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Biomedical subjects

W G Stevenson

Publications and source records attributed to W G Stevenson.

At least 73 records · Page 4Linked to original sources
PubMed1996

Should survivors of myocardial infarction with low ejection fraction be routinely referred to arrhythmia specialists?

Because survivors of myocardial infarction are at risk for ventricular arrhythmias and sudden death, physicians must decide whether to refer these patients to specialists for arrhythmia assessment and therapy. However, this decision is complex as few randomized data are available concerning either diagnostic or therapeutic options. Therefore, we modeled the potential impact of current arrhythmia detection and management strategies on mortality in survivors of myocardial infarction with reduced left ventricular function who are managed in a contemporary manner. Based on recent data we estimated that the mortality for myocardial infarction survivors with left ventricular ejection fraction less than 0.40 is 20 percent over 3.5 years and that half of the deaths are sudden. The sensitivity and specificity of a Holter electrocardiogram (ECG), a signal-averaged ECG, and an invasive electrophysiology study for predicting sudden death were obtained from a literature review of trials published after 1990 that included more than 300 patients. A series of models were constructed to predict mortality achieved by different arrhythmia management strategies that reduced sudden death by 50 percent and 75 percent--reductions estimated to be within the range for amiodarone and implantable defibrillators. We found that, when routinely applied to all infarct survivors with depressed ventricular function, a therapy that reduces sudden death by 50 percent with 1 percent fatal adverse effects (potentially amiodarone) saves approximately 1 life for every 25 patients treated. Therapy that reduces sudden death by 75 percent with 2 percent fatal adverse effects (potentially implantable defibrillators) saves 1 life for every 14 patients treated. Using Holter ECG recordings, a signal-averaged ECG, or an invasive electrophysiology study to select higher-risk groups, 1 life can be saved for every 4 to 11 patients treated, and the negative impact of adverse effects can be reduced. However, to achieve this benefit, additional and potentially invasive arrhythmia testing must be applied to 28 to 47 patients for each life saved. Thus, with contemporary management of acute myocardial infarction, the risk of sudden death for survivors is sufficiently low that broad application of available antiarrhythmic therapies has limited potential for further improving survival, particularly if therapy also has significant adverse effects. Thus, routine referral to arrhythmia specialists is not warranted for the majority of infarct survivors and should be largely reserved for patients with serious, symptomatic arrhythmias.

Amiodarone↗
PubMed1996

Effects of isoflurane on electrophysiological measurements in children with the Wolff-Parkinson-White syndrome.

This study was designed to assess the effects of isoflurane (ISO) on the electrophysiological properties of the accessory pathway, atrium, ventricle, and AV node in children with the Wolff-Parkinson-White (WPW) syndrome. The results of programmed electrical stimulation were analyzed in 51 patients (4 months to 17 years of age) with WPW. The study population was divided into two groups. Twenty-seven patients received local anesthesia and intramuscular injection of meperidine, promethazine, and chlorpromazine (MPC group). Twenty-four patients received general anesthesia with ISO inhalation (ISO group). We compared the antegrade effective refractory period of the accessory pathway (antegrade APERP), ventricular effective refractory period (VERP), atrial effective refractory period (AERP), AH interval, and cycle length of circus movement tachycardia (CMT-CL) in 12 pairs of age and sex matched patients selected from the MPC and ISO groups. Of the 12 pairs of age and sex matched patients, antegrade APERP in patients who received ISO (299 +/- 17 ms, mean +/- SEM) was significantly longer as compared with matched patients in the MPC group (262 +/- 5 ms, P < 0.025). The VERP and AERP in patients from the ISO group were significantly prolonged compared with the MPC patients (239 +/- 7 vs 210 +/- 8 ms, P < 0.025, and 228 +/- 11 vs 180 +/- 6 ms, P < 0.01, respectively). There was no significant difference in the AH interval or CMT-CL between the two subgroups. Thus, ISO prolongs the antegrade APERPs as well as the effective refractory periods of atrial and ventricular muscle in children with WPW, while the AH interval and CMT-CL appear to be unaffected. Care must be taken in interpreting measurements of the antegrade APERP made in patients under general anesthesia for RF ablation of accessory pathways.

