal (AVN) pathways. To further explore the electrophysiologic effects of intravenous magnesium sulfate (MgSO(4)) on supraventricular tachycardia, with particular reference to AVN conduction pathways, we studied 23 patients with supraventricular tachycardia at the time of electrophysiologic study. Tachycardia cycle length; AH, HV, and VA intervals; anterograde and retrograde Wenckebach thresholds; slow and fast pathway effective refractory periods (ERPs); accessory pathway ERP; right atrial and ventricular ERPs; blood pressure; and serum magnesium were evaluated before and after administration of MgSO(4) during sustained tachycardia. AVN reentry was induced in 14 patients and atrioventricular reentry was induced in 9; 1 of the latter had dual AVN physiology with tachycardia using the slow pathway. Serum magnesium level increased from 0.88 +/- 0.11 to 1.79 +/- 0.14 mmol/L (p <0.0001). Magnesium increased tachycardia cycle length to a greater extent in those with dual AVN physiology than those without: 340 +/- 54 to 370 +/- 57 ms versus 347 +/- 29 to 350 +/- 30 ms (p = 0.01). This was associated with greater increase in AH interval in those with dual AVN physiology than in those without: 241 +/- 59 to 270 +/- 60 ms versus 144 +/- 16 to 140 +/- 20 ms (p = 0.003). Presence of dual AVN physiology was more frequently associated with reversion to sinus rhythm: 5 of 15 versus 0 of 8 (p = 0.06). MgSO(4) did not alter other measured parameters. In conclusion, magnesium increases tachycardia cycle length and AH interval in patients with dual AVN physiology through a dominant effect on the slow AVN pathway.     

“Paradoxical” AH Shortening Caused By Proximal Coronary Sinus Stimulation During Orthodromic Reciprocating Tachycardia

AH Shortening During ORT. Introduction: During extrastimulation or entrainment of orthodromic atrioventricular (AV) reciprocating tachycardia (ORT), the atriuni-His (AH) interval as measured at the His-bundle recording site is expected to lengthen due to extrastimu-Lation-dependent or pacing rate-dependent slowing of AV nodal conduction by impulses that penetrate the tachycardia circuit. We report 6 patients in whom the AH interval “paradoxically” shortened during ORT in response to extrastimulation and rapid pacing from the proximal coronary sinus. Methods and Results: Accessory pathway location was right anterior (1 patient), right anteroseptal (1 patient), and left anterior (4 patients). Cycle length of ORT was stahle (variation ≤ 5 msec) and ranged from 325 to 410 msec. During ORT, extrastimulation and rapid pacing were performed from the proximal coronary sinus and the right atrium. Extrastimulation from the proximal coronary sinus late in diastole caused significant shortening of AH interval in all patients hy a mean of 18 ± 3 msec (range 15 to 20 msec). AH shortening was demonstrated without a change of either the timing or morphologic appearance of the low septal right atrium at the H is-bundle recording site. This phenomenon was not ohserved during right atrial extrastimulation. Rapid pacing from the proximal coronary sinus at cycle lengths of 305 to 390 msec (i.e., 15 to 20 msec shorter than the cycle length of each ORT) again demonstrated shortening of AH interval in all patients by a mean of 15 ± 3 msec (range 10 to 20 msec). By contrast, rapid pacing from the right atrium demonstrated classical AH prolongation at any paced cycle length. Conclusion: AH shortening without a change of either the timing or morphologic appearance of the low septal right atrium at the His-handle recording site confirms the existence of a distinct posterior atrial input to the AV node. In this setting low septal right atrial activation is not requisite for AV nodal conduction. Whether activation of the low septal right atrium is essential for. or contributes to, AV nodal conduction of atrial impulses from locations other than the proximal coronary sinus needs to he determined.     

