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Biomedical subjects

P R Reid

Publications and source records attributed to P R Reid.

At least 37 records · Page 2Linked to original sources
PubMed1986

Treatment of malignant ventricular arrhythmias with endocardial resection and implantation of the automatic cardioverter-defibrillator.

Although ventricular resection guided by endocardial mapping has been a successful treatment for drug-refractory ventricular arrhythmias, 20 to 30 percent of patients still have postoperative sustained ventricular tachycardia or sudden death. To improve the outcome of the procedure, we implanted an automatic cardioverter-defibrillator in conjunction with endocardial resection in 28 patients, all of whom had had previous myocardial infarctions and between one and five cardiac arrests. There were three perioperative deaths. During follow-up of 8 to 51 months (mean, 25), 4 of the 25 survivors had recurrences of hypotensive ventricular tachycardia, which in all instances were automatically terminated by the implanted device. One patient, whose automatic cardioverter-defibrillator was not functional, died suddenly. We conclude that patients undergoing mapping-directed endocardial resection can be provided with additional protection against recurrent ventricular tachyarrhythmias or sudden death by implantation of an automatic cardioverter-defibrillator.

Adult↗
PubMed1986

The use of ambulatory monitoring in the prognostic evaluation of patients with sustained ventricular tachycardia treated with amiodarone.

We recently reported a retrospective experience with serial Holter monitoring as a guide to therapy in patients with sustained ventricular tachycardia treated with amiodarone. To confirm and substantiate these findings, a prospective study was designed that included baseline 24 hr Holter monitoring and serial Holter monitoring after 1 week of therapy with amiodarone. Fifty-two patients with documented sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring were treated with amiodarone. Thirty-four patients (group I) had nonsustained ventricular tachycardia completely suppressed and 18 patients (group II) had continued nonsustained ventricular tachycardia on serial Holter monitoring performed on days 8, 9, and 10 of therapy. At 11.6 +/- 1.0 (mean +/- SE) months follow-up, three (9%) group I patients and 12 (67%) group II patients had recurrent sustained ventricular tachycardia or sudden cardiac death (p less than .01). The sensitivity, specificity, positive and negative predictive value, and predictive accuracy of ventricular tachycardia on 24, 48, and 72 hr Holter monitoring over days 8, 9, and 10 for predicting recurrent sustained ventricular tachycardia or sudden cardiac death were analyzed. The positive and negative predictive values were 89% and 84%, 69% and 89%, and 67% and 91% for 24, 48, and 72 hr Holter monitoring, respectively. Overall predictive accuracy was 85%, 83%, and 83%, respectively. We conclude that early Holter monitoring is useful in assessing the clinical efficacy of amiodarone in patients with sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring.

Amiodarone↗
PubMed1985

Ambulatory electrocardiographic recordings at the time of fatal cardiac arrest.

The relation between arrhythmias at cardiac arrest and the outcome of arrest is poorly understood. The Holter monitor tracings of 13 patients were reviewed after they sustained an in-hospital cardiac arrest during ambulatory electrocardiographic monitoring. All had a prior cardiac arrest or cardiac syncope. Twelve patients had ventricular tachycardia (VT) as their initial arrest arrhythmia and 1 patient had bradycardia followed by ventricular fibrillation (VF). VT degenerated to VF in 10 of 12 patients after a mean interval of 96 +/- 31 seconds (+/- standard error of the mean). The number of VT runs increased significantly during the hour immediately preceding arrest (p = 0.004). Despite prompt resuscitation efforts in 12 patients, only 6 survived. The 6 survivors and 6 nonsurvivors were not different with regard to age, ejection fraction, extent of coronary artery narrowing and time to first defibrillation. However, degeneration to VF within 30 seconds of arrest (5 of 6 nonsurvivors and 1 of 6 survivors, p = 0.04) and a slower rate of VT at the onset of arrest (166 beats/min in nonsurvivors and 227 beats/min in survivors, p = 0.02) were associated with unsuccessful resuscitation.

Adult↗
PubMed1985

Programmed electrical stimulation and long-term follow-up in asymptomatic, nonsustained ventricular tachycardia.

Thirty-three patients with ventricular tachycardia (VT) (3 or more beats, less than 30 seconds in duration, rate more than 100 per minute) on 24-hour Holter monitoring and no history of clinical arrhythmia (presyncope, syncope or sudden death) were studied using programmed electrical stimulation (PES). PES induced VT in 14 patients (42%), sustained VT in 7 (21%) and nonsustained VT in 7 (21%). Inducible VT was associated with underlying heart disease in 9 of 19 patients with coronary artery disease, 3 of 6 patients with idiopathic dilated cardiomyopathy and 2 of 4 patients with mitral valve prolapse. Patients without structural heart disease did not have inducible VT. Ejection fraction (EF) was not significantly different in patients with or without inducible VT. Twenty-three patients were discharged with drug therapy and 10 patients without therapy. At 23 +/- 16 months (mean +/- standard deviation) follow-up, 28 patients (85%) were alive, 4 (12%) had died from a cardiac cause (EF 49 +/- 17% vs 28 +/- 20%, p less than 0.03). Another patient died from cerebrovascular accident. Twenty-six patients (79%) were free of clinical arrhythmia and 7 patients (21%) had arrhythmic events (EF 49 +/- 18% vs 31 +/- 17%, p less than 0.04). Two of 8 patients with noninducible VT who were discharged without drug treatment had clinical arrhythmic events and neither of 2 patients with inducible VT discharged off drugs had such events.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1985

Nonsustained ventricular tachycardia during programmed ventricular stimulation: criteria for a positive test.

Controversy persists among groups carrying out programmed ventricular stimulation (PVS) as to which criteria should be used to define a positive test. To examine this question, the results of PVS carried out in 50 patients with documented sustained ventricular tachycardia (VT) or ventricular fibrillation were retrospectively analyzed. All patients underwent serial PVS using single and double extrastimuli and ventricular burst pacing in the right ventricle and, when necessary, the left ventricle, with sustained VT elicited during the control study in each patient. Antiarrhythmic drugs were then administered, with therapy tailored to both PVS result and ambulatory Holter monitoring, when possible. All patients were maintained and followed on the same drugs and dosages as at the time of predischarge PVS. After mean 20 months follow-up, 28 patients either died suddenly (8 patients) or had documented sustained VT (20 patients). The ability to induce nonsustained or sustained VT on predischarge PVS was associated with a significantly higher likelihood of subsequent sudden death or VT recurrence than if VT could not be induced (p less than 0.001). In addition, using the criterion of 5 or more beats of induced VT to define a positive study maximized the predictive value of PVS and provided a significantly higher predictive accuracy than if only sustained VT were used to define a positive study.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1985

Flecainide: electrophysiologic and antiarrhythmic properties in refractory ventricular tachycardia.

Twenty-two patients with coronary artery disease and spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) underwent intracardiac electrophysiologic evaluation and, when possible, ambulatory monitoring before and after therapy with flecainide (mean dose 418 +/- 87 mg [mean +/- standard deviation]). An average of 4 antiarrhythmic agents were used and were unsuccessful before therapy with flecainide was begun. During 64 +/- 16 hours of control Holter monitoring in 16 patients, all had 1 or more salvos of VT, as well as ventricular premature complexes (VPCs). Programmed stimulation during the control period induced VT in 17 of 22 patients. After flecainide therapy, Holter monitoring showed elimination of all forms of VT in all but 1 patient, as well as significant reduction of paired VPCs by 95% (p less than 0.03) and single VPCs by 70% (p less than 0.005). Electrophysiologic study during flecainide therapy showed significant increases in AH, HV, PR, QRS and QTc intervals, and the ventricular effective refractory period. Programmed stimulation in 17 patients taking flecainide, with a mean plasma level of 1,075 +/- 521 ng/ml, showed ablation of inducible VT in only 2 patients, a worsening in 5 and continued VT inducibility in 10. Adverse effects that required drug withdrawal were infrequent and encountered in patients who received higher drug levels: 1 patient with congestive heart failure and 1 with severe sinus bradycardia. Thus, although flecainide suppresses complex ventricular arrhythmias on Holter recordings, it rarely alters the response to programmed stimulation. Caution is recommended in its use for recurrent sustained VT or VF and in the interpretation of electrophysiologic studies until the predictive value of programmed stimulation with flecainide therapy is established.

Adult↗
PubMed1985

Results of late programmed electrical stimulation and long-term electrophysiologic effects of amiodarone therapy in patients with refractory ventricular tachycardia.

Thirteen patients with refractory, recurrent, life-threatening ventricular tachycardia (VT) underwent electrophysiologic testing before and after long-term amiodarone therapy. Nine patients (69%) had coronary artery disease, 3 (23%) had nonischemic cardiomyopathy and 1 patient (8%) had mitral valve prolapse. At control electrophysiologic study, programmed electrical stimulation (PES) induced VT in all patients: sustained VT in 11 and nonsustained VT in 2 (9 beats and 31 beats). After oral loading with amiodarone, 1200 mg/day for 14 days, followed by maintenance therapy with 408 +/- 20 mg/day (mean +/- standard error of the mean), repeat PES at 6 +/- 1.6 months revealed inducible VT in 12 of 13 patients: sustained VT in 11 and nonsustained VT (32 beats) in 1 patient. Inducible VT was suppressed in only 1 patient. Amiodarone significantly increased sinus cycle length, PR interval, QRS duration and right ventricular effective refractory period. Insignificant increases in AH, HV and QTc intervals were noted. At 24 +/- 2 months, 8 patients (62%) (all with inducible VT at late PES) were free of clinical arrhythmic events (syncope or sudden death), compared with 5 patients (38%) (4 with inducible VT at late PES) with events. There were no significant differences in the induced VT cycle length, VT cycle length change, ease of inducibility or hemodynamic response to induced VT at late PES in patients with and without arrhythmic events.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗
PubMed1985

Effect of electrical activation site on left ventricular performance in ventricular tachycardia patients with coronary heart disease.

Some patients with ventricular tachycardia (VT) remain virtually asymptomatic, whereas others have syncope despite similar VT rates. The role of ventricular activation site on left ventricular (LV) function was examined in 10 patients undergoing electrophysiologic evaluation for recurrent ventricular arrhythmias. Radionuclide ventriculograms were acquired to calculate LV volumes and aortic or LV pressure was measured during right atrial and right ventricular (RV) pacing. RV apical pacing resulted in end-diastolic volumes similar to those achieved with right atrial pacing (171 +/- 27 vs 175 +/- 19 ml), whereas RV outflow tract pacing showed a trend toward lower volumes (168 +/- 32 vs 177 +/- 33 ml). Comparison between RV apical and RV outflow tract pacing showed that apical activation resulted in higher end-diastolic volumes (216 +/- 26 vs 194 +/- 22 ml, p = 0.020), end-systolic volumes (175 +/- 25 vs 158 +/- 20 ml, p = 0.041), stroke volumes (42 +/- 4 vs 36 +/- 6 ml, p = 0.046), peak rates of LV ejection (309 +/- 57 vs 245 +/- 40 ml/s, p = 0.034) and peak rates normalized for differences in end-diastolic volume (1.5 +/- 0.3 vs 1.3 +/- 0.3; p = 0.047) without a significant increase in peak pressures (131 +/- 12 vs 127 +/- 14 mm Hg, p greater than 0.30) or ejection fractions (24 +/- 5 vs 22 +/- 4%, p = 0.187). These changes were accompanied by an increase in LV/RV stroke count ratios during RV apical vs RV outflow tract pacing (1.6 +/- 0.2 vs 1.2 +/- 0.2, p = 0.030), suggesting the development of mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Management of the prolonged QT syndrome and recurrent ventricular fibrillation with an implantable automatic cardioverter-defibrillator.

Two patients with the prolonged QT syndrome and recurrent ventricular tachyarrhythmias are presented, one of them refractory to combination antiarrhythmic drug therapy and bilateral stellate ganglion blockade. We implanted and tested in vivo an automatic cardioverter-defibrillator to provide a cardiac monitoring system with the capability of delivering a 25 J electrical discharge to the heart if rapid ventricular tachycardia or ventricular fibrillation is detected. Arrhythmia induction in the electrophysiology laboratory confirmed the appropriate recognition of the arrhythmias in each patient, with prompt discharge of the device and resultant termination of the tachycardias. We suggest that implantation of such a device may provide an effective adjunct to antiarrhythmic drug therapy in the management of infrequent, but potentially lethal, ventricular arrhythmias occurring in patients with the prolonged QT syndrome.

Adult↗
PubMed1985

Comparison of acebutolol and propranolol therapy for ventricular arrhythmias.

The effects of acebutolol, a new investigational cardioselective beta blocker, and propranolol on ventricular arrhythmias were compared in 14 patients with more than 30 premature ventricular contractions (PVCs) per hour. Each patient served as their own control, receiving both drugs and placebo in random sequence and in double-blind fashion, with an intervening one-week, drug-free period. Each drug was given for a two-month period, the maximum acebutolol dosage reaching 600 mg tid and the maximum propranolol dosage 80 mg tid. Seventy-two-hour ambulatory electrocardiographic monitoring assessed arrhythmia frequency for each study period. Mean PVC counts did not significantly differ during the two control periods. Acebutolol decreased mean PVC count by 65% (P less than .02), with eight patients exhibiting a 70% or greater decrease. Only three patients exhibited a similar decline with propranolol. The incidence of PVCs was not significantly decreased by propranolol. Acebutolol reduced the number of couplets by 70% (P less than .04), whereas propranolol did not significantly affect couplets. At the dosage of 600 mg tid, acebutolol was well tolerated, effectively suppressed total PVCs and couplets, and appeared to be more effective than propranolol administered at 80 mg tid.

Acebutolol↗
PubMed1985

Meobentine sulfate: antiarrhythmic and electrophysiologic effects assessed by programmed electrical stimulation and ambulatory monitoring in patients with complex ventricular tachyarrhythmia. Report of a multicenter evaluation.

Five cardiology centers conducted open-label prospective trials of meobentine sulfate, an intravenously and orally available analog of bethanidine, to assess its potential for treatment of recurrent, drug refractory ventricular tachycardia (VT) or fibrillation (VF), and complex ventricular arrhythmias. The study population comprised 26 patients (mean age, 61 years); 18 were men. Coronary artery disease was present in 15, cardiomyopathy in six, and valvular heart disease in three. Patients presented with both VT and VF (seven), sustained VT alone (12), or frequent ventricular ectopy (PVCs) and nonsustained VT (seven). Of the 26 patients, 5 were enrolled in antiarrhythmic studies (chronic PVC suppression) and 21 were enrolled in programmed electrical stimulation (PES) studies. Two of five in the chronic PVC study showed greater than 75% arrhythmia suppression. Among 21 patients in PES studies, there were eight intravenous (16 mg/kg) and 19 oral trials (400 to 1000 mg every 6 hours, 3 days/dose interval). Five of 22 patients showed efficacy at repeat PES study (neither VT nor VF), one showed partial efficacy, and four were not restudied because of clinical arrhythmia (three) and/or adverse effects (two). Overall, three patients (12%) were continued on the drug for an extended period of time. Adverse experience included hypotension in 50% and gastrointestinal effects (nausea, vomiting, or diarrhea) in 56% (oral trials only). Adverse reactions led to drug discontinuation in six and dosage reduction in eight patients. Thus, meobentine may prevent induction of VT or VF or reduce frequency of complex PVCs in selected patients refractory to other antiarrhythmic agents, but the response rate is relatively low. Symptomatic hypotension or gastrointestinal adverse effects are common and may limit utility of meobentine as a chronic oral antiarrhythmic agent.

Administration, Oral↗
PubMed1985

The utility of aprindine blood levels in the management of ventricular arrhythmias.

Sixty-four patients with a history of ventricular tachycardia and ventricular fibrillation refractory to conventional therapy received aprindine to abolish recurrent episodes of symptomatic ventricular tachycardia. Fifty-six patients became asymptomatic and were followed up for a mean period of 23 months. Aprindine dose was adjusted to minimize adverse reactions but still control arrhythmia. Survival analysis was performed for the group with aprindine levels greater than 1.5 micrograms/ml and the group with levels of 1.5 micrograms/ml or less. At the end of the study, 65% of the patients with a high level were alive and asymptomatic as compared with only 35% of the patients with a low level (p less than 0.036). In patients at risk of recurrent sudden cardiac death, high aprindine levels maintained after abolition of symptomatic ventricular tachycardia were associated with improved survival.

Aprindine↗
PubMed1985

Amiodarone pulmonary toxicity: early changes in pulmonary function tests during amiodarone rechallenge.

Amiodarone is an investigational antiarrhythmic agent known to cause pulmonary toxicity. This report describes two patients with previous amiodarone pulmonary toxicity and complete resolution who at rechallenge 5 to 6 months later developed within 2 weeks of therapy a significant reduction in lung diffusion capacity before overt clinical toxicity occurred. This suggests that toxicity may present early with reduction in diffusion capacity and that such changes may warrant the need to alter treatment.

Aged↗
PubMed1985

Amiodarone in the treatment of life-threatening ventricular tachycardia: role of Holter monitoring in predicting long-term clinical efficacy.

Forty-two patients with refractory, recurrent life-threatening ventricular tachycardia and spontaneous ventricular tachycardia (greater than or equal to 3 beats, heart rate greater than 100 beats/min) on baseline 24 hour Holter recording were treated with amiodarone. After 1 week of amiodarone therapy and during the follow-up period (22 +/- 11 months, mean +/- SD), patients had serial 24 hour Holter recordings (10.6 +/- 3.8 per patient). Twenty-four hour, 48 hour or 72 hour Holter monitoring was performed during the second week of therapy. Ventricular tachycardia was suppressed on all follow-up serial Holter recordings in 17 patients (40%). Ventricular tachycardia was suppressed in 34 (81%) of 42 patients with 24 hour Holter recordings, 21 (72%) of 29 patients with 48 hour recordings and 20 (69%) of 29 patients with 72 hour recordings during the second week of therapy. At follow-up 24 patients (57%) were free of clinical arrhythmic events (Sustained ventricular tachycardia or sudden death). The sensitivity, specificity, positive and negative predictive values and predictive accuracy of ventricular tachycardia on 24, 48 and 72 hour Holter recordings during the second week of therapy for predicting subsequent events were analyzed. The positive and negative predictive values were 100 and 71% for 24 hour Holter recordings, 88 and 71% for 48 hour recordings and 89 and 75% for 72 hour recordings. Overall predictive accuracy was 76, 76 and 79%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Recent clinical experience with the automatic implantable cardioverter-defibrillator.

The automatic implantable cardioverter-defibrillator is an electronic device designed to monitor the heart continuously, identify ventricular tachycardias and ventricular fibrillation, and terminate the life-threatening arrhythmias with an internal countershock. This device has been proved to be safe and effective, and its use has led to a significant decrease of arrhythmic mortality in the implantees.

Arrhythmias, Cardiac↗
PubMed1985

Clinical experience with the automatic implantable defibrillator.

Since February 1980, worldwide, over 400 survivors of sudden arrhythmic death have been treated with the automatic implantable defibrillator. Recently, the device has been further improved; it is now a cardioverter-defibrillator (AICD), able to treat ventricular tachycardias as well as ventricular fibrillation. There are two defibrillating electrodes which are used also for waveform analysis; one is located in the superior vena cava, the other is placed over the cardia apex. A third bipolar right ventricular electrode serves for rate counting and R-wave synchronization. When ventricular fibrillation occurs, a 25-joule pulse is delivered; when ventricular tachycardia faster than a preset rate is detected, the discharge is R-wave synchronized. Special batteries can deliver over 100 shocks or provide a three-year monitoring life. Implantation of the device can be achieved through a thoracotomy or by a subxiphoid or a subcostal approach. Thus far, the longest follow-up period has been 58 months. Actuarial analysis shows the one-year mortality attributed to arrhythmias reduced to less than 2%. Thus, the automatic cardioverter-defibrillator can reliably identify and correct potentially lethal ventricular tachyarrhythmias, leading to a substantial increase in survival in properly selected high-risk patients.

Death, Sudden↗
PubMed1985

Assessment of the site of ventricular activation by Fourier analysis of gated blood-pool studies.

We studied the use of first-harmonic Fourier analysis of gated blood-pool images to assess the site of ventricular activation in a group of 12 patients undergoing electrophysiologic pacing studies. We acquired gated blood-pool studies during pacing at up to four sites at each of two different rates. A total of 50 studies were made. At a pacing rate of 100 beats/min, when the pacing electrode was at the right-ventricular apex, 9/13 times the Fourier activation site agreed; at the right-ventricular outflow tract, 7/8; at the anterolateral left-ventricular wall, 4/4. When the Fourier activation site was at the right-ventricular apex, 9/9 times the pacing electrode was there; at the right-ventricular outflow tract, 7/10; in the left ventricle, 4/4. Fourier analysis of gated blood-pool studies can help identify the site of ventricular activation but is not sufficiently accurate to fully replace endocardial mapping.

Cardiac Pacing, Artificial↗