Biomedical subjects

A H Kadish

Publications and source records attributed to A H Kadish.

At least 91 records · Page 5Linked to original sources

PubMed1990

Effect of atrioventricular relationship on ventricular refractoriness in humans.

Right ventricular refractory periods obtained using atrial and ventricular pacing with an atrioventricular (AV) interval of 160 ms were compared with those obtained with an AV interval of 0 ms in a group of 53 patients. The mean right ventricular effective refractory periods were longer at an AV interval of 160 ms than at an AV interval of 0 ms at pacing cycle lengths of 600 (mean 2.5 +/- 1.8 ms difference) and 400 ms (mean 3.8 +/- 2.4 ms difference; P less than 0.01). In a subset of 10 patients, left ventricular volumes measured by two-dimensional echocardiography demonstrated that pacing with an AV interval of 160 ms was associated with a higher end-diastolic volume and stroke volume than pacing with an AV interval of 0 ms (P less than 0.001). Autonomic blockade did not alter the relationship between AV interval and ventricular refractoriness. We conclude that 1) right ventricular refractory periods are shorter at an AV interval of 0 ms than at an AV interval of 160 ms; 2) these differences are not caused by changes in autonomic tone but are associated with differences in ventricular volumes; and 3) if precise determinations of ventricular refractoriness are desired, then the timing of atrial systole should be controlled by atrial pacing.

Aged↗

PubMed1990

Paradoxical effects of exercise on the QT interval in patients with polymorphic ventricular tachycardia receiving type Ia antiarrhythmic agents.

We analyzed the results of exercise testing performed in the absence of all antiarrhythmic drugs in 11 case patients with newly documented polymorphic ventricular tachycardia in response to type Ia antiarrhythmic agents. These results were compared with those found in 11 control patients matched for age, sex, and heart disease to determine whether the response of the QT interval to exercise testing was abnormal in patients who developed worsening of arrhythmia while taking antiarrhythmic drugs. QT, RR, and QTc intervals (by Bazett's method) were evaluated at rest and at 3 minutes of exercise in both groups. At rest, there was no significant difference in the QT interval (410 +/- 13 vs. 386 +/- 11 msec), RR interval (890 +/- 56 vs. 781 +/- 43 msec), or corrected QT interval (438 +/- 10 vs. 438 +/- 4 msec) in the case patients and the control patients. Both groups demonstrated a similar chronotropic response to exercise. The QT interval shortened in both groups with exercise (p less than 0.001), but the degree of shortening tended to be greater in the control patients (to 310 +/- 9 msec) than in the case patients (to 357 +/- 11 msec) (p = 0.06). Thus, there was a paradoxical increase in the QTc interval in the patients who experienced a proarrhythmic effect of type Ia drugs but not in the control patients (to 482 +/- 8 vs. 431 +/- 5 msec; p less than 0.001). Ten of 11 case patients but only one of 11 control patients had an increase in QTc interval of more than 10 msec with exercise (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗

PubMed1990

Effects of resting vagal tone on accessory atrioventricular connections.

The purpose of this study was to determine the effects of resting vagal tone on accessory atrioventricular (AV) connections. Atropine (0.04 mg/kg) was administered to 13 patients with the Wolff-Parkinson-White syndrome and was found to have the following effects on the accessory AV connection: the anterograde block cycle length shortened from 305 +/- 51 to 279 +/- 54 msec (mean +/- SD; p less than 0.001); the retrograde block cycle length shortened from 288 +/- 57 to 251 +/- 50 msec (p less than 0.001); and the effective refractory period measured at a basic drive cycle length of 400 msec shortened from 295 +/- 45 to 265 +/- 47 msec in the anterograde direction (p less than 0.001) and from 283 +/- 18 to 261 +/- 12 msec in the retrograde direction (p less than 0.01). During atrial fibrillation, the mean ventricular cycle length decreased from 434 +/- 88 to 352 +/- 56 msec (p less than 0.001), and the shortest preexcited RR interval decreased from 302 +/- 56 to 256 +/- 43 msec (p less than 0.01). In another seven patients, propranolol (0.2 mg/kg) was administered before atropine, and atropine lengthened the anterograde block cycle length and the effective refractory period of the accessory AV connection; the magnitude of these effects was similar to that in the patients who did not receive propranolol. In conclusion, these data demonstrate that resting vagal tone exerts a direct depressant effect on accessory AV connections that does not require background sympathetic activity to be manifest.

Adult↗

PubMed1990

Long-term results of catheter ablation of idiopathic right ventricular tachycardia.

Ten consecutive patients with recurrent episodes of symptomatic, idiopathic, sustained monomorphic ventricular tachycardia (VT) originating in the right ventricle underwent an attempt at catheter ablation of the ventricular tachycardia. There were seven women and three men, with a mean age of 39 +/- 14 years (+/- SD). None of the patients had any evidence of structural heart disease. The VT had a left bundle branch block configuration and an inferior axis in each patient, and the mean cycle length was 313 +/- 75 msec. Based on the methods of induction of the VT and the response of the VT to verapamil, the VT mechanism was presumed to be reentry in six patients, triggered activity in three patients, and catecholamine-sensitive automaticity in one patient. Sites for ablation were guided by pace mapping, and an appropriate target site was identified in the right ventricular outflow tract in each patient. From one to three shocks of 100-360 J (mean total, 336 +/- 195 J) were delivered from a defibrillator between the tip of the ablation catheter (cathode) and a patch electrode on the anterior chest (anode). An electrophysiology test 7-9 days after ablation demonstrated that VT was still inducible in only one patient, who was treated with amiodarone. One other patient had a recurrence of VT 3 weeks after ablation and was treated with verapamil. Eight of 10 patients were not treated with antiarrhythmic medications and have had no episodes of symptomatic VT during 15-68 months of follow-up (mean follow-up, 33 +/- 18 months). There were no acute or long-term complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Effect of cellular uncoupling by heptanol on conduction in infarcted myocardium.

Experiments were performed in vitro on six normal thin ventricular epicardial tissue strips and 10 strips removed from the infarcted regions of dogs 21-60 days after experimental myocardial infarction. Conduction was evaluated by mapping activation sequences at 40-45 sites over an area of 1 x 2 cm during pacing at a basic cycle length of 2,000 msec. The amplitude and length of recorded electrograms were also determined at each site. After control recordings, heptanol, which increases gap junctional resistance, was added to the tissue bath at concentrations ranging between 0.2 and 1.0 mM. In contrast to its effect on normal tissues, heptanol caused 75 of 260 previously active sites in the infarcted tissues to become inactive. The affected sites were located in areas of very slow conduction and/or adjacent to areas of preexisting conduction block. In addition, heptanol decreased the length and degree of fractionation of electrograms recorded in slowly conducting regions of the infarcted tissues. The magnitude of the decrease in electrogram length following heptanol was related to the degree of electrogram abnormality during control as reflected in the ratio of electrogram length to amplitude. Heptanol shortened electrograms by causing local conduction block, which eliminated some components of the fractionated electrograms. In an additional eight epicardial strips removed from the infarcted region, 0.5 mM heptanol had only a slight effect (10.7% decrease) on the maximum rate of membrane depolarization. Thus, heptanol does not act primarily by way of depressing the fast inward current. We conclude from heptanol's effects on conduction and electrogram characteristics that slow and dissociated conduction in the infarcted region is due to an abnormality in gap junctional distribution between surviving cells and/or an abnormality in individual gap junctional function.

Action Potentials↗

PubMed1989

Sequelae of nonsustained polymorphic ventricular tachycardia induced during programmed ventricular stimulation.

The results of 206 programmed ventricular stimulation studies performed in 130 patients (100 men and 30 women, mean age 62 +/- 12 years, +/- standard deviation) were examined prospectively to determine the sequelae of nonsustained polymorphic ventricular tachycardia (VT) induced during programmed ventricular stimulation. The clinical indication for the electrophysiologic study was either documented monomorphic VT or unexplained syncope. The pacing protocol included 2 right ventricular pacing sites, 2 basic drive cycle lengths and up to 3 extrastimuli. In 111 studies, nonsustained polymorphic VT was induced and with continuation of the programmed stimulation protocol, sustained monomorphic VT was induced in 48 studies (43%) and polymorphic VT was induced in 13 studies (12%). Overall, sustained monomorphic VT was induced in 110 studies and sustained polymorphic VT in 18 studies. The incidence of nonsustained polymorphic VT preceding the induction of sustained polymorphic VT was significantly greater than the incidence of nonsustained polymorphic VT preceding the induction of sustained monomorphic VT (72 vs 44%, p less than 0.05). Nonsustained polymorphic VT is not a useful predictor of the outcome of programmed ventricular stimulation. The use of nonsustained polymorphic VT as an endpoint for stimulation would be likely to improve the specificity of programmed ventricular stimulation by limiting the induction of sustained nonclinical arrhythmias that require countershock, but at the cost of significantly impairing the yield of monomorphic VT.

Cardiac Pacing, Artificial↗

PubMed1989

Natural history of patients with unexplained syncope and a nondiagnostic electrophysiologic study.

The purpose of this study was to define the natural history of 99 patients with unexplained syncope who underwent an electrophysiologic test that either was entirely normal or demonstrated nonspecific abnormalities that were nondiagnostic (inducible polymorphic ventricular tachycardia or ventricular fibrillation, a mildly prolonged sinus node recovery time of less than 2 s, a His-ventricular interval of 55 to 99 ms or supraventricular tachycardia not associated with hypotension). The mean age (+/- SD) of the patients was 56 +/- 19 years; structural heart disease was present in 47 patients and absent in 52. Complete follow-up was available in 95 patients. During 20 +/- 11 months of follow-up, 2 patients (2%) died suddenly, 19 patients (20%) had recurrent syncope and 74 patients (78%) had no further episodes of syncope. Among the 19 patients who continued to have syncope after the electrophysiologic testing, the cause of syncope was established clinically in 4 and was found to be high degree atrioventricular (AV) block (2 patients) or sinus node dysfunction (2 patients). No clinical or laboratory findings distinguished patients who had sudden death or syncope during follow-up from patients who did not. In conclusion, in patients with unexplained syncope who undergo an electrophysiologic test that is nondiagnostic 1) the incidence of sudden death is low (2%); 2) the remission rate of syncope is high (80%); 3) the electrophysiologic test may be documented to have been falsely negative in greater than or equal to 20% of patients who continue to have syncope, syncope in these patients being caused by AV block or sinus node dysfunction; and 4) patients at risk of sudden death or recurrent syncope, or both, cannot be readily identified prospectively.

Arrhythmia, Sinus↗

PubMed1989

Sinus mapping in patients with cardiac arrest and coronary disease--results and correlation with outcome.

Electrophysiological testing and left ventricular endocardial mapping in sinus rhythm were performed in 61 patients with coronary artery disease who presented with cardiac arrest in an attempt to relate the results of these studies to clinical outcome. Forty-one patients (67%) had inducible sustained arrhythmias (18 uniform ventricular tachycardia, 23 polymorphic ventricular tachycardia/ventricular fibrillation) and 20 had no inducible arrhythmia. Patients with inducible arrhythmia had 45% abnormal and 6% fractionated electrograms versus 31% and 0% for those without inducible arrhythmia (P greater than 0.05 for both comparisons). Sixteen of 59 patients (27%) with adequate follow-up had arrhythmia recurrence (11/39 [31%] with inducible arrhythmia and 5/20 [25%] without inducible arrhythmia) over a mean follow-up period of 27 months. Of five patients without inducible arrhythmia who experienced recurrence, two did so despite the anti-ischemic therapy. In the 20 patients without inducible arrhythmia, the 15 who remained arrhythmia-free had a mean of 78 +/- 22% normal sites versus 46 +/- 24% normal sites in those with recurrence (P greater than 0.05). We conclude that in patients with coronary artery disease and cardiac arrest: 1) patients without inducible arrhythmia have less marked endocardial electrical abnormality than those with inducible arrhythmia, 2) those patients who have marked endocardial abnormality despite the lack of inducible arrhythmia are at risk for clinical recurrence which suggests that these abnormalities may represent an anatomic substrate for arrhythmia which cannot be identified by programmed stimulation. These patients are candidates for AICD implantation and 3) patients with relatively normal endocardial electrograms do well with anti-ischemic therapy alone.

Aged↗

PubMed1989

Comparison of ventricular refractory periods determined by incremental and decremental scanning of an extrastimulus.

This study compared the ventricular effective refractory periods measured by scanning diastole with an extrastimulus in incremental and decremental steps of 5 msec. The subjects of the study were 80 patients undergoing a clinically indicated electrophysiological test. Eight beat basic drive trains at a cycle length of 600 msec and an intertrain pause of 4 seconds were used to measure the ventricular effective refractory period (VERP). In the incremental method, the extrastimulus initially was positioned at a coupling interval shorter than the VERP and the coupling interval then was progressively increased until ventricular capture occurred. In the decremental method, the initial extrastimulus coupling interval was longer than the VERP and the coupling interval was progressively shortened until ventricular capture was lost. In 50 subjects, the mean VERP determined by the incremental method, 252 +/- 18 (+/- standard deviation), was significantly longer than the mean VERP determined in the same patients by the decremental method, 248 +/- 18 msec (P less than 0.0001). In ten subjects, a subthreshold stimulus (S') positioned 10 msec earlier than the VERP had an inhibitory effect that lengthened the VERP by an average of 7 msec; however, when S' was positioned after the seventh beat of an eight beat drive train, no inhibitory effect could be demonstrated. In 20 subjects, VERP's were determined by the incremental and decremental methods using intertrain pauses of 1, 4, 8, 12, and 20 seconds.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗

PubMed1989

The effect of electrode configuration on the unipolar His-bundle electrogram.

Although "unipolar electrograms" recorded from the His-bundle position have been used to help position catheters for His-bundle ablation, the techniques used to record such electrograms have not been standardized. The effects of five anode locations (right chest wall, anterior chest wall, left chest wall, posterior chest wall, and inferior vena cava) on unipolar atrial, His bundle and ventricular electrograms recorded from the His-bundle position were examined in ten patients undergoing clinical electrophysiology studies. Electrograms were recorded at filter settings of 50-500 as well as 0.05-1000 Hz. The location of the anode had no consistent effect on the amplitude, duration or morphology of any of the electrograms at either filter setting, but signals recorded with the inferior vena cava anode had the highest signal-to-noise ratio. A filter setting of 50-500 Hz decreased the amplitude of atrial (0.72 to 0.33 mV-P less than 0.01), His bundle (0.38 vs 0.32 mV-P less than 0.01) and ventricular electrograms (3.71 vs 2.01 mV-P less than 0.001) compared to a filter setting of 0.05-1,000 Hz. The filter setting did not affect electrogram duration. We concluded that the use of an electrode catheter in the inferior vena cava as the anode when recording "unipolar electrograms" from the His-bundle position yields a better signal-to-noise ratio than a skin patch on the chest and appears to be the optimal method for recording unipolar electrograms.

Bundle of His↗

PubMed1989

Epinephrine-induced reversal of verapamil's electrophysiologic and therapeutic effects in patients with paroxysmal supraventricular tachycardia.

The purpose of our study was to determine whether an infusion of epinephrine reverses the electrophysiologic effects of verapamil and whether reversal of verapamil's effects on the induction of paroxysmal supraventricular tachycardia (PSVT) by epinephrine during electropharmacologic testing is predictive of stress-related recurrences of PSVT during long-term treatment with verapamil. The infusion rates of epinephrine used in this study were 25 and 50 ng/kg/min, which previously have been demonstrated to result in plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. The subjects of this study were 17 patients with recurrent PSVT who underwent an electrophysiologic study in the control state and after at least 2 days of treatment with 240-480 mg/day verapamil. After assessing the response to verapamil, epinephrine was infused and testing was repeated. Verapamil significantly slowed atrioventricular conduction and prolonged refractoriness in the atrium and atrioventricular node. The effects of the two infusion rates of epinephrine were generally similar in magnitude and, therefore, the results were pooled. Epinephrine partially or completely reversed all of verapamil's electrophysiologic effects. Verapamil suppressed the induction of sustained PSVT in 15 patients. Epinephrine facilitated the induction of PSVT in seven of these 15 patients. All 15 patients were treated on a long-term basis with verapamil. The eight patients in whom epinephrine did not facilitate the induction of PSVT had no recurrences of PSVT during 9-18 months of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Atenolol↗

PubMed1989

Long-term results of catheter ablation of a posteroseptal accessory atrioventricular connection in 48 patients.

Forty-eight patients with a posteroseptal accessory atrioventricular (AV) connection underwent catheter ablation of the accessory AV connection with 200-400 J shocks delivered by a standard defibrillator. Cathodal shocks were delivered through the proximal pair of electrodes of a 6F quadripolar electrode catheter positioned in the coronary sinus such that the proximal electrodes straddled the ostium (12 patients) or the third electrode from the tip was at the ostium (36 patients). A 16-cm patch electrode positioned on the back or anterior chest served as the anode. Two to 4 shocks were delivered (total, 635 +/- 198 J, mean +/- SD). The cathether ablation procedure was clinically successful in eliminating symptomatic tachycardias in in 32 of 48 patients (67%) during a mean follow-up of 26 +/- 19 months. A long-term follow-up electrophysiology study was performed in 27 of the 32 patients who had a successful clinical outcome, and this showed that conduction through the accessory AV connection was completely absent in 25 patients and present but impaired in two patients. The success rate was significantly higher in patients with a concealed accessory AV connection (13 of 13, 100%) than in patients with manifest preexcitation (19 of 35, 54%; p less than 0.001). Among the 12 patients in whom the proximal electrodes of the ablation catheter straddled the ostium of the coronary sinus, one patient developed cardiac tamponade requiring needle pericardiocentesis; there were no instances of cardiac tamponade among the 36 patients in whom the third electrode from the tip was at the ostium of the coronary sinus. Other complications were AV block requiring a permanent pacemaker and transient atrial tachycardia in one patient each and an asymptomatic pericardial effusion in three patients. In conclusion, with the catheter ablation technique described in this study, a successful clinical outcome may be achieved in approximately two thirds of patients who have a posteroseptal accessory AV connection, and the risk of serious complications is low. This technique is particularly well suited to patients with a concealed posteroseptal accessory AV connection, in whom the success rate is higher than in patients with manifest preexcitation.

Adult↗

PubMed1989

Mechanisms and risk factors for proarrhythmia with type Ia compared with Ic antiarrhythmic drug therapy.

Proarrhythmia defined as the exacerbation of existing arrhythmias or the genesis of new arrhythmias de novo may result from any antiarrhythmic agent. The two general clinical syndromes of sustained arrhythmias that result appear to have distinct clinical properties that are consistent with the proposed basic mechanisms of arrhythmogenesis. Torsades de points occurs most commonly in association with administration of type Ia antiarrhythmic agents and has characteristics most consistent with triggered activity mediated by early after depolarization. Conversely, incessant, sustained, monomorphic, wide complex ventricular tachycardia occurs most commonly in association with type Ic antiarrhythmic agents and has characteristics most consistent with incessant reentry. These general subdivisions are probably oversimplified, and in fact, much overlap likely exists. In addition, these proposed mechanisms may not apply to other forms of proarrhythmia such as an increased frequency of isolated ventricular premature couplets or repetitive forms. Furthermore, proarrhythmia may also occur during treatment of supraventricular arrhythmias; although some of these described syndromes are consistent with incessant reentry, the clinical syndromes are not sufficiently defined to better characterize potential mechanisms. Further investigation, therefore, is needed to better define the mechanisms in question, but the mechanisms proposed in this article help to provide a rational approach toward understanding and dealing with clinical proarrhythmia.

Animals↗

PubMed1988

Effects of epinephrine in patients with an accessory atrioventricular connection treated with quinidine.

The purpose of this study was to determine whether physiologic doses of epinephrine reverse the electrophysiologic effects of quinidine in patients with an accessory atrioventricular (AV) connection. Eighteen patients with an accessory AV connection who had inducible sustained orthodromic tachycardia underwent an electrophysiologic study in the baseline state and after at least 2 days of treatment with 1.4 to 1.9 g/day of quinidine gluconate. The effects of epinephrine were then determined. Epinephrine infusion rates of 25 and 50 ng/kg/min were used in 9 patients each because these doses of epinephrine previously have been demonstrated to result in elevated plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. Quinidine prolonged refractoriness in the atrium and accessory AV connection and slowed conduction through the accessory AV connection. These effects were partially or completely reversed by epinephrine. Among 8 patients in whom quinidine resulted in orthodromic tachycardia becoming noninducible or nonsustained, sustained tachycardia became inducible again in 5 patients after infusion of epinephrine. After quinidine, atrial fibrillation was either noninducible or nonsustained in 8 patients; however, sustained atrial fibrillation could be induced in 4 of these patients after infusion of epinephrine. The results of this study demonstrate that the therapeutic effect of quinidine in patients who have an accessory AV connection are often reversed by physiologic increases in circulating epinephrine.

Adult↗

PubMed1988

Differential effects of procainamide, lidocaine and acetylstrophanthidin on body surface potentials and epicardial conduction in dogs with chronic myocardial infarction.

Twenty-eight anesthetized mongrel dogs were studied 2 to 74 months after experimental myocardial infarction in order to examine the effects of procainamide, lidocaine and acetylstrophanthidin on conduction within the infarcted region and the way such effects relate to changes in body surface potentials and antiarrhythmic efficacy. In each animal, 100 to 200 QRS complexes in the X, Y, Z leads were signal averaged, vector summed and high pass filtered at 50 Hz. Susceptibility to ventricular arrhythmia was evaluated using routine programmed ventricular extrastimulation in the anesthetized open chest animal. Epicardial electrograms were sequentially recorded at 45 standard sites within the infarcted region and referenced to the beginning of the QRS complex. Of the three agents, only procainamide exhibited antiarrhythmic action whereas lidocaine and acetylstrophanthidin produced inconsistent effects. Procainamide prolonged the time at which activity in the epicardial electrographic recordings ended relative to the beginning of the body surface QRS complex. This effect was significantly greater in electrograms that ended late in the QRS complex in the control state than for those that ended earlier. Such preferential effect on more abnormal sites was reflected on the body surface as a greater effect of procainamide in prolonging the lower energy terminal portion of the signal-averaged QRS complex than the earlier high energy portion. In contrast, lidocaine significantly prolonged the time at which electrograms ended only for those relatively normal electrograms that ended early in the QRS complex in the control state. In the signal-averaged body surface QRS complex, lidocaine produced a small but significant prolongation of the early high energy portion of the QRS complex but no change in the late portion. Acetylstrophanthidin produced a significant prolongation in early-ending electrograms and, surprisingly, significantly shortened the end time of electrograms that ended late in the QRS complex in the control state. Such effects were not reflected, however, on the body surface because acetylstrophanthidin had no significant effect on either the early or the late portion of the QRS complex. It is concluded that procainamide's differential effect between early- and late-ending electrograms is detected on the body surface by a greater prolongation in the terminal portion of the QRS complex. The signal-averaged body surface QRS complex is less sensitive in detecting the more subtle effects on conduction caused by lidocaine and acetylstrophanthidin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Antagonism of quinidine's electrophysiologic effects by epinephrine in patients with ventricular tachycardia.

The purpose of this study was to determine whether pharmacologically induced elevations in the plasma epinephrine concentration within reported physiologic limits alter the response to quinidine during electropharmacologic testing. Twenty-one patients with coronary artery disease and a history of unimorphic ventricular tachycardia were found to have inducible sustained unimorphic ventricular tachycardia that was suppressed by treatment with oral quinidine gluconate. Epinephrine was then infused at a rate of either 25 or 50 ng/kg per min and testing was repeated. These infusion rates of epinephrine were previously demonstrated to result in elevations of the plasma epinephrine concentration in the range of concentrations that occur during a variety of stresses. Quinidine significantly lengthened the ventricular refractory periods and the QRS duration at a ventricular pacing cycle length of 350 ms, which was used as an index of intraventricular conduction. Epinephrine partially or completely reversed the effects of quinidine on ventricular refractory periods, but had no effect on QRS duration. During electropharmacologic testing of quinidine, no ventricular tachycardia was inducible in 12 patients, and only nonsustained ventricular tachycardia, 8 to 48 beats in duration, was inducible in 9 patients. Retesting during infusion of epinephrine demonstrated inducible sustained unimorphic ventricular tachycardia in 2 of the 12 patients in whom quinidine had completely suppressed the induction of ventricular tachycardia and in 8 of the 9 patients in whom only nonsustained ventricular tachycardia had been inducible during testing of quinidine. In conclusion, physiologic elevations in the plasma epinephrine concentration may reverse quinidine-induced prolongation of ventricular refractoriness but not intraventricular conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1988

Cycle length-dependent effects on normal and abnormal intraventricular electrograms: effect of procainamide.

The effect of procainamide (mean concentration 9.1 +/- 2.0 micrograms/ml) on cycle length-dependent changes in electrographic characteristics was determined in 10 patients with prior myocardial infarction. Intracardiac bipolar electrograms were recorded from an abnormal left ventricular site in the distribution of prior (greater than 6 month) myocardial infarction and from a normal right ventricular site. Pacing was performed for 15 beats from the right ventricular apex at cycle lengths of 600 (or 500), 400 and 300 ms. In the control state, the QRS width, the normal electrogram and in 9 of the 10 patients the abnormal electrogram did not change with decreasing cycle lengths. After procainamide the mean QRS width increased from 203 +/- 32 to 240 +/- 50 ms (+18%, p less than 0.01) at a paced cycle length of 600 (or 500) ms, from 198 +/- 34 to 245 +/- 59 ms (+24%, p less than 0.01) at a paced cycle length of 400 ms and from 197 +/- 36 to 258 +/- 67 ms (+31%, p less than 0.01) at a paced cycle length of 300 ms.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗

PubMed1988

The maximum effect of an increase in rate on human ventricular refractoriness.

The purpose of this study was to determine the maximum shortening of ventricular refractoriness that occurs following an increase in rate and to quantitate the duration of ventricular pacing required to obtain this maximum shortening of refractoriness. The subjects of the study consisted of 41 patients who underwent a clinically indicated electrophysiologic study. Ventricular refractory periods were measured with an extrastimulus (S2) at basic cycle lengths of 600 and 400 ms by Method A (8 beat basic drive trains and 4 second intertrain paue and Method B (drive train duration of 3 minutes, then an S2 after every eighth basic drive beat, with no pause after the S2). In 23 subjects, the mean ventricular effective refractory period determined by Method B was 12 +/- 7 ms (+/- standard deviation) shorter than when determined by Method A at a basic drive cycle length of 600 ms (p less than 0.0001) and 33 +/- 9 ms shorter at a basic drive cycle length of 400 ms (p less than 0.001). In these 23 subjects, the drive train duration required for maximum shortening of ventricular refractoriness was estimated by counting the number of drive train beats preceding ventricular capture by an S2 inserted after every fourth basic drive beat at a coupling interval fixed at 5 ms longer than the ventricular effective refractory period determined in that subject by Method B. The mean number of basic drive beats preceding capture by S2 was 114 +/- 84 beats at a basic drive cycle length of 600 ms and 233 +/- 85 beats at a BDCL of 400 ms. In six subjects the ventricular effective refractory period was measured by Methods A and B before and after autonomic blockade with propranolol and atropine, and the amount of shortening in the ventricular effective refractory period with Method B was not affected by autonomic blockade. In conclusion, the basic drive train has a cumulative effect on ventricular refractoriness in humans, and a drive train duration substantially longer than 50 beats often is required to obtain the maximum shortening of ventricular effective refractory period after an increase in rate. Therefore, ventricular effective refractory periods determined conventionally using 8 beat drive trains and a 4 second intertrain pause often may be overestimates of the actual ventricular effective refractory period. The shortening of ventricular refractoriness with long drive train durations is probably related to a prolonged duration of pacing required to obtain a steady-state action potential duration after an increase in rate.

Action Potentials↗