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Biomedical subjects

W G Stevenson

Publications and source records attributed to W G Stevenson.

At least 91 records · Page 5Linked to original sources
PubMed1995

Entrainment techniques for mapping atrial and ventricular tachycardias.

Many atrial tachycardias, atrial flutter, and postmyocardial infarction ventricular tachycardias are due to reentry through large "macroreentrant" circuits. These circuits can be difficult to define by catheter mapping of the activation sequence. Entrainment techniques allow the relation of a mapping site to the reentrant circuit to be assessed on a site-by-site basis during catheter mapping. Regions of abnormal conduction that are in the reentrant circuit can be distinguished from bystander sites outside the circuit. A mapping site classification to guide catheter ablation is reviewed.

Atrial Flutter↗
PubMed1994

Complex heart rate variability and serum norepinephrine levels in patients with advanced heart failure.

OBJECTIVES: This study was designed to examine the relation of the Poincaré plot heart rate variability pattern to sympathetic nervous system activity as assessed by serum norepinephrine. BACKGROUND: Poincaré plots demonstrate a complexity of beat to beat behavior not readily detected by other heart rate variability measures. Previous studies have described two abnormal Poincaré patterns in patients with heart failure: a torpedo pattern with reduced beat to beat variability and a complex pattern with clustering of points. METHODS: To assess the relation of these plots to sympathetic activity, plasma norepinephrine at rest and a standard deviation measure of heart rate variability were analyzed in 21 patients with heart failure (mean left ventricular ejection fraction [+/- SD] 0.22 +/- 0.05). RESULTS: Eleven subjects had a torpedo-shaped and 10 subjects had a complex Poincaré plot pattern. These two groups did not differ significantly in age, functional class, disease etiology, left ventricular ejection fraction, heart rate, ventricular ectopic activity or in a standard deviation measure of heart rate variability. However, patients with a complex Poincaré plot pattern had higher norepinephrine levels (722 +/- 373 pg/ml) than patients with torpedo-shaped plots (309 +/- 134 pg/ml) (p = 0.003). Patients with a complex pattern also had more severe hemodynamic decompensation, as evidenced by their higher levels of pulmonary capillary wedge and mean pulmonary artery pressures and lower values for cardiac index than those of patients with a torpedo-shaped plot. CONCLUSIONS: Complex Poincaré plots are associated with marked sympathetic activation and may provide additional prognostic information and insight into autonomic alterations and sudden cardiac death in patients with heart failure.

Electrocardiography, Ambulatory↗
PubMed1994

Activation times in and adjacent to reentry circuits during entrainment: implications for mapping ventricular tachycardia.

Myocardial infarct scars giving rise to reentrant ventricular tachycardia can contain "bystander" areas of abnormal electrical activity that are difficult to distinguish from reentry circuit sites. Pacing to entrain ventricular tachycardia with analysis of electrograms at the pacing site is useful to identify reentry circuit sites but assumes that electrograms reflect activation times at the recording site. The purpose of this study was to determine whether a similar analysis could be applied to electrograms recorded from sites distant from the pacing site. In computer simulations, activation times at sites in and adjacent to figure-eight reentry circuits were analyzed during entrainment of tachycardia by pacing at various sites. During entrainment, activation at reentry circuit sites activated by the stimulated orthodromic wavefronts maintains the same relation to the QRS complex as that during tachycardia. The return cycle from the last entrained electrogram to the following electrogram equals the tachycardia cycle length. The same findings occur, however, at bystander sites activated by stimulated wavefronts that have propagated orthodromically through the circuit. When a reentry circuit site is activated by stimulated antidromic wavefronts, the electrogram to QRS interval is shorter than that during tachycardia, the return cycle may be less than the tachycardia cycle length, and the site may appear to be dissociated from the tachycardia, despite its location in the circuit. If the entrained electrogram to QRS interval exceeds the tachycardia electrogram to QRS interval and the return cycle length exceeds the tachycardia cycle length, it is likely that both pacing and recording sites are outside the reentry circuit. Thus, during entrainment, failure to dissociate an electrogram from the QRS complex and the return cycle length does not reliably indicate the relation of the recording site to the reentry circuit when the recording and pacing sites are separate.

Cardiac Pacing, Artificial↗
PubMed1994

Timing of sudden death in patients with heart failure.

OBJECTIVES: The purpose of this study was to determine the timing of sudden death in patients with advanced heart failure. BACKGROUND: The frequency of sudden cardiac death and myocardial infarction is greatest in the morning hours, suggesting that physiologic processes associated with morning activities may trigger these events. In patients with advanced heart failure, a variety of mechanisms may cause sudden death, and the frequency of their occurrence may differ from that in other patient groups, perhaps altering the timing of sudden death in heart failure. METHODS: Deaths among 566 consecutive patients followed up after treatment for advanced heart failure were prospectively categorized as sudden death, death due to heart failure or noncardiac death. For 72 sudden deaths the time of death was determined from witnesses to the event and from death certificates. RESULTS: Sudden death occurred 2.5 times more frequently between 6:01 AM and 12 noon than in the three other 6-h intervals, with 46% of deaths occurring during this period (p < 0.005). The morning peak occurred both in patients with coronary artery disease and in those with nonischemic causes of heart failure. CONCLUSIONS: Despite a variety of potential mechanisms of sudden death and underlying causes of heart disease in patients with heart failure, the 24-h distribution of sudden death in these patients is similar to that observed in other patient groups. Morning surges in sympathetic nervous system activity may promote a variety of sudden death mechanisms, including ischemic and nonischemic arrhythmias.

Adult↗
PubMed1993

Low-dose amiodarone for atrial fibrillation.

Concerns about proarrhythmia risk and inefficacy associated with class I antiarrhythmic drugs have revived interest in low-dose amiodarone (maintenance dose 200-400 mg/day) for suppression of atrial fibrillation. In nonrandomized trials of amiodarone for atrial fibrillation refractory to conventional agents, amiodarone has been successful in maintaining sinus rhythm in 53-79% of patients during a mean follow-up of 15-27 months. Intolerable side effects, including pulmonary toxicity, are in the range of 1-12% per year and resolve following amiodarone withdrawal in the majority of cases. Proarrhythmia risk associated with amiodarone, even in the setting of left ventricular dysfunction, is extremely low. In patients with congestive heart failure, in whom other pharmacologic options are limited by proarrhythmia risk and negative inotropism, preliminary experience with amiodarone is especially promising. Randomized trials are needed, directly comparing amiodarone to conventional antiarrhythmic therapy for atrial fibrillation suppression and comparing amiodarone to warfarin for thromboembolism prevention in patients with atrial fibrillation refractory to conventional antiarrhythmic drugs.

Amiodarone↗
PubMed1993

Transesophageal echocardiography during radiofrequency catheter ablation of ventricular tachycardia.

Radiofrequency lesion formation requires stable catheter tip/endocardial contact. Energy delivery is limited when temperatures are > 100 degrees C due to coagulum formation at the catheter tip. Transesophageal echocardiographic imaging may be useful for monitoring catheter position and detecting boiling. Transesophageal echocardiographic images were recorded during production of 22 radiofrequency lesions in bovine myocardium in a saline bath. Lesion size, tissue temperature and appearance of echo contrast (bubbles) were assessed. In 11 patients, transesophageal echocardiography was used to guide catheter movement and detect boiling during radiofrequency ablation for ventricular tachycardia. In the tissue bath, the appearance of echo bubbles was associated with visual bubbling at the catheter tip, tissue temperatures > 60 degrees C and larger lesions (284 +/- 165 vs 30 +/- 54 mm3; p < 0.001). In humans, transesophageal images easily identified the catheter tip in either ventricle and enabled continuous observation of electrode-tissue contact during radiofrequency application. Transesophageal echocardiographic bubbles appeared in 59 of 217 radiofrequency applications (27%). Continued radiofrequency application after appearance of bubbles was followed by an increase in impedance. Prolonged placement of the probe in heavily sedated patients resulted in a mild sore throat, but no other complications. Transesophageal echocardiographic imaging enables continuous monitoring of catheter position during radiofrequency energy application. The abrupt appearance of echo bubbles indicates boiling and impending coagulum formation at the catheter tip.

Adult↗
PubMed1993

Predicting death from progressive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Data were retrospectively reviewed on 528 consecutive patients hospitalized for treatment of advanced heart failure (left ventricular ejection fraction 0.2 +/- 0.07) and cardiac transplant evaluation, who were stabilized with medical therapy and discharged home. Predictors of heart failure death or rehospitalization for urgent transplantation were identified using the Cox proportional-hazards model. Within 1 year, 59 patients (11%) died suddenly and 70 (13%) died of heart failure or required urgent transplantation. A serum sodium < or = 134 mEq/liter, pulmonary arterial diastolic pressure > 19 mm Hg, left ventricular diastolic dimension index > 44 mm/m2, peak oxygen consumption during exercise testing < 11 ml/kg/min and the presence of a permanent pacemaker were independent predictors of hemodynamic deterioration. In the absence of these risk factors the risk of hemodynamic deterioration within 1 year from this study was only 2%. This risk increased to > 50% in the presence of hyponatremia and any 2 additional risk factors. Thus, patients with advanced heart failure at highest risk for progressive hemodynamic deterioration can be identified from clinical variables that could aid in triaging such patients to earlier cardiac transplantation.

Actuarial Analysis↗
PubMed1993

Prognosis after syncope: impact of left ventricular function.

A cardiac cause of syncope has been associated with increased sudden death risk, whereas unexplained syncope has a benign prognosis. However, in patients who have depressed left ventricular function, the accuracy of diagnostic tests and the efficacy of therapy, such as antiarrhythmic drugs, are reduced. Previous studies of patients with syncope have not evaluated the contribution of left ventricular performance in risk stratification for sudden death. The purpose of our study of a large population of patients with syncope was to determine the impact of left ventricular dysfunction on sudden death risk if syncope is caused by a cardiac cause or remains unexplained after electrophysiologic testing. We retrospectively evaluated the relationship of left ventricular ejection fraction to sudden death prognosis in 88 consecutive patients referred for electrophysiologic testing to determine a cause of syncope. The mean age was 57 +/- 18 years, left ventricular ejection fraction was 0.41 +/- 0.20, and 66 patients (75%) had structural heart disease. In 49 patients (56%) a cardiac cause of syncope was diagnosed, and in 39 patients (44%) the cause of syncope remained unexplained after evaluation. Cardiac syncope was attributed to ventricular tachycardia in 27 patients, bradyarrhythmia in 11 patients, and supraventricular tachyarrhythmia in 11 patients. By logistic regression only structural heart disease was independently associated with cardiac cause of syncope (p = 0.003). After a mean follow-up of 790 +/- 688 days, nine patients had died suddenly, eight (89%) of whom had left ventricular ejection fraction less than 0.30.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Increasing catheter ablation lesion size by simultaneous application of radiofrequency current to two adjacent sites.

Treatment of ventricular tachycardia by radiofrequency current application can be difficult, partly because of the larger size of the reentry circuit in relation to the lesion generated. Larger lesions than those currently achieved with single radiofrequency applications are desirable. This study evaluated simultaneous radiofrequency application to two adjacent electrodes to determine the effects of inter-electrode distance and configuration (bipolar serial vs parallel) on lesion size and tissue temperature. Two 6F electrodes were placed, with the tips facing each other, on bovine myocardium in a saline bath at 37 degrees C. Radiofrequency current was applied to a single electrode, or simultaneously to two electrodes connected either in series or in parallel. Tissue temperature, power, and lesion size were measured. Lesions produced by simultaneous radiofrequency delivery to both electrodes were more than twice the size of those produced by a single electrode alone (> 100 mm3 vs 33.2 mm3, p < 0.01). Temperatures between electrodes were greater than those temperatures at the same distances from a single electrode (p < 0.001). The size of the lesions increased as inter-electrode distance decreased below 3.5 mm (p < 0.030) because of the increasing depth of the lesion between the electrodes. Two electrodes placed in a bipolar as opposed to a parallel configuration were most efficient, as this configuration produced greater lesion sizes for a given level of power delivery (p < 0.0001). The bipolar lesion size decreased by > 50% if one electrode was not in contact with the tissue (p < 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Increased risk of progressive hemodynamic deterioration in advanced heart failure patients requiring permanent pacemakers.

To determine the influence of long-term permanent pacing systems on survival in patients with severe left ventricular dysfunction, data from 557 consecutive patients hospitalized with advanced heart failure for cardiac transplant evaluation and discharged on medical therapy were reviewed. Permanent pacemakers were identified in 42 (8%) patients. One-year actuarial risk of death from heart failure or urgent transplantation in paced patients was higher (49%) than that of a control group, matched for the severity of heart failure (15%, p = 0.003). Sudden death did not differ between paced patients and controls.

Actuarial Analysis↗
PubMed1993

Syncope in advanced heart failure: high risk of sudden death regardless of origin of syncope.

OBJECTIVES: The purpose of this study was to assess the importance of syncope as a warning sign for sudden death in advanced heart failure and to determine the relative importance of cardiac syncope and syncope from other causes. BACKGROUND: Despite remarkable advances in the pharmacologic approach to advanced heart failure, 20% to 40% of patients with advanced heart failure will die each year. In such patients, the relation between sudden death and the etiology of syncope has not been evaluated. METHODS: The relation of syncope to sudden death was evaluated in 491 consecutive patients with advanced heart failure (New York Heart Association functional class III or IV), no history of cardiac arrest and a mean left ventricular ejection fraction of 0.20 +/- 0.07. Patients were evaluated for the presence and origin of syncope. The severity of heart failure was assessed from serum sodium levels, ejection fraction, functional class and echocardiographic and hemodynamic variables. RESULTS: Sixty patients (12%) had a history of syncope; the condition had a cardiac origin in 29 (48%) and was due to other causes in 31 (52%). The origin of heart failure was coronary artery disease in 234 patients (48%) and dilated cardiomyopathy in 253 (51%) and its severity was similar in patients with and without syncope. During a mean follow-up interval of 365 +/- 419 days, 69 patients (14%) died suddenly and 66 patients (13%) died of progressive heart failure. The actuarial incidence of sudden death by 1 year was significantly greater in patients with (45%) than in those without (12%, p < 0.00001) syncope. In the Cox proportional hazards model, syncope predicted sudden death independent of atrial fibrillation, serum sodium, cardiac index, angiotensin-converting enzyme inhibition and patient age. The actuarial risk of sudden death by 1 year was similarly high in patients with either cardiac syncope or syncope from other causes (49% vs. 39%, p = NS). CONCLUSIONS: Patients with advanced heart failure are at especially high risk for sudden death regardless of the etiology of syncope.

Adult↗
PubMed1993

Amiodarone and post-MI patients.

Amiodarone is a viable drug for preventing sudden cardiac death, particularly during the first year after MI. If larger trials confirm the aforementioned prospective trials of Ceremuzynski et al, Cairns et al, and the BASIS trial, the efficacy of amiodarone would outweigh the risk of its side effects during the first year after MI. Based on the long-term observation from the BASIS trial, the duration of amiodarone therapy need not be more than 1 year--which, as we have learned, is when these post-MI patients would benefit most from the drug. It is also likely that the effects of amiodarone would complement those of aspirin and angiotensin converting enzyme inhibitors. The SAVE, CONSENSUS II, and SOLVD trials demonstrated that captopril and enalapril did not reduce the mortality rate during the first year after MI, nor did they reduce the sudden cardiac death rate. Their beneficial effects became evident only during the second year and thereafter. Unlike other antiarrhythmic agents of various classes, amiodarone possesses antiarrhythmic properties but does not exert deleterious effects on ventricular function. More studies are needed to determine if the benefit of amiodarone could be enhanced by combination therapy (eg, angiotensin converting enzyme inhibitors, aspirin, or beta-blockers). Whether amiodarone will provide the same protection for patients who have poor left ventricular function or congestive heart failure is not known. The European and VA cooperative studies should help answer this question. If it turns out that amiodarone is beneficial, one must then determine whether higher doses of the drug will offer more protection, and, if so, if that greater protection would be offset by increased toxicity. How much amiodarone should be given to offer the most protection with the least risk? Another intriguing research question is this: If we treat patients with amiodarone for more than 1 year, would the drug continue to improve the mortality rate in subsequent years? Other studies are needed in patients at very high risk of sudden cardiac death (ie, those who have a low ejection fraction and high-density VPDs). A study comparing amiodarone and sotalol in high-risk patients for sudden cardiac death is also needed. These clinical studies should be carried out with basic science research investigating the actions of amiodarone at the molecular and cellular level in order to give us a better understanding of how the drug works.

Amiodarone↗
PubMed1993

Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction.

BACKGROUND: Ventricular tachycardia reentry circuits in chronic infarct scars can contain slow conduction zones, which are difficult to distinguish from bystander areas adjacent to the circuit during catheter mapping. This study developed criteria for identifying reentry circuit sites using computer simulations. These criteria then were tested during catheter mapping in humans to predict sites at which radiofrequency current application terminated ventricular tachycardia. METHODS AND RESULTS: In computer simulations, effects of single stimuli and stimulus trains at sites in and adjacent to reentry circuits were analyzed. Entrainment with concealed fusion, defined as ventricular tachycardia entrainment with no change in QRS morphology, could occur during stimulation in reentry circuit common pathways and adjacent bystander sites. Pacing at reentry circuit common pathway sites, the stimulus to QRS (S-QRS) interval equals the electrogram to QRS interval (EG-QRS) during tachycardia. The postpacing interval from the last stimulus to the following electrogram equals the tachycardia cycle length. Pacing at bystander sites the S-QRS exceeds the EG-QRS interval when the conduction time from the bystander site to the circuit is short but may be less than or equal to the EG-QRS interval when the conduction time to the circuit is long. The postpacing interval, however, always exceeds the tachycardia cycle length. When conduction in the circuit slows during pacing, the S-QRS and postpacing intervals increase and the slowest stimulus train most closely reflects conduction times during tachycardia. Endocardial catheter mapping and radiofrequency ablation were performed during 31 monomorphic ventricular tachycardias in 15 patients with drug refractory ventricular tachycardia late after myocardial infarction. During ventricular tachycardia, trains of electrical stimuli or scanning single stimuli were evaluated before application of radiofrequency current at the same site. Radiofrequency current terminated ventricular tachycardia at 24 of 241 sites (10%) in 12 of 15 patients (80%). Ventricular tachycardia termination occurred more frequently at sites with entrainment with concealed fusion (odds ratio, 3.4; 95% confidence interval [CI], 1.4 to 8.3), a postpacing interval approximating the ventricular tachycardia cycle length (odds ratio, 4.6; 95% CI, 1.6 to 12.9) and an S-QRS interval during entrainment of more than 60 milliseconds and less than 70% of the ventricular tachycardia cycle length (odds ratio, 4.9; 95% CI, 1.4 to 17.1). Ventricular tachycardia termination was also predicted by the presence of isolated diastolic potentials or continuous electrical activity (odds ratio, 5.2; 95% CI, 1.8 to 15.5), but these electrograms were infrequent (8% of all sites). Combinations of entrainment with concealed fusion, postpacing interval, S-QRS intervals, and isolated diastolic potentials or continuous electrical activity predicted a more than 35% incidence of ventricular tachycardia termination during radiofrequency current application versus a 4% incidence when none suggested that the site was in the reentry circuit. Analysis of the postpacing interval and S-QRS interval suggested that 25% of the sites with entrainment with concealed fusion were in bystander areas not within the reentry circuit. At restudy 5 to 7 days later, 6 patients had no monomorphic ventricular tachycardia inducible, and inducible ventricular tachycardias were modified in 4 patients. None of these 10 patients have suffered arrhythmia recurrences during a follow-up of 316 +/- 199 days, although 4 continue to receive previously ineffective medications. CONCLUSIONS: Regions giving rise to reentry after myocardial infarction are complex and can include bystander areas, slow conduction zones, and isthmuses for impulse propagation at which radiofrequency current lesions can interrupt reentry.

Aged↗
PubMed1992

Low-dose amiodarone for atrial fibrillation: time for a prospective study?

Because atrial fibrillation is associated with substantial morbidity, restoration of sinus rhythm is desirable. Long-term maintenance of sinus rhythm often requires chronic antiarrhythmic therapy. Class I antiarrhythmic drugs such as quinidine or propafenone maintain sinus rhythm in approximately 50% of patients at 1 year and have risks for proarrhythmia and noncardiac toxicity. Studies of low-dose amiodarone for atrial fibrillation have reported sinus rhythm maintenance in 53% to 79% of patients during a mean follow-up of 27 months. Amiodarone has a lower incidence of proarrhythmia and heart failure exacerbation compared with class I drugs. Most noncardiac side effects are dose related, and low-dose amiodarone (less than 300 mg/d) is well tolerated. The time has come for a large-scale prospective evaluation of low-dose amiodarone treatment early in the course of atrial fibrillation.

Amiodarone↗