Frequency-dependent effects of verapamil on atrioventricular nodal conduction in man

We sought to determine if verapamil induces frequency-dependent prolongation of atrioventricular nodal conduction in 10 consecutive patients studied in the electrophysiology laboratory. We used a maintenance infusion of verapamil designed to produce plasma concentrations of verapamil in the "therapeutic" range and that did not alter heart rate or blood pressure significantly. Frequency-dependent prolongation of atrioventricular nodal conduction (AH interval) was demonstrated in all 10 patients (p less than .001), and no change in HV conduction time with decreasing cycle length was noted in any patients while receiving verapamil. Two patterns of use-dependent response were seen. In four patients frequency-dependent prolongation of the delta(AH) interval [delta(AH) = AHverapamil - AHcontrol at a given cycle length] was seen with each decrement in pacing cycle length. In six patients frequency-dependent prolongation of the delta(AH) interval was not manifest until the fifth to eighth pacing cycle length tested. There was no association between the pattern observed and the initial heart rate or AH interval. After an abrupt change in pacing cycle length, the kinetics of delta (AH) interval prolongation were rapid; equilibrium was achieved by five to eight pulses in all patients. There was no correlation between the magnitude of prolongation of the AH interval noted at a particular cycle length and the concentration of verapamil during the maintenance infusion. These results indicate that verapamil causes use-dependent prolongation of atrioventricular nodal conduction in man.     

Electrophysiologic effects of verapamil in children

The electrophysiologic effects of verapamil, a slow channel blocker, were investigated during diagnostic cardiac catheterization in 24 children premedicated with lytic cocktail. The ages ranged from 50 days to 12 years. Twenty had congenital and 4 had rheumatic heart disease. Surface EKG, high intra-atrial and His bundle electrograms were obtained in all before and 5 min after a single dose of verapamil (0.15 mg/Kg, max 5 mg iv). In 14 cases complete electropysiologic studies were performed using the atrial pacing and extrastimulus technique. Due to variability of the resting heart rates and the effect of cycle length on refractory periods each paced with identical S1-S1 interval before and after verapamil, thus allowing each case to serve as his own control. Verapamil prolonged the corrected AH interval in all (mean +/- SD; from 116 +/- 37 to 152 +/- 41 msec, p less than 0.01) and shortened the HV interval in 15/24 (mean +/- SD: from 55 +/- 13 to 47 +/- 9.9 msec, p less than 0.05). The effective and functional refractory periods of the total conduction system, the AV node (ERPAVN) and atrium (ERPA) increased significantly in 10/14. The most profound effect was on ERPAVN and ERPA (25.54 +/- 29 and 19.27 +/- 21.81 percent mean percent increase +/- SD respectively, p less than 0.01 and p less than 0.02). Our findings show that verapamil prolongs the effective and functional refractory periods of the cardiac conduction system with maximal effects on the AV node, thus suggesting the mechanism of its effectiveness in the treatment of reentrant supraventricular arrhythmias.     

Effect of pindolol and propranolol on sinus node recovery time and atrioventricular conduction intervals

In a randomized, observer-blind study, the effect of incremental doses of pindolol 0.001, 0.002, 0.003, and 0.004 mg/kg IV and propranolol 0.01, 0.02, 0.03, and 0.04 mg/kg IV on SA nodal recovery time (SNRT) and atrioventricular conduction interval (AH) was assessed in 20 patients (15 men and 5 women age range thirty to seventy-two, mean age fifty-three). AH and His bundle-to-ventricle (HV) intervals and SNRT were measured at spontaneous heart rate and at incremental atrial pacing rates (80, 100, 120, 140 bpm). Both drugs caused significant beta blockade as estimated by the percentage suppression of heart rate increment induced by 3 mcg isoproterenol administered intravenously (pindolol 67.6 +/- 5.3%, P less than 0.007; propranolol 38.6 +/- 10.6%, P less than 0.001). Propranolol significantly prolonged SNRT (P less than 0.05) and AH interval (P less than 0.05). Pindolol did not significantly affect either SNRT (P = 0.25) or AH intervals (P = 0.78). Significant effects on HV interval were not seen. Thus, in the doses tested that resulted in significant beta blockade, propranolol prolonged SA nodal recovery times and depressed AV nodal conduction while pindolol did not affect these variables.     

Electrophysiologic effects of cibenzoline in humans related to dose and plasma concentration

The electrophysiologic effects of a new antiarrhythmic agent, cibenzoline, were investigated in 25 patients with an average age of 62 years. The compound was administered intravenously, as a bolus given over 2 minutes, then as a slow infusion over 40 minutes. Each subject was randomly allocated to receive one of the following four doses: 1.55 mg/kg (six patients), 1.8 mg/kg (six patients), 2.2 mg/kg (six patients), or 2.6 mg/kg (seven patients). Plasma cibenzoline concentrations at these doses were 378 +/- 80,525 +/- 194, 618 +/- 72, and 731 +/- 196 ng/ml, respectively. Administration of 1.55 mg/kg cibenzoline significantly shortened the sinus cycle (60 msec on average; p less than 0.025) and increased intraatrial (+8 msec; p less than 0.05) and His-Purkinje conduction times (HV interval + 13 msec; p less than 0.001). At 1.80 mg/kg, prolongation occurred in the HV interval (+9 msec; p less than 0.02), the duration of the QRS complex (+20 msec; p greater than 0.05), and the QT interval (+18 msec; p less than 0.025). At the higher doses these changes became more marked (maximum increase: HV = +16 msec, p less than 0.001; QRS + 25 msec; p less than 0.001; QT + 26 msec, p less than 0.05), and additional effects on atrioventricular nodal conduction time (AH interval + 17 msec; p less than 0.05) and atrial (+20 msec; p less than 0.05) and ventricular (+10 msec; p greater than 0.05) effective refractory periods were observed. Prolongation of the QRS duration was the effect that correlated best with plasma cibenzoline levels (r = 0.47; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of intravenous adenosine on antegrade refractoriness of accessory atrioventricular connections

BACKGROUND. Several groups have suggested the use of intravenous adenosine or adenosine triphosphate in the diagnosis of regular broad complex tachycardias. However, the short half-life of these agents has precluded assessment of their effects on refractoriness of accessory connections, and their safety in preexcited arrhythmias has not been demonstrated. METHODS AND RESULTS. We examined the effects of intravenous adenosine on accessory atrioventricular (AV) connections in 30 patients with the Wolff-Parkinson-White syndrome. Intravenous adenosine (12 mg, rapid bolus) was administered to 14 patients (group 1) during continuous atrial pacing at a cycle length 20 msec below that required to cause 2:1 conduction block in the accessory connection (mean pacing cycle length 261 +/- 41 msec). After adenosine, transient 1:1 conduction occurred via the accessory connection in 12 of 14 patients, indicating a shortening of antegrade refractoriness. In three of seven patients, this effect was abolished after intravenous propranolol (0.2 mg/kg). Nineteen patients (group 2) received adenosine (0.17 +/- 0.04 mg/kg) during induced, preexcited atrial arrhythmias. The minimum RR interval during preexcited atrial fibrillation transiently decreased (252 +/- 44 msec to 224 +/- 35 msec, p less than 0.01) after adenosine, but no change in average RR interval was observed (360 +/- 59 msec to 357 +/- 60 msec, NS). The preexcited ventricular response to atrial flutter was transiently accelerated in five of eight patients (415 +/- 21 msec to 360 +/- 49 msec, p less than 0.05) due to shortening of flutter cycle length (207 +/- 10 msec to 180 +/- 24 msec, p less than 0.05). However, 2:1 accessory connection conduction was maintained in all eight patients. All effects were short lived, with the decrease in RR interval during atrial fibrillation occurring for a maximum of two RR intervals only. No patient suffered ventricular arrhythmias or hemodynamic deterioration. CONCLUSIONS. Adenosine shortens antegrade refractoriness of accessory AV connections, and in some patients this action is mediated by beta-adrenergic stimulation. Adenosine may cause acceleration of preexcited atrial arrhythmias, but these effects are transient and should not discourage the use of adenosine as a diagnostic agent in broad complex, regular tachycardias of uncertain origin.     

Effects of upright posture on anterograde and retrograde atrioventricular conduction in patients with coronary artery disease, mitral valve prolapse or no structural heart disease

To assess the effects of posture on anterograde and retrograde atrioventricular conduction, electrophysiologic testing was performed in 25 patients in both the supine and 45 degrees upright positions on a tilt table. Retrograde conduction was present during ventricular pacing in 17 patients in the supine position; all 17 continued to manifest retrograde conduction in the upright position. In all patients with absent retrograde conduction while supine, retrograde conduction could not be demonstrated while upright. Upright posture significantly (p less than 0.05) shortened the sinus cycle length (from 808 +/- 34 to 678 +/- 26 ms, mean +/- standard error of the mean), AH interval during sinus rhythm (78 +/- 6 to 69 +/- 6 ms), and AH interval during atrial pacing at cycle length 500 ms (123 +/- 13 to 91 +/- 9 ms). Total atrioventricular conduction time during atrial pacing shortened significantly (from 169 +/- 13 to 136 +/- 10 ms), as did ventriculoatrial conduction time during ventricular pacing (from 192 +/- 9 to 178 +/- 7 ms). Upright posture also significantly shortened both anterograde block cycle length (390 +/- 20 to 328 +/- 17 ms) and retrograde block cycle length (466 +/- 27 to 354 +/- 18 ms). However, the effect of upright posture on retrograde block cycle length was significantly greater than on anterograde block cycle length: a 21% decrease retrograde vs a 14% decrease anterograde (p less than 0.05). These effects may produce clinically important changes in characteristics of arrhythmias that depend on the properties of anterograde and retrograde conduction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Procainamide and retrograde atrioventricular nodal conduction in man

Recent studies that show a depressant effect of procainamide (PA) on retrograde conduction in patients with atrioventricular (AV) nodal reentrant tachycardia (RT) have suggested possible incorporation of AV nodal bypass tracts. Electrophysiologic effects of i.v. PA, 10 mg/kg, on retrograde AV nodal conduction were examined in 13 patients without RT, demonstrable AV nodal refractory period curves, or accessory pathways. Ventriculoatrial (VA) conduction was recorded before and after PA using intracardiac electrograms, incremental ventricular pacing and extrastimulation. With incremental pacing during the control, VA block occurred at a mean cycle length (CL) of 364.6 +/- 87.9 msec. After PA, VA conduction was abolished in five of 13 patients due to onset of retrograde block in the AV node; in seven of 13, VA block occurred at a longer paced CL after PA (344.2 +/- 51.2 msec vs 477.1 +/- 93.2 msec). In one patient, PA did not affect VA conduction. PA invariably produced prolongation in the VA interval at comparable CL of pacing. With ventricular premature stimulation, the retrograde H2A2 intervals during the control period were short (less than 50 msec) in seven of 13, intermediate (60-100 msec) in three of 13 and long (greater than 100 msec) in three of 13 cases. PA either abolished H2A2 conduction (H2 but no A2) or prolonged the H2A2 intervals by 5-20 msec in most cases in this series. The data suggest that i.v. PA almost uniformly depresses retrograde AV nodal conduction in the intact human heart. This depressant response to PA is not indicative of presence of partial or complete AV nodal bypass tracts.     

Differential effects of autonomic blockade on sinus and atrioventricular nodal function in normals and in intrinsic sinus node dysfunction

The effect of pharmacologic total autonomic blockade on sinus and atrioventricular nodes was studied in 10 normals and 21 patients with sick sinus syndrome with abnormal intrinsic corrected sinus node recovery time. In normals the intrinsic heart rate (113.3 +/- 11.6 beats/min) was higher than the resting heart rate (87.3 +/- 12 beats/min; P less than 0.001). The AH interval at an identical paced rate decreased from 119 +/- 36 msec to 93 +/- 17.6 msec after autonomic blockade (P less than 0.05). Mean atrial paced cycle length at AH Wenckebach block was not different during control and after drugs (319 +/- 46 msec vs. 311.5 +/- 39 msec; P = NS). Although sinus cycle length shortened in all cases after autonomic blockade, paced cycle length at AH Wenckebach increased (4) or remained unchanged (3) in 7 cases. Maximum normal "intrinsic" paced cycle length at AH Wenckebach was 390 msec (mean +/- 2 SD). In sick sinus syndrome, resting heart rate (66.3 +/- 18.8 beats/min) and intrinsic heart rate (74.6 +/- 16.4 beats/min) were similar (P = NS); AH at identical paced rate: control 136.6 +/- 54 msec, after drugs 130.5 +/- 35 msec (P = NS); cycle length at AH Wenckebach: control 380.5 +/- 73 msec, after autonomic blockade 383 +/- 49 msec (P = NS). Two of 3 cases with abnormal atrioventricular nodal response to atrial pacing during control normalized after autonomic blockade; 9/21 (42.8%) cases developed AH Wenckebach at cycle length greater than 390 msec after autonomic blockade. The data suggest that the autonomic nervous system has differential effects on sinus and atrioventricular nodes. Patients with sick sinus syndrome frequently have abnormalities of "intrinsic" atrioventricular nodal conduction unmasked by autonomic blockade.     

Demonstration of the presence of slow conduction during sustained ventricular tachycardia in man: use of transient entrainment of the tachycardia

To test the hypothesis that an area of slow conduction is present during reentrant ventricular tachycardia in man, and that the earliest activation site during ventricular tachycardia is within or orthodromically just distal to the area of slow conduction in the reentry loop, we studied 12 episodes of ventricular tachycardia (mean rate 185 +/- 32 beats/min) that were induced in nine patients with ischemic heart disease. Rapid ventricular pacing was performed at selected sites during ventricular tachycardia while recording electrograms from an early activation site relative to the onset of the QRS complex (site A) and from a site close to the pacing site (site B). Rapid pacing from the right ventricular apex during ventricular tachycardia with a right bundle branch block pattern and from selected left ventricular sites during ventricular tachycardia with a left bundle branch block pattern (mean pacing rate 202 +/- 38 beats/min) resulted in constant ventricular fusion beats on the electrocardiogram except for the last captured beat (i.e., the ventricular tachycardia was entrained) in 11 of 12 episodes. During entrainment: sites A and B were activated at the pacing rate, conduction time from the last pacing impulse to the last captured ventricular electrogram at site A (St-A interval) was 359 +/- 69 msec and spanned the diastolic interval, while that at site B (St-B interval) was only 28 +/- 13 msec, site A had the same ventricular electrogram morphology as that during ventricular tachycardia, while site B had a different electrogram morphology, indicating that site A was activated in the same direction during entrainment as during ventricular tachycardia. Eight episodes of ventricular tachycardia were entrained at two or more different pacing rates. The St-A interval increased during pacing at the faster rate(s) in four of eight episodes, while the St-B interval remained unchanged. Rapid ventricular pacing performed from the same site during sinus rhythm (mean pacing rate 201 +/- 37 beats/min) resulted in an St-A interval of 103 +/- 37 msec (p less than .001 vs the value during entrainment) and an St-B interval of 31 +/- 15 msec (p = NS vs the value during entrainment). It is concluded that an area of slow conduction not demonstrable during sinus rhythm exists during ventricular tachycardia, and that the earliest activation site during ventricular tachycardia is at or orthodromically distal to this area of slow conduction.     

Abnormal parasympathetic vagal function in patients with spasmodic dysphonia

Gastric vagal function was assessed in 15 patients with spasmodic dysphonia by measuring gastric acid output in response to sham feeding. Patients secreted significantly less acid than controls (p less than 0.001). Cardiac vagal function was assessed in 11 patients by measuring heart rate during deep respiration and also during and after Valsalva maneuver. Patients with spasmodic dysphonia had a significantly reduced fluctuation of heart rate during deep respiration (sinus arrhythmia). The expiratory to inspiratory R-R interval averaged 1.08 +/- 0.08 (mean +/- SD) in patients and 1.22 +/- 0.10 in controls (p less than 0.005). The ratio of tachycardia during Valsalva maneuver to bradycardia after Valsalva maneuver was also lower in patients than in controls (p less than 0.005). The auditory brainstem response was abnormal in 11 of 15 patients. Our results show either a central brainstem abnormality or several cranial nerve abnormalities in some patients with spasmodic dysphonia.