Joseph Anthony C. Gomes

Antegrade and retrograde conduction characteristics in three patterns of paroxysmal atrioventricular junctional reentrant tachycardia.

Abstract In 20 patients with PSVT without ventricular pre-excitation, the site of reentry and functional characteristics of Ant. and Ret. pathways were studied. Three distinct patterns of PSVT were observed. In 13 patients (group I) in whom A-V node was the site of reentry, the interval between the Ant. H bundle deflection and the following atrial echo response (H-Ae) measured 30 to 85 msec. and the Ae was partially or completely obscured by ventricular electrogram. The ratio between the H-Ae and the subsequent Ae-H interval ranged 1:3.1–17.3. In a majority of Group I patients (eight out of 13) the Ret. conduction was better than Ant. conduction, as the VACS sustained a 1:1 response at faster paced rates than AVCS. The FRP of the AVCS in Group I was determined by the A-V node in all patients and significantly exceeded the FRP of the VACS; the latter was determined by the HPS in 12 out of 13 patients. In four patients (Group II) a V-A AP silent antegradely was operative during PSVT. The H-Ae in Group II valued 145 to 200 msec. and the Ae clearly followed the ventricular electrogram, the H-Ae: Ae-H being 1:0.5–1.7. The V-A conduction in all Group II patients was better than the A-V conduction. A-V node determined the FRP of the AVCS, whereas AP determined the FRP of the VACS in Group II patients, and the former significantly exceeded the latter. Good correlation existed between PSVT, Ant. and Ret. conduction patterns in Group I and Group II patients. In three patients (Group III) the H-Ae measured 270 to 470 msec. with an H-Ae:Ae-H of 1:0.2–0.4, a relationship quite the opposite of Group I patients. No definite relationship existed between PSVT, Ant. and Ret. conduction patterns in Group III patients. The data in Group III patients were compatible with (1) A-V nodal reentry with reversal of conduction balance compared to Group I, (2) intra-atrial reentry, and (3) enhanced atrail automaticity. It is concluded (1) the site of reentry in patients with PSVT is variable, (2) a fair estimation of reentry site can be made from H-Ae and Ae-H relationship, (3) all patients with PSVT have intact V-A conduction and in most the V-A conduction is better than A-V conduction, and (4) in the majority of patients with PSVT refractoriness of the AVCS exceeds that of the VACS.

Electrophysiologic evidence for selective retrograde utilization of a specialized conducting system in atrioventricular nodal reentrant tachycardia

Abstract In 12 patients with atrioventricular (A-V) nodal reentrant tachycardia, the existence and utilization of retrograde ventriculoatrial bypass tracts in the reentrant process were excluded, and the characteristics of the anterograde and retrograde limbs of the reentrant circuits were studied using His bundle electrograms, incremental atrial and ventricular pacing and atrial and ventricular extrastimulus techniques before and after the administration of 0.01 mg/kg of intravenous ouabain. Similar studies were also performed in five control patients without tachycardia. Paroxysmal supraventricular tachycardia could be induced in all 12 patients during atrial pacing-induced A-V nodal Wenckebach periods or premature atrial stimulation, or both. On the basis of conduction time in the retrograde limb during tachycardia and during retrograde studies, two groups were identified. Group I (seven patients) had (1) short (39 ± 10 msec) and constant conduction time in the retrogarde limb measured from the anterograde His bundle deflection to the retrograde atrial echo response (H-Ae interval), (2) no change in ventriculoatrial conduction time up to maximal ventricular pacing rates, (3) H2-A2 intervals during retrograde refractory period studies that were identical to the H-Ae intervals and that did not increase with decreasing V1-V2 intervals, and (4) increased conduction time of the anterograde limb (Ae-H intervals) after the administration of ouabain without any effect on retrograde limb conduction (H-Ae and H2-A2 intervals) and refractoriness. Group II (five patients) had (1) long and variable H-Ae intervals (60 to 180 msec), (2) a progressive increase in ventriculoatrial intervals during incremental ventricular pacing, (3) an increase in H2-A2 intervals in response to decreasing V1-V2 intervals, and (4) increased anterograde (Ae-H interval) and retrograde limb (H-Ae and H2-A2 intervals) conduction and refractoriness after the administration of ouabain. Changes in the H2-A2 interval corresponded to the changes in four of the five control patients. These findings suggest that (1) in group I the anterograde limb was the A-V node, whereas the retrograde limb was an A-V nodal bypass tract or an insulated intranodal tract physiologically unlike the A-V node; and (2) in group II the A-V node comprised both the anterograde and retrograde limbs of the reentrant circuit.

Incidence, determinants and significance of fixed retrograde conduction in the region of the atrioventricular node: Evidence for retrograde atrioventricular nodal bypass tracts

Of 104 consecutive patients studied in our laboratory with His bundle electrograms, atrial and ventricular pacing and the atrial and ventricular extrastimulus techniques, 18 patients in whom the existence and utilization of ventriculoatrial (V-A) bypass tracts were excluded demonstrated evidence for fixed and rapid retrograde conduction in the region of the atrioventricular node (A-V) as suggested by the following: (1) short (36 +/- 2 msec [mean +/- standard error of mean]) and constant retrograde H2-A2 intervals during retrograde refractory period studies; (2) significantly (P less than 0.025) better V-A than A-V conduction; (3) significantly (P less than 0.025) shorter retrograde functional refractory period of the V-A conducting system than of the A-V conduction system; and (4) the retrograde effective refractory period of the A=V nodal region was not attainable in any of the 18 patients. Fourteen of the 18 patients (77 percent) had a history of palpitations and 10 (51 percent) had documented paroxysmal supraventricular tachycardia; in 13 (72 percent) single echoes or sustained reentrant supraventricular tachycardia, or both, could be induced during atrial pacing or atrial premature stimulation studies, or both. During tachycardia all these 13 patients had a short (37 +/- 2.4 msec) and constant conduction time in the retrograde limb (H-Ae interval) of the reentrant circuit that was identical to the H2-A2 interval. In conclusion, fixed and rapid retrograde conduction in the region of the A-V node (1) is seen in approximately 17 percent of patients, (2) is associated with a large incidence of reentrant paroxysmal supraventricular tachycardia, and (3) suggests the presence of A-V nodal bypass tracts (intranodal or extranodal functioning in retrograde manner).

Ventricular septal motion and left ventricular dimensions during abnormal ventricular activation

To determine the effect of abnormal ventricular activation on ventricular septal motion, left ventricular endocardial motion and left ventricular dimensions, 12 patients with normal motion were studied with echocardiography during incremental pacing of the right ventricular apex, outflow and inflow regions. Three types of abnormal ventricular septal motion were seen: The type I pattern was characterized by an early rapid preejection posterior ventricular septal motion followed by another posterior systolic motion that lasted throughout ejection, both of which were associated with septal thickening. In the type II pattern an early rapid preejection posterior ventricular septal motion was followed by an anterior ejection motion; the latter was not accompanied by septal thickening. The type III pattern consisted of an early preejection posterior ventricular septal motion followed by a mid and late systolic posterior motion: the latter motion extended through diastole. During right ventricular apical pacing, 8 of 11 patients showed a type 1 pattern, 1 a type II pattern and 2 a normal septal motion. During right ventricular outflow pacing,seven of nine patients showed a type II pattern, one a type III pattern and one a type I pattern. During right ventricular inflow pacing, eight of nine patients showed a type II pattern and one a type III pattern. At faster pacing rates patterns of types I and III changed to a type II pattern (five patients). End-diastolic dimensions decreased significantly during incremental right ventricular pacing when compared with those during sinus rhythm. End-systolic dimensions decreased significantly only during right ventricular apical and outflow pacing at maximal rates. In the seven patients who had pacing from all three sites, the decrease in left ventricular dimensions did not significantly differ when the three pacing sites were compared. These findings suggest that (1) abnormal ventricular septal motion during right ventricular pacing (induced left bundle branch block patterns) is dependent on the sequence of ventricular activation; (2) ventricular septal motion during right ventricular outflow and inflow pacing is similar to that seen in spontaneous left bundle branch block, whereas the pattern of septal motion during right ventricular apical pacing is different from that of spontaneous left bundle branch block; and (3) changes in left ventricular dimension are dependent on ventricular pacing rate but independent of pacing site.

Effect of Procainamide on Reentry Within the His-Purkinje System in Man

Abstract The effects of a single intravenous infusion of 500 mg of procainamide on macro-reentry within the His-Purkinje system were assessed, in 10 patients using bundle of His electrograms and the ventricular extrastimulus method. Procainamide did not abolish reentry in any of the 10 patients and produced repetitive reentry (two or more consecutive reentrant beats) in 8 of 10 patients. On the average, procainamide caused reentry to be initiated at longer S 1 -S 2 intervals, widening the zone of reentry. In all but one patient reentry was manifest at significantly longer S 2 -H 2 intervals than control values. The H-V intervals of reentrant beats (H 2 -V 3 intervals) after procainamide were longer than control values at comparable S 2 -H 2 intervals. Procainamide shortened or abolished the retrograde gap zones thereby causing reentry to be present more frequently within the zone of reentry. No significant change was seen in effective refractory period of ventricular muscle. On the assumption that many clinically encountered ventricular arrhythmias that respond to procainamide result from micro-reentry, the observed differences between the effects of procainamide on macro- and micro-reentry may be explained on the basis of the relation between drug effect and size of the reentrant circuit. Procainamide may produce a greater increase in refractoriness in a micro-reentrant circuit than in macro-reentry, thereby producing bilateral block and abolishing reentry in the former; or if the degree of electrophysiologic changes produced by procainamide were the same in both types of circuits, then for a given change, the pathway in a micro-reentrant circuit may be too small to sustain reentry.

The effect of vitamin E on platelet aggregation

Platelet aggregation studies were performed in five men with coronary artery disease and angina pectoris and five men with nonspecific chest pain before and after receiving 1,000 I.U. of alpha-tocopherol acetate orally per day for 8 days. There was no significant difference in the platelet aggregation response to three concentrations of ADP and two concentrations of epinephrine between the pre- and post-vitamin E periods among the 10 patients. If tocopherol acetate (vitamin E) has any beneficial effect on the prevention of thromboemolism or in the treatment of angina pectoris and peripheral vascular disease, it is not via inhibition of platelet aggregation.

Effects of digitalis on ventricular myocardial and His-Purkinje refractoriness and reentry in man.

The effects of digitalis on retrograde conduction and refractoriness of the His-Purkinje system, ventricular myocardium and reentry within the His-Purkinje system were studied in 17 patients using the ventricular extrastimulus (V2) technique. Studies were performed, before and 30 minutes after intravenous administration of ouabain, 0.01 mg/kg. After treatment with ouabain, there was a significant decrease in the functional refractory period (266 +/- 19 to 254 +/- 18 msec, P less than 0.001), relative refractory period (253 +/- 17 to 240 +/- 16 msec, P less than 0.001) and effective refractory period (242 +/- 23 to 231 +/- 24 msec, P less than 0.005) of the ventricular muscle. In contrast, there was no significant change in retrograde His-Purkinje conduction and refractoriness. The phenomenon of reentry within the His-Purkinje system characterized by the reentrant beat (V3) at critical retrograde conduction delays in the His-Purkinje system (V2-H2) within a narrow range of V1-V2 intervals was seen in 10 of 17 patients. Ouabain increased and shifted to the left the zone of reentry within the His-Purkinje system in 7 of 10 patients (36 +/- 23 to 55 +/- 23 msec, P less than 0.001) and decreased it by 10 to 30 msec in the remaining 3 patients. The critical V2-H2 (186 +/- 29 to 193 +/- 27 msec, difference not significant [NS]) and V1-V2 (299 +/- 30 to 294 +/- 36 msec, NS) intervals for reentry did not significantly change after ouabain. However, the minimal V1-V2 intervals (266 +/- 26 to 253 +/- 25 msec, P less than 0.025) decreased significantly, whereas the maximal V2-H2 intervals (266 +/- 40 to 239 +/- 37 msec, P less than 0.01) increased significantly. Thus, in the intact human heart, digitalis (1) significantly decreased all measures of ventricular myocardial refractoriness, (2) had no significant effect on retrograde conduction and refractoriness of the His-Purkinje system, and (3) widened the zone of reentry within the His-Purkinje system due to shortening of the functional refractory period of the ventricular muscle with attainment of longer V2-H2 delays.

The effect of isosorbide dinitrate on left ventricular size, wall stress and left ventricular function in chronic refractory heart failure: An echocardiographic study

Abstract To determine the effect of a long-acting vasodilator isosorbide dinitrate (ID) on ventricular performance, 16 patients with refractory congestive heart failure underwent echocardiographic studies during control and for a period of 2 hours after the administration of 10 mg of sublingual ID. The effects of ID were seen in 5 to 10 minutes, reached maximum at 30 ± 3 minutes lasted for 60 minutes and dissipated thereafter. At the maximal drug effect, a significant decline in mean blood pressure (74 ± 2 versus 81 ± 3 mm Hg, p 3 ± 9 × 10 3 dynes/cm 2 versus 273 × 10 3 ± 12 × 10 3 dynes/cm 2 p −1 , p

Study of the temporal effects on conduction and refractoriness of the His-Purkinje system in man

Temporal effects on refractoriness within the His-Purkinje system (HPS) were studied in 14 patients in whom effective refractory period (ERP) of HPS could be determined, using His bundle electrograms, incremental atrial pacing, and atrial extrastimulus method. His-Purkinje conduction times (H-V interval) and relative (R), effective (E), and functional (F) refractory periods (RP) of HPS were measured during the control period and repeat measurements were made after a 30 minute interval. H-V intervals were unchanged from control in all patients. Although changes of the magnitude of 5 to 25 msec. in either direction from control values commonly occurred, on the average, no statistically significant changes were seen in RRP, ERP, or FRP of HPS. The results of the present study confirm the stability of refractoriness of HPS over a 30 minute period and provide baseline data for future investigations of cardiovascular drugs which act primarily on the distal part of the A-V conduction system.

Inotropic effect of post-stimulation potentiation in man: An echocardiographic study☆

To determine the magnitude of enhancement of the inotropic state in the intact human left ventricle, echocardiographic studies were performed in 11 subjects during pacing-induced changes in heart rate. Incremental atrial or ventricular pacing (80 to 160 beats/min) was performed for 1 minute at each rate, and echocardiographic variables of left ventricular function and indexes of left ventricular thickening were assessed for the post-stimulation beats and compared with the values obtained during sinus rhythm before pacing. For the first post-stimulation beat at maximal paced rates (146 ± 3 beats/min, mean ± standard error of mean), the ejection fraction (+23 percent P < 0.001), percent fractional shortening (+45 percent, P < 0.001) and mean velocity of circumferential fiber shortening (+45 percent, P < 0.001) increased significantly, whereas the end-systolic dimension (−22.4 percent, P < 0.001) and volume (− 52 percent, P < 0.001) decreased significantly. The end-diastolic dimension (+1.42 percent) and volume (+4.8 percent) did not change significantly. Similarly, septal thickening (+21.89 percent, P < 0.005), posterior wall thickening (+23.4 percent, P < 0.001), left ventricular thickening (+21.91 percent, P < 0.001) and the mean rate of left ventricular thickening (+33 percent, P < 0.001) increased significantly. Similar significant changes, although of a lesser magnitude, occurred at lower paced rates; the magnitude of these changes was proportional to the pacing rate. Decay in potentiation occurred within four to five beats after pacing was stopped at any given rate. Thus, in the intact human heart (1) the positive inotropic effects of stimulation on the left ventricle are reflected as post-stimulation potentiation, (2) potentiation is related to the pacing rate, and (3) decay in potentiation occurs rapidly when pacing is stopped.