Adjuvants, Anesthesia↗
PubMed1996

Autonomic dysfunction after catheter ablation.

Autonomic dysfunction may occur as a consequence of radiofrequency (RF) catheter ablation of a variety of supraventricular tachycardias. Effects suggestive of autonomic dysfunction that may be seen acutely during the ablation procedure include sudden profound slowing of the sinus rate or transient AV block. These abnormalities may occur during application of RF current, typically along the tricuspid or mitral annulus, at sites distant from both the sinus and AV nodes; they resolve quickly when RF current delivery is terminated. The most common long-term indication of autonomic dysfunction after ablation is inappropriate sinus tachycardia. This complication, rarely a lasting significant clinical problem, is seen after AV node modification and after ablation of accessory pathways. It usually resolves within several months. The mechanism appears to be loss of parasympathetic influence on the sinus node. Autonomic dysfunction after ablation of ventricular tachycardia has not yet been described, but could occur as newer catheter technologies capable of producing larger lesions are perfected.

Autonomic Nervous System↗
PubMed1996

Comparison of four methods of assessing heart rate variability in patients with heart failure.

BACKGROUND: Heart rate variability reflects autonomic tone and is used to assess progression and prognosis in a variety of illnesses. However, multiple heart rate variability methods exist and are not necessarily equivalent. OBJECTIVES: To compare four methods of heart rate variability in heart failure patients and healthy subjects. METHODS: Twenty-four-hour Holter recordings were obtained in 50 heart failure patients and 50 age- and gender-matched control patients. From these recordings, heart rate variability was assessed by histograms, standard deviation, Poincaré plots, and spectral analysis. RESULTS: For R-R interval histograms, standard deviation, and Poincaré plots, diminished heart rate variability was identified in 65% to 100% of heart failure patients versus 0% to 8% of controls. Agreement among these tests ranged from 69% to 96%. Spectral values varied greatly over the recording period, even in the same subject, possibly because of variations in activity. Only 16% of heart failure patients had spectral values that were identified as abnormal. Agreement between spectral analysis and the other methods ranged between 58% and 67%. CONCLUSIONS: Heart rate variability assessed over a 24-hour period with different techniques yields similar but not identical results. Heart rate variability assessed from spectral analysis of short periods of data varied markedly in a 24-hour period and should not be compared with measures obtained from 24-hour methods. Standardization of subject activity and recording time is necessary for comparison of spectral analysis of brief periods. Further research is required to determine if differences among methods assessing 24-hour heart rate variability yield complementary information.

Arrhythmias, Cardiac↗
PubMed1995

Improving survival for patients with advanced heart failure: a study of 737 consecutive patients.

OBJECTIVES: This study sought to determine whether survival and risk of sudden death have improved for patients with advanced heart failure referred for consideration for heart transplantation as advances in medical therapy were systematically implemented over an 8-year period. BACKGROUND: Recent survival trials in patients with mild to moderate heart failure and patients after a myocardial infarction have shown that angiotensin-converting enzyme inhibitors are beneficial, type I antiarrhythmic drugs can be detrimental, and amiodarone may be beneficial in some groups. The impact of advances in therapy may be enhanced or blunted when applied to severe heart failure. METHODS: One-year mortality and sudden death were determined in relation to time, baseline variables and therapeutics for 737 consecutive patients referred for heart transplantation and discharged home on medical therapy from 1986 to 1988, 1989 to 1990 and 1991 to 1993. Medical care was directed by a single team of physicians with policies established by consensus. From 1986 to 1990, the hydralazine/isosorbide dinitrate combination or angiotensin-converting enzyme inhibitors were the initial vasodilators, and class I antiarrhythmic drugs were allowed. After 1990, captopril was the initial vasodilator, given to 86% of patients compared with 46% of patients before 1989. After mid-1989, class I agents were routinely withdrawn, and amiodarone was used for frequent ventricular ectopic beats or atrial fibrillation (53% of patients after 1990 vs. 10% before 1989). RESULTS: The total 1-year mortality rate decreased from 33% before 1989 to 16% after 1990 (p = 0.0001), and sudden death decreased from 20% to 8% (p = 0.0006). Adjusted for clinical and hemodynamic variables in multivariate proportional hazards models, total mortality and sudden death were lower after 1990. CONCLUSIONS: The large reduction in mortality, particularly in sudden death, from advanced heart failure since 1990 may reflect an enhanced impact of therapeutic advances shown in large randomized trials when they are incorporated into a comprehensive approach in this population. This improved survival supports the growing practice of maintaining potential heart transplant candidates on optimal medical therapy until clinical decompensation mandates transplantation.

Adult↗
PubMed1995

Age- and anesthesia-related changes in accessory pathway conduction in children with Wolff-Parkinson-White syndrome.

The anterograde effective refractory period of the accessory pathway is age-dependent in pediatric patients with the WPW syndrome. Thus, age should be considered when developing electrophysiologic criteria for the risk of hypotensive arrhythmias in these patients. In addition, general anesthesia must also be considered in interpreting age-related changes in the anterograde APERP, especially in children.

Adolescent↗
PubMed1995

Amiodarone and torsades de pointes in patients with advanced heart failure.

Amiodarone is considered to be safe in patients with prior QT prolongation and torsades de pointes taking class I antiarrhythmic agents who require continued antiarrhythmic drug therapy. However, the safety of amiodarone in advanced heart failure patients with a history of drug-induced torsades de pointes, who may be more susceptible to proarrhythmia, is unknown. Therefore, the objective of this study was to assess amiodarone safety and efficacy in heart failure patients with prior antiarrhythmic drug-induced torsades de pointes. We determined the history of torsades de pointes in 205 patients with heart failure treated with amiodarone, and compared the risk of sudden death in patients with and without such a history. To evaluate the possibility that all patients with a history of torsades de pointes would be at high risk for sudden death regardless of amiodarone treatment, we compared this risk in patients with a history of torsades de pointes who were and were not subsequently treated with amiodarone. Of 205 patients with advanced heart failure, 8 (4%) treated with amiodarone had prior drug-induced torsades de pointes. Despite similar severity of heart failure, the 1-year actuarial sudden death risk was markedly increased in amiodarone patients with than without prior torsades de pointes (55% vs 15%, p = 0.0001). Similarly, the incidence of 1-year sudden death was markedly increased in patients with prior torsades de pointes taking amiodarone compared with such patients who were not subsequently treated with amiodarone (55% vs 0%, p = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Long-term efficacy of amiodarone for the maintenance of normal sinus rhythm in patients with refractory atrial fibrillation or flutter.

The purpose of this study was to examine the efficacy and safety of amiodarone to maintain sinus rhythm in patients with refractory atrial fibrillation or flutter. One hundred ten patients with atrial fibrillation or flutter, refractory to > or = 1 class I antiarrhythmic agents (mean +/- SD 2.5 +/- 1.5, median 2), were given low-dose amiodarone (mean maintenance dose 268 +/- 100 mg/day) to determine its efficacy to maintain normal sinus rhythm after chemical or electrical cardioversion. Fifty-three patients had chronic and 57 patients had paroxysmal atrial fibrillation or flutter. Mean age of the study population was 60 +/- 13 years, and the mean follow-up was 36 +/- 38 months (range 31 days to 137 months). Actuarial rates for maintenance of sinus rhythm were 0.87, 0.70, and 0.55 at 1, 3, and 5 years, respectively. Twenty-one patients (19%) with arrhythmia recurrence had an increase in amiodarone dose, and after a mean additional follow-up of 2.5 years, 86% remained in normal sinus rhythm. The only observed predictor of atrial fibrillation or flutter recurrence was paroxysmal arrhythmia (40% recurrence vs 9% in patients with chronic atrial fibrillation or flutter; p < 0.001). Actuarial rates for withdrawal because of adverse effects were 0.08, 0.22, and 0.30 at 1, 3, and 5 years, respectively. The most frequent adverse effects necessitating withdrawal were skin discoloration (4.5%), pulmonary fibrosis (3.6%; none fatal), and thyroid toxicity (2.7%). No deaths occurred during the study period. In conclusion, amiodarone sinus rhythm in patients with atrial fibrillation or flutter, with a relatively low incidence of adverse effects necessitating withdrawal.

Aged↗
PubMed1995

Antiarrhythmic prophylaxis vs warfarin anticoagulation to prevent thromboembolic events among patients with atrial fibrillation. A decision analysis.

BACKGROUND: Patients with atrial fibrillation compared with those with sinus rhythm are at increased risk for thromboembolism, often mandating therapy directed at thromboembolism prevention. However, the safest, most efficacious strategy to prevent thromboembolism associated with atrial fibrillation is unknown. We developed a decision analysis to compare the risks and benefits of two common clinical strategies to prevent thromboembolism in the patient with atrial fibrillation: (1) sinus rhythm maintenance with quinidine sulfate or with amiodarone hydrochloride after cardioversion and (2) long-term anticoagulation with warfarin sodium. METHODS: A search was conducted of the English-language MEDLINE databases of the National Library of Medicine dated 1966 through December 1992. The search was conducted by intersecting "quinidine," "warfarin," or "amiodarone" with "atrial fibrillation." Six of 249 articles concerning quinidine and five of 20 articles concerning warfarin were judged by multiple reviewers to meet predetermined inclusion and exclusion criteria. To our knowledge, no randomized, placebo-controlled trials of amiodarone therapy for atrial fibrillation have been published. Five of 112 identified articles concerning amiodarone involved nonrandomized trials that met the remaining selection criteria and were included in this analysis. RESULTS: Thromboembolic events and fatal nonthromboembolic adverse events during the course of therapy (defined as fatal proarrhythmia, fatal hemorrhage, and fatal noncardiac toxic effects) were considered to have equivalent weight. The total risk during therapy, defined as thromboembolic and fatal nonthromboembolic adverse events during the course of therapy, was evaluated over a range of baseline thromboembolism risks, from 1% to 20% per patient-year. Quinidine therapy compared with no therapy was associated with increased total risk, unless baseline thromboembolism risk exceeded 11% per patient-year. Total risk during warfarin therapy was less than total risk during quinidine therapy for the entire range of baseline thromboembolism risks, from 1% to 20% per patient-year. Total risk during warfarin or amiodarone therapy was similar and less than that with no therapy for the entire range of baseline risks. CONCLUSIONS: Based on data from randomized, controlled trials of quinidine and warfarin, warfarin therapy appears to be the safest strategy for thromboembolism prevention in the patient with atrial fibrillation. The role of low-dose amiodarone therapy appears promising and warrants further study in randomized, controlled trials.

Adolescent↗
PubMed1995

Risk of arterial embolization in 224 patients awaiting cardiac transplantation.

Of patients awaiting cardiac transplantation, 10% to 20% die before a donor heart becomes available. Embolization of left ventricular thrombus is a source of morbidity and mortality in this population. To define the incidence and possible risk factors for systemic arterial embolization, we examined the frequency of arterial embolic events and their relation to clinical, hemodynamic, and echocardiographic variables in 224 consecutive outpatients awaiting cardiac transplantation (left ventricular ejection fraction 0.20 +/- 0.07 and left ventricular end-diastolic dimension 76 +/- 11 mm). Over a follow-up period of 301 +/- 371 days, during which 82 (37%) patients received warfarin, arterial embolization occurred in 6 (3%) patients, 1 of whom was receiving and 5 of whom were not receiving warfarin (difference not specifically significant). The risk of embolization was not statistically different in patients with atrial fibrillation, previous embolization, or left ventricular thrombus on transthoracic echocardiogram, regardless of warfarin therapy. Cumulative risk of sudden death was similar for patients with or without echocardiographically documented left ventricular thrombus. Nonfatal bleeding complications associated with warfarin therapy occurred in 2 (2%) patients. Thus in patients who are awaiting cardiac transplantation and who receive anticoagulation therapy for left ventricular thrombus, atrial fibrillation, or previous arterial embolization, the incidence of clinically detectable arterial embolization is low despite severe ventricular dilatation. Embolization is not likely a major cause of sudden death or morbidity in this population.

Cardiomyopathy, Dilated↗
PubMed1995

Implantable defibrillators for high-risk patients with heart failure who are awaiting cardiac transplantation.

The objective of this study was to assess the operative risk and efficacy of implantable defibrillators for preventing sudden death in patients with heart failure awaiting transplantation. The average waiting time for elective cardiac transplantation is 6 months to 1 year. Sudden cardiac death is the major source of mortality in outpatients in stable condition awaiting cardiac transplantation. The efficacy of implantable defibrillator therapy in this population is not established. We analyzed the operative risk, time to appropriate shock, and sudden death in 15 patients determined to be at high risk of sudden death who were accepted onto the outpatient cardiac transplant waiting list. Nonfatal postoperative complications occurred in two (13%) subjects with epicardial defibrillating lead systems and in none with transvenous lead systems. Defibrillation energies were 16 +/- 2 J versus 24 +/- 2 J with epicardial and transvenous lead systems, respectively. Sudden death free survival until transplantation was 93%. Most of the patients (60%) had an appropriate shock during a mean follow-up of 11 +/- 12 months. The mean time to an appropriate shock was 3 +/- 3 months. Hospital readmission was required in three (20%) subjects to await transplantation on an urgent basis. However, two of these subjects had received appropriate shocks before readmission. In selected patients at high risk for sudden death while on the outpatient cardiac transplant waiting list, the operative risk is low and adequate defibrillation energies can be obtained to allow implantable defibrillator placement. Most subjects will have an appropriate shock as outpatients before transplantation, and sudden death free survival is excellent.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1995

Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars.

OBJECTIVES: This study sought to determine the relation of the paced QRS configuration and conduction delay during pace mapping to reentry circuit sites in patients with ventricular tachycardia late after myocardial infarction. BACKGROUND: The QRS configuration produced by ventricular pacing during sinus rhythm (pace mapping) can locate focal idiopathic ventricular tachycardias during catheter mapping, but postinfarction reentry circuits may be relatively large and contain regions of slow conduction. We hypothesized that for postinfarction ventricular tachycardia, 1) pacing during sinus rhythm at reentry circuit sites distant from the exit from the scar would produce a QRS configuration different from the tachycardia; and 2) a stimulus to QRS delay during pace mapping may be a useful guide to reentry circuit slow conduction zones. METHODS: Catheter mapping and ablation were performed in 18 consecutive patients with ventricular tachycardia after myocardial infarction. At 85 endocardial sites in 13 patients, 12-lead electrocardiograms (ECGs) were recorded during pace mapping, and participation of each site in a reentry circuit was then evaluated by entrainment techniques during induced ventricular tachycardia or by application of radiofrequency current. RESULTS: Pace maps resembled tachycardia at < 30% of likely reentry circuit sites identified by entrainment criteria and at only 1 (9%) of 11 sites where radiofrequency current terminated tachycardia. Analysis of the stimulus to QRS interval during entrainment with concealed fusion showed that the conduction time from the pacing site to the exit from the scar was longer at sites where the pace map did not resemble tachycardia. Evidence of slow conduction during pace mapping, with a stimulus to QRS interval > 40 ms was observed at > or = 70% of reentry circuit sites. CONCLUSIONS: At many sites in postinfarction ventricular reentry circuits, the QRS configuration during pace mapping does not resemble the ventricular tachycardia QRS complex, consistent with relatively large reentry circuits or regions of functional conduction block during ventricular tachycardia. A stimulus to QRS delay during pace mapping is consistent with slow conduction and may aid in targeting endocardial sites for further evaluation during tachycardia.

Aged↗
PubMed1995

Mechanisms and management of arrhythmias in heart failure.

Ventricular arrhythmias are a common problem in patients with heart failure and are an important cause of sudden death. Sustained ventricular arrhythmias are due either to reentry in an old infarct scar, bundle branch reentry, or the electrophysiologic abnormalities that accompany heart failure and hypertrophy. In animal models, ventricular hypertrophy that accompanies heart failure increases susceptibility to polymorphic ventricular tachycardias. Patients resuscitated from a sustained ventricular arrhythmia have a high risk of recurrence. Antiarrhythmic drug toxicity and inefficacy are increased in heart failure. Amiodarone or an implantable defibrillator are the first-line options, and have not been directly compared. Amiodarone appears to be the safest antiarrhythmic drug for treatment of nonsustained arrhythmias and atrial fibrillation. In one randomized trial, amiodarone improved survival in patients with advanced heart failure.

Animals↗
PubMed1995

Ventricular tachycardia after myocardial infarction: from arrhythmia surgery to catheter ablation.

Ventricular tachycardia due to prior myocardial infarction is caused by reentry. Intraoperative mapping at the time of arrhythmia surgery has shown that the reentry circuits are diverse in size and location. Many circuits are large, extending over several square centimeters. Endocardial excision guided by activation sequence mapping, fractionated sinus rhythm electrograms, or visual identification of scarred subendocardium renders 69% to 95% of patients free from inducible ventricular tachycardia, but with an operative mortality that exceeds 8% at most centers. Catheter ablation is difficult due to limitations of catheter mapping, relatively small size of lesions produced with current techniques, and limited access to intramural and epicardial portions of the reentry circuits. Many problems need to be overcome for catheter ablation to achieve success comparable to that of surgery. At present, only hemodynamically tolerated ventricular tachycardias can be mapped. Progress is being made, and it is likely that catheter ablation will become a viable therapy for subgroups of patients with postmyocardial infarction ventricular tachycardia.

Cardiac Surgical Procedures↗
PubMed1995

Histologic evolution of radiofrequency lesions in an old human myocardial infarct causing ventricular tachycardia.

INTRODUCTION: Radiofrequency (RF) ablation of ventricular tachycardia (VT) late after myocardial infarction may be difficult due to characteristics of the infarct containing the reentry circuit. RF lesions in these infarcts in humans have not been characterized. METHODS AND RESULTS: Catheter mapping and ablation of VT originating from an anterior wall infarct was performed 8 days and again 12 hours prior to death. Pacing identified a region of abnormal conduction where RF ablation terminated VT. This region contained strips of myocytes sandwiched between endocardial fibrosis and dense scar. RF lesions ranged from 2 x 2 mm to 5 x 10 mm and were up to 3 mm in depth. Acute lesions showed superficial thrombus and early coagulation necrosis without inflammation. Older lesions showed coagulation necrosis, sparse neutrophil infiltrate, minimal granulation tissue, hemorrhage, and mixed inflammatory infiltrate along the lumen without re-endothelialization. CONCLUSION: In this patient, RF lesions had sufficient depth but not width to interrupt the thin, but potentially broad, sheets of myocytes in the reentry circuit. In thinned areas, RF lesions can extend to the epicardium. Selecting sites with abnormal electrograms confines RF lesions to the infarct region. Inflammation and hemorrhage could conceivably cause delayed effects of RF.

Aged↗