Influence of residual blood flow in the infarct-related artery on ventricular tachycardia after myocardial infarction.
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Aged↗
Biomedical subjects
W G Stevenson
Publications and source records attributed to W G Stevenson.
Patterns of beat-to-beat heart rate variability in advanced heart failure.
Diminished heart rate variability is associated with high sympathetic tone and an increased mortality rate in heart failure cases. We constructed Poincaré plots of each sinus R-R interval plotted against the subsequent R-R interval from 24-hour Holter recordings of 24 healthy subjects (control group) and 24 patients with heart failure. Every subject in the control group had a comet-shaped Poincaré plot resulting from an increase in beat-to-beat dispersion as heart rate slowed. No patient with heart failure had this comet-shaped pattern. Instead, three distinctive patterns were identified: (1) a torpedo-shaped pattern resulting from low R-R interval dispersion over the entire range of heart rates, (2) a fanshaped pattern resulting from restriction of overall R-R interval ranges with enhanced dispersion, and (3) complex patterns with clusters of points characteristic of stepwise changes in R-R intervals. Poincaré pattern could not be predicted from standard deviations of R-R intervals. This first use of Poincaré plots in heart rate variability analysis reveals a complexity not readily perceived from standard deviation information. Further study is warranted to determine if this method will allow refined assessment of cardiac-autonomic integrity in heart failure, which could help identify patients at highest risk for sudden death.
Death, Sudden↗
Optimal late potential criteria for reducing false positive signal-averaged electrocardiograms.
The purposes of this study were to determine for signal-averaged electrocardiograms in normal subjects: (1) the incidence of false positives for various filter frequencies and late potential criteria and (2) reproducibility over time. In 46 normal volunteers, the QRS vector magnitude was bidirectionally high-pass filtered at 25, 40, and 100 Hz. As high-pass filter frequency increased, QRS duration decreased from 98 +/- 9 to 92 +/- 9 msec (p less than 0.0001), terminal QRS root mean square voltage decreased from 60 +/- 41 to 14 +/- 9 microV (p less than 0.0001), and terminal QRS low amplitude signal duration increased from 27 +/- 7 to 41 +/- 14 msec (p less than 0.0001). For individual parameters, the incidence of false positive tests ranged from 2% to 41%, whereas there were no false positive tests for the combination of abnormal QRS duration plus either root mean square voltage or low amplitude signal duration. Measurements were repeated after 6.4 +/- 0.3 months in 26 subjects and were highly reproducible at all filter settings. The potentially high incidence of false positive tests with some criteria has important implications for the use of signal-averaged electrocardiography as a screening test in patient populations with various arrhythmia risks.
Adult↗
Prevention of sudden death in survivors of myocardial infarction: a decision analysis approach.
During the first year after myocardial infarction, 5% to 15% of patients die, and the majority of deaths occur suddenly. Highly efficacious therapy, such as the implantable cardioverter-defibrillator, may reduce the chance of sudden death, but broad application is limited by associated risks. Hence, attempts to identify patients at high risk so they can receive therapy are desirable. Subgroups with high or low sudden death risks can be identified based on left ventricular function. Further risk stratification using programmed electrical stimulation and the signal-averaged ECG has been advocated, but the best strategy is unknown. Using a decision analysis model, we compared the 1-year survival rates in survivors of myocardial infarction treated with the implantable cardioverter-defibrillator either empirically or based on screening with the signal-averaged ECG and programmed electrical stimulation. The best strategy for selecting patients for therapy depended on the pre-therapy sudden death risk. For patients at low risk, such as those with well-preserved ventricular function, antiarrhythmic therapy selected with screening tests or given empirically increased both the mortality rate resulting from the adverse effects of therapy and the excellent survival rate without therapy. In the moderate-risk population, both empiric and stratified approaches reduced mortality, but stratification substantially limited the number of patients receiving unnecessary therapy. In the high-risk population, empiric treatment achieved the best survival rate, and screening resulted in only a small reduction in the number of patients treated unnecessarily.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac Pacing, Artificial↗
Ventricular tachycardia after infarction: sources of coronary blood flow to the infarct zone.
The purpose of this study was to determine the sources of coronary blood flow to infarct scars in patients with sustained ventricular tachycardia occurring late after myocardial infarction, which is necessary for transcoronary sclerosis or embolization. Angiograms of 32 consecutive patients (age 63 +/- 8 years, ejection fraction 0.30 +/- 0.10) were reviewed. Sources of blood flow to the infarct zone were identified as coming from a recanalized infarct-related artery, side branch, collateral, or coronary bypass graft. Eighty-four percent of patients in the study had an identifiable blood supply to the area of previous infarction. More than one source of blood flow to anterior infarct locations were observed more often than to inferior infarct locations (53% vs 17%, p = 0.03). Transcoronary mapping for possible chemical ablation should be technically feasible in the majority of patients with ventricular tachycardia. Infarct zone blood flow arises from any of several sources and varies somewhat depending on infarct location.
Collateral Circulation↗
Significance of aborted cardiac arrest and sustained ventricular tachycardia in patients referred for treatment therapy of advanced heart failure.
Cardiac arrest in patients with heart failure may be the result of remediable factors such as pulmonary edema, drug toxicity, or electrolyte abnormalities, or it may be due to primary arrhythmias. The relation of prior aborted cardiac arrest or sustained ventricular tachycardia to subsequent prognosis was assessed in 458 consecutive patients referred for management of advanced heart failure (left ventricular ejection fraction 0.2 +/- 0.07). All patients received tailored vasodilator and diuretic therapy and were then followed as outpatients. Patients were divided into four groups: 388 patients (85%) with no prior cardiac arrest or sustained ventricular tachycardia, 31 patients (7%) with a primary arrhythmia cardiac arrest, 22 patients (5%) with a secondary cardiac arrest, and 17 patients (4%) with sustained ventricular tachycardia without cardiac arrest. Patients with cardiac arrest resulting from a primary arrhythmia were usually treated with antiarrhythmic drugs (25 patients), and five patients received an implantable defibrillator. After hospital discharge actuarial 1-year sudden death risk (17%) and total mortality (24%) rates for the group with primary arrhythmia were similar to corresponding values in patients with no history of cardiac arrest or sustained ventricular tachycardia (17% and 30%, respectively). In patients with a secondary cardiac arrest as a result of exacerbation of heart failure (11 patients), torsade de pointes (10 patients), or hypokalemia (one patient), therapy focused on removal of aggravating factors. Actuarial 1-year sudden death (39%) and total mortality (54%) rates for the group with secondary arrest were higher than for patients without a history of cardiac arrest (p = 0.003 and 0.005, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Actuarial Analysis↗
Amiodarone therapy does not compromise subsequent heart transplantation.
OBJECTIVES: The objective of this study was to determine the frequency of pulmonary complications, feasibility of early hospital discharge and requirements for postoperative inotropic and chronotropic support in patients receiving amiodarone therapy before heart transplantation. BACKGROUND: Although many patients waiting for heart transplantation will die of arrhythmias before a donor heart is found, the use of amiodarone has been limited by concern about increased complications in the perioperative period. METHODS: The 29 patients receiving amiodarone at the time of heart transplantation at University of California, Los Angeles Medical Center between October 1986 and September 1990 were compared with 29 control recipients to evaluate postoperative morbidity. Patients were receiving amiodarone for recurrent ventricular tachyarrhythmias (n = 11), atrial fibrillation (n = 2) or complex ventricular ectopic activity (n = 16). The average daily dose was 360 +/- 230 mg/day for an average of 11 +/- 22 months before transplantation. Amiodarone and control groups had a similar ejection fraction (0.18 +/- 0.07 vs. 0.20 +/- 0.08), frequency of coronary disease, age and gender. There were three more status I patients in the control group. OKT3 was given to only two patients receiving amiodarone and 12 control patients at high risk for renal dysfunction. RESULTS: Postoperatively, the duration of assisted ventilation was 21 +/- 19 h after amiodarone therapy versus 26 +/- 2 h in the control group (20 +/- 18 h vs. 15 +/- 9 h after excluding patients receiving OKT3), discharge arterial oxygen saturation was > 95% in both groups. Two patients in the amiodarone group with a smoking history of > 100 pack-years developed bilateral pulmonary infiltrates of brief duration. Although patients receiving amiodarone required atrial pacing more frequently (eight vs. two patients) and had a lower heart rate at discharge (75 +/- 18 vs. 86 +/- 11 beats/min), the duration of inotropic support (2.1 +/- 1.5 vs. 3.5 +/- 2.5 days) and of hospital stay (10 +/- 3 vs. 15 +/- 10 days) was not higher in the amiodarone than in the control group. The mortality rate at 30 days was similar in the two groups (6.8% vs. 3.4%, p = NS). CONCLUSIONS: Amiodarone therapy before heart transplantation may contribute to occasional pulmonary complications but does not significantly increase perioperative morbidity or mortality with the regimens used in this retrospective study.
Aged↗
Identifying sites for catheter ablation of ventricular tachycardia.
The approach to localizing sites for catheter ablation of ventricular tachycardia foci depends on the type of tachycardia. In large reentry circuits such as those arising from infarct scars, areas of slow conduction in and around the scar should be targeted. During sinus rhythm, these can be suspected from the presence of fractionated electrograms and, at some sites, long stimulus to QRS delays during pacing. Slow conduction areas can be classified as: 1. central slow conduction zone sites, 2. exits from the slow conduction zone, 3. entrances to the slow conduction zone, and 4. bystander areas which are not involved in the tachycardia circuit. In the central slow conduction zone stimulation entrains or resets tachycardia with a long stimulus to QRS (S-QRS) delay (40 to greater than 300 ms) without altering the QRS morphology (entrainment with concealed fusion). At slow conduction zone exits, presystolic electrograms are recorded during VT, the pacemap matches the VT QRS morphology, and with pacing during VT the S-QRS interval is relatively short and VT may or may not be entrained. At entrances to the slow conduction zone electrogram timing is variable but early diastolic electrograms are expected and the pace-map QRS may differ from the VT QRS morphology. Relatively late stimuli or slow trains of stimuli entrain VT with concealed fusion with a relatively longer S-QRS interval than observed in the central slow conduction zone. Early stimuli may entrain VT while altering the QRS morphology due to propagation of the stimulated antidromic wavefront out of the scar from a site other than the tachycardia exit. At bystander sites electrogram timing, pace-mapping, and the effects of programmed stimulation are variable but may occasionally mimic reentry circuit sites. Relatively late stimuli are likely to capture the site without altering the VT. If discrete electrograms are present, analysis of these during pacing may provide further evidence that the site is not in the reentry circuit. Catheter ablation will probably be most effective at central slow conduction zone sites. When VT originates from a small focus surrounded by normal myocardium, such as is likely for idiopathic RV outflow tract and some idiopathic left ventricular tachycardias, presystolic electrical activity and pacemapping are likely to identify the tachycardia focus. For macroreentry involving the bundle branches, the right bundle branch can be easily targeted.
Animals↗
Ventricular arrhythmias in ischemic heart disease.
Ventricular arrhythmias remain the leading cause of death from coronary artery disease. This review summarizes current thinking in several areas relating to the pathophysiology, prognosis, and therapy of ventricular arrhythmias associated with acute and chronic coronary artery disease syndromes. The experimental basis of arrhythmias in the setting of acute myocardial ischemia and chronic myocardial infarction is described, stressing the important pathophysiologic differences between these two conditions. The effects of the autonomic nervous system as a key modulator of ischemic arrhythmogenesis are discussed. Insights, derived from endocardial mapping studies, into the nature of ventricular tachycardia in humans with chronic myocardial infarction are described, including implications for risk stratification and therapy to prevent arrhythmia recurrence. Current therapeutic principles are discussed in the management of ventricular arrhythmias associated with coronary artery disease, including pharmacologic approaches, surgical and catheter ablation, and automatic implantable cardioverting and defibrillating devices.
Acute Disease↗
Frequency of late potentials in systemic sclerosis.
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Adult↗
Hearts too good to die: ventricular fibrillation due to small infarctions or ischemia.
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Aged↗
Late potentials are unaltered by ventricular filling pressure reduction in heart failure.
Exacerbation of heart failure may increase susceptibility to arrhythmias. Therefore tests to assess the risk of arrhythmia, performed after hemodynamic improvