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Biomedical subjects

A H Dougherty

Publications and source records attributed to A H Dougherty.

At least 19 recordsLinked to original sources
PubMed1996

Interactions between antiarrhythmic drugs and implantable cardioverter-defibrillators.

Despite the efficacy of implantable cardioverter-defibrillators in preventing sudden death associated with ventricular arrhythmias, 40% to 70% of patients with an implantable cardioverter-defibrillator receive adjunctive antiarrhythmic drug therapy. The most common aims of drug therapy are to reduce the frequency of ventricular tachycardia and fibrillation triggering shock, to alter the tachycardia characteristics in order to enhance the efficacy of antitachycardia pacing, and to suppress supraventricular tachyarrhythmias. Antiarrhythmic drugs may, however, interfere with implantable cardioverter-defibrillator function by raising defibrillation and pacing thresholds. Furthermore, drugs may adversely affect the sensing of ventricular tachycardia and fibrillation by the implantable cardioverter defribillator. Careful prescription and follow-up electrophysiologic testing is critical in ensuring a cooperative effect of drug and implantable cardiovascular-defibrillator after initiation of new therapy.

Anti-Arrhythmia Agents↗
PubMed1993

Provocation of atrioventricular reentry tachycardia: a paradoxical effect of adenosine.

Adenosine has been used to diagnose latent preexcitation in patients with the Wolff-Parkinson-White syndrome. A case is reported in which intermittent preexcitation had been previously observed, however only retrograde accessory pathway conduction was documented at the time of invasive electrophysiological study. Administration of intravenous adenosine during sinus rhythm resulted in provocation of orthodromic atrioventricular reentry tachycardia.

Adenosine↗
PubMed1992

Acute conversion of paroxysmal supraventricular tachycardia with intravenous diltiazem. IV Diltiazem Study Group.

Diltiazem has electrophysiologic effects similar to those of verapamil. Its efficacy and safety in 4 doses for treatment of induced supraventricular tachycardia (SVT) were examined and compared with those of placebo in 87 patients (25 with atrioventricular [AV] nodal reentry tachycardia, 60 with AV reentry associated with an accessory AV connection, and 2 with atrial tachycardia). Conversion to sinus rhythm occurred in 4 of 14 patients (29%) with 0.05 mg/kg of diltiazem, 16 of 19 (84%) with 0.15 mg/kg, 13 of 13 (100%) with 0.25 mg/kg, and 14 of 17 (82%) with 0.45 mg/kg compared with 6 of 24 (25%) treated with placebo. Conversion rates in groups receiving doses of 0.15 to 0.45 mg/kg of diltiazem were superior to that in the placebo group (p less than 0.001). Time to conversion was 3.0 +/- 2.6 minutes in responding diltiazem patients compared with 5.9 +/- 6.1 minutes in responding control patients. Diltiazem administration resulted in significant lengthening of SVT cycle length, AH interval, and AV nodal effective refractory period and block cycle length. The most frequent adverse response to diltiazem was hypotension (7 of 63 patients); however, only 4 patients had symptoms related to hypotension. Thus, intravenous diltiazem in doses of 0.15, 0.25 and 0.45 mg/kg is an effective and safe treatment for the acute management of SVT.

Cardiac Pacing, Artificial↗
PubMed1988

Encainide for treatment of atrioventricular reciprocating tachycardia in the Wolff-Parkinson-White syndrome.

Oral encainide, varying from 75 to 300 mg/day (mean 174 mg/day), was administered to 52 patients with drug-resistant atrioventricular reciprocating tachycardia (AVRT) associated with the Wolff-Parkinson-White syndrome. Electrophysiologic studies were performed before and during drug treatment. Encainide resulted in anterograde accessory pathway block in 15 of 37 (41%) and retrograde accessory pathway block in 11 of 46 (24%) patients. In patients with residual accessory pathway conduction, encainide significantly prolonged the shortest pacing cycle length maintaining anterograde (261 +/- 26 to 404 +/- 85 ms) and retrograde (279 +/- 46 to 436 +/- 87 ms) accessory pathway conduction, as well as the anterograde accessory pathway effective refractory period (271 +/- 32 to 329 +/- 73 ms). AVRT could not be induced during encainide therapy in 20 of 49 patients (41%). In the remaining patients, AVRT cycle length increased (319 +/- 44 to 426 +/- 90 ms, p less than 0.001) due to prolongation of HV and ventriculoatrial intervals. During follow-up (mean 38.5 months), 30 patients continued to take the drug and 7 patients with favorable drug response subsequently elected to undergo surgical accessory pathway ablation (71% overall favorable response). Encainide was ineffective in 11 patients, was discontinued because of drug intolerance in 2 patients and exacerbated ventricular tachycardia in 2 patients. Lack of AVRT inducibility at encainide electrophysiologic study did not always predict recurrence-free follow-up. Encainide is an effective and well-tolerated drug to prevent recurrence of AVRT in patients with Wolff-Parkinson-White syndrome.

Administration, Oral↗
PubMed1988

Encainide for atrial fibrillation associated with Wolff-Parkinson-White syndrome.

Thirty-six patients with a history of atrial fibrillation and Wolff-Parkinson-White syndrome were treated with oral encainide, 175 +/- 44 mg/day, after undergoing baseline drug-free electrophysiologic studies. The mean age was 38 +/- 15 years, with structural heart disease present in only 3 patients. Nine patients had only paroxysmal atrial fibrillation and 27 patients had both atrial fibrillation and atrioventricular reciprocating tachycardia (AVRT). Symptoms were present for a mean of 195 +/- 168 months and were treated with an average of 2.7 +/- 1.6 drugs before encainide. Anterograde block in the accessory pathway occurred in 12 of 30 patients (40%) and retrograde block accessory pathway occurred in 10 of 24 patients in whom comparison could be made. AVRT was initiated in 29 of 36 patients during the control study and could be initiated in 19 of 29 patients while receiving encainide. Drug efficacy was determined by the clinical response judged completely effective, partially effective or ineffective. During a mean follow-up of 30.1 +/- 25 months, 24 patients (67%) continued to take encainide. Encainide was completely effective in 14 of 24 patients and partially effective in another 7 patients. Noncardiac side effects were mild and generally resolved, and required discontinuance in only 1 patient. More frequent AVRT occurred in 2 patients, but was managed with dose reduction and the addition of a beta blocker. Three patients had ventricular tachycardia requiring discontinuance; however 2 of 3 patients had a history of ventricular tachycardia before receiving encainide. Encainide is an effective and safe agent for treating atrial fibrillation in patients with Wolff-Parkinson-White syndrome.

Adolescent↗
PubMed1988

Efficacy and electrophysiologic effects of encainide for atrioventricular nodal reentrant tachycardia.

To prospectively determine the clinical efficacy and electrophysiologic effects of encainide in atrioventricular nodal reentrant tachycardia (AVNRT), 49 patients refractory to 2.7 +/- 1.5 previous antiarrhythmic drug trials underwent electrophysiologic study before and 47 did so after administration of oral encainide (75 to 240 mg/day). Encainide prolonged the minimum atrial pacing cycle length maintaining 1:1 atrioventricular (AV) nodal conduction from 334 +/- 55 to 391 +/- 55 ms (p = 0.0001). Encainide induced ventriculoatrial (VA) block in 12 patients (25%) and slowed the minimum ventricular pacing cycle length maintaining 1:1 VA conduction from 315 +/- 46 to 485 +/- 89 ms (p = 0.0001) in the remaining 35 patients. After encainide, AVNRT was not inducible in 32 of 47 patients (68%) primarily because of the effects on retrograde AV nodal conduction. In the remaining 15 (32%) patients, AVNRT remained inducible; however, the tachycardia cycle length slowed from 397 +/- 86 to 492 +/- 90 ms (p = 0.0001). There was no significant difference in the baseline minimum ventricular pacing cycle length maintaining 1:1 VA conduction in patients whose inducible tachycardia was or was not suppressed. Forty-seven patients were treated for 18.9 +/- 12.9 months (range 1 to 50) with oral encainide. Encainide was completely effective in eliminating recurrences of supraventricular tachycardia in 26 of 47 patients (55%) and partially effective in an additional 42%. Recurrences of arrhythmia occurred in 15 of 32 patients (47%) whose inducible tachycardia was suppressed by encainide and 7 of 15 patients (47%) whose inducible tachycardia was not suppressed by encainide (p = not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Role of adrenergic stimulation by isoproterenol in reversal of effects of encainide in supraventricular tachycardia.

Reversal of the electrophysiologic effects of oral encainide with isoproterenol was evaluated in 16 patients with atrioventricular (AV) nodal reentry (group A) and in another 16 patients with Wolff-Parkinson-White syndrome (group B). Sustained AV nodal reentry was induced in all group A cases before administration of encainide, in 2 cases after oral encainide, and in 12 patients during infusion of isoproterenol. Among group B cases, 14 of 16 had sustained AV reentry during control, 6 of 16 after receiving encainide, and 8 of 16 with addition of isoproterenol. During a mean follow-up of 19 +/- 10 months in group A and 17 +/- 9 months in group B, clinical tachycardia recurred in 8 patients (4 from each group). These 8 patients were among the 20 patients who demonstrated (1) isoproterenol-induced reversibility of encainide-suppressed tachycardia, or (2) acceleration of tachycardia rate slowed by encainide. No recurrences were seen among any of the 12 cases in which isoproterenol failed to reverse the encainide-induced tachycardia suppression. Patients with clinical recurrences were controlled with a variety of means, which included beta blockers in 3 and nonpharmacologic methods in the remaining 5. In patients with AV junctional tachycardia treated with oral encainide, our findings suggest that lack of tachycardia inducibility with isoproterenol predicts freedom from clinical recurrences. Furthermore, addition of a beta blocker to oral encainide may prevent clinical recurrence in some who demonstrate adrenergic reversal of encainide effect.

Administration, Oral↗
PubMed1988

Efficacy and safety of class IC antiarrhythmic agents for the treatment of coexisting supraventricular and ventricular tachycardia.

Thirty-three patients with concurrent supraventricular (SVT) and ventricular tachycardia (VT) were treated with class IC antiarrhythmic agents. Twenty-two patients had atrial fibrillation (17 with paroxysmal and 5 with chronic fibrillation), 1 patient had ectopic atrial tachycardia and 11 patients had reentrant paroxysmal SVT (8 with atrioventricular node reentrant tachycardia, 3 with atrioventricular reentrant tachycardia). Of 5 patients with Wolff-Parkinson-White syndrome, 2 had only atrial fibrillation. Six patients had sustained VT and 27 had nonsustained VT. Twenty-nine patients had organic heart disease (16 with coronary artery disease, 8 with cardiomyopathy and 5 with valvular heart disease) and 4 had primary electrical disease. The mean ejection fraction was 40 +/- 14% (range 15 to 66%). The study population's arrhythmias were not controlled despite having received 2 to 5 (mean 3.1) previous drug trials. Eighteen patients were referred for treatment of SVT and 15 were referred for treatment of VT (mean symptom duration 107 months). Efficacy was determined in 13 of 33 patients with sustained SVT or VT by programmed electrical stimulation and in 20 of 33 by telemetry and 24-hour Holter response. Twenty-two flecainide and 15 encainide trials were conducted in the 33 patients. Four patients underwent trials with both drugs. Of 33 patients with coexisting SVT and VT, 15 (45%) were controlled with an IC agent alone and 3 continued therapy with an IC agent plus additional therapy (2 drugs, 1 antitachycardia pacing). During the follow-up period (mean 10.4 months), flecainide produced a complete response in 9 patients and encainide in 9 patients. SVT was not controlled in 7 patients and VT was not controlled in 7 patients. One patient had neither arrhythmia controlled. Atrial or ventricular proarrhythmia was seen in 9 of 33 patients (27%) (5 with ventricular and 4 with atrial arrhythmia). Noncardiac side effects were uncommon. Oral class IC agents may be effective therapy for some patients with coexisting VT and SVT of different mechanisms. Patients with such complex arrhythmias should be evaluated carefully because there is a potential for both atrial and ventricular proarrhythmia.

Anilides↗
PubMed1987

Efficacy and safety of flecainide acetate for atrial tachycardia or fibrillation.

Thirty-nine patients with symptomatic ectopic atrial tachycardia (9 paroxysmal, of which 5 were incessant) and atrial fibrillation (AF) (25 paroxysmal, 5 chronic) were treated with oral flecainide acetate (100 to 400 mg/day). Thirty-two patients had organic heart disease (16 coronary artery disease, 6 valvular, 10 cardiomyopathy, 7 primary electrical abnormality). Previous antiarrhythmic trials consisted of 0 to 5 drugs (mean 2.2). Of 39 patients with atrial tachycardia or AF, a complete response (no recurrent symptomatic atrial arrhythmia) was achieved in 22 (56%), a partial response (more than 95% reduction in arrhythmia occurrence) in 3 (8%) and no response in 14 (36%). Left atrial size, ejection fraction, underlying heart disease, duration of symptoms before treatment and drug levels were not useful for predicting clinical response. Therefore, during the follow-up period of 5.4 +/- 6.7 months (range 4 weeks to 2.5 years), flecainide had a complete or partial effect in 25 patients (64%). Complete or partial responses were noted in 8 of 9 patients (90%) with ectopic atrial tachycardia and 17 of 30 (57%) with AF. In 14 patients with concurrent ventricular arrhythmias, a significant reduction in episodes of nonsustained ventricular tachycardia was also achieved. Treatment was discontinued in 8 patients (20%) because of cardiac adverse reactions, including pulmonary edema and ventricular or atrial proarrhythmic response. Thus, oral flecainide acetate is effective therapy for some patients with ectopic atrial tachycardia or AF.

Arrhythmias, Cardiac↗
PubMed1987

Characteristics of ventriculoatrial conduction in patients with enhanced atrioventricular nodal conduction.

To study the characteristics of the ventriculoatrial conduction system in patients capable of rapid antegrade atrioventricular conduction, electrophysiologic studies were performed in 23 subjects capable of 1:1 atrioventricular conduction at atrial cycle lengths less than or equal to 300 ms (Group I), and in 23 subjects with normal 1:1 atrioventricular conduction (Group II). During ventricular pacing, ventriculoatrial block at all cycle lengths was seen in 5/23 (22%) in Group I and in 7/23 (30%) in Group II patients (p = NS). In the remainder, the minimum ventricular pacing cycle length maintaining 1:1 ventriculoatrial conduction was 359 +/- 85 ms in Group I, compared to 444 +/- 118 ms in Group II (p less than .02). Both flat and exponential VA conduction interval curves, drawn as a function of pacing cycle length, were observed in both groups. Discontinuous ventriculoatrial conduction curves were seen in 5/18 (28%) Group I and 1/16 (6%) Group II patients (p = NS). In conclusion, retrograde ventriculoatrial conduction, when present in patients capable of rapid 1:1 atrioventricular conduction, is maintained at shorter cycle lengths than in patients with normal atrioventricular conduction. Quantitative, rather than qualitative, differences distinguish the two groups.

Adult↗
PubMed1986

Assessment of antiarrhythmic drug efficacy in the treatment of supraventricular arrhythmias.

Few guidelines exist for judging the efficacy of antiarrhythmic drugs in patients with supraventricular arrhythmias. Useful definitions concerning the frequency and duration of supraventricular arrhythmias are offered, and complete and partial efficacy criteria are outlined for noninvasive electrocardiographic and invasive electrophysiologic techniques. Several open label, double-blind, parallel and crossover study designs are suggested for efficacy studies concerning the termination and prevention of supraventricular tachycardia. These recommendations are useful for designing new drug trials needed to evaluate properly the efficacy of antiarrhythmic agents in the treatment of various supraventricular arrhythmias.

Adult↗
PubMed1986

Effect of pharmacologic autonomic blockade on ventriculoatrial conduction.

To determine the influence of autonomic tone on retrograde ventriculoatrial (VA) conduction, incremental atrial and ventricular pacing was performed before and after pharmacologic autonomic blockade in 28 patients. VA conduction during ventricular pacing was demonstrated, with highest frequency in patients capable of 1:1 atrioventricular (AV) conduction at atrial paced cycle lengths of 300 ms or less (7 of 7, 100%). In subjects with 1:1 AV conduction at minimum cycle lengths of 300 to 500 ms, 14 of 21 (67%) demonstrated VA conduction in the control state; however, only 12 of 21 (57%) did so after autonomic blockade. The lowest frequency was observed in those capable of 1:1 AV conduction at minimum cycle lengths of 505 ms or more before and after autonomic blockade (2 of 7, [29%], p less than or equal to 0.02 compared with values in the first group). No change in the mean minimum ventricular paced cycle length at which 1:1 VA conduction could be maintained was demonstrated after autonomic blockade. In individual subjects, incremental change in this cycle length after autonomic blockade correlated positively with the corresponding change in minimum atrial cycle length at which 1:1 AV conduction could be maintained (r = 0.62, p less than 0.005), and was concordant in direction in 18 of 21. In conclusion, the sympathetic and parasympathetic modulation of VA conduction is balanced and concordant in direction to the effect on AV nodal conduction.

Adolescent↗
PubMed1986

Electrophysiologic effects of milrinone in patients with congestive heart failure.

The electrophysiologic effects of milrinone, a new inotropic agent, have not been characterized in humans. Accordingly, 10 patients with class III or IV congestive heart failure underwent hemodynamic and electrophysiologic testing before and during an infusion of milrinone (0.5 micrograms/kg/min). Cardiac index increased from a mean of 1.65 +/- 0.51 to 2.19 +/- 0.68 liters/min/m2 (p less than 0.03) and pulmonary artery capillary pressure decreased from 30 +/- 9 to 22 +/- 9 mm Hg (p less than 0.01), without a significant change in systemic arterial pressure. Holter monitoring was performed for 48 hours at baseline and during infusion of milrinone. Frequency of ventricular premature complexes and ventricular couplets did not change significantly. Frequency of ventricular tachycardia (VT) increased significantly, although no patients would be classified as having a proarrhythmic effect based on a clinical model. PR, QRS, QTc, heart rate, AH, HV, atrial, atrioventricular and ventricular effective and functional refractory periods were not affected. Milrinone decreased 1:1 atrioventricular maximal conduction from 399 +/- 133 to 374 +/- 111 ms (p less than 0.01); ventriculoatrial conduction was not significantly affected. During programmed right ventricular stimulation, 5 patients had inducible VT at baseline (3 sustained, 2 non-sustained), whereas after drug administration, none had it (p less than 0.05). Thus, intravenous milrinone is an effective inotropic drug that also enhances atrioventricular conduction and may decrease the incidence of inducible VT in patients with congestive heart failure.

Adult↗
PubMed1986

Flecainide in the treatment of nonsustained ventricular tachycardia.

Thirty-two patients received flecainide acetate for nonsustained ventricular tachycardia after having had unsuccessful treatment with a mean of four antiarrhythmic drugs. The mean left ventricular ejection fraction was 41% in 27. Thirty-one patients had organic heart disease, and 22 patients had arrhythmia-related symptoms. Total suppression of ventricular tachycardia occurred in 22 patients. Thirty patients were discharged from the hospital receiving flecainide at a mean (+/- SD) dosage of 315 +/- 76 mg/d and 26 of these patients attained a mean trough plasma drug level of 567 +/- 254 ng/mL. One patient had proarrhythmia and 3 had worsening of heart failure. Twenty-two patients remained in the trial for a mean follow-up of 13 +/- 7 months. Five patients died (1 suddenly) during the follow-up period. Our data indicate that flecainide suppresses refractory nonsustained ventricular tachycardia in 69% of patients who have organic heart disease. Serious adverse effects were minimized by initiation of treatment in the hospital and careful surveillance of electrocardiograms and plasma drug levels.

Adult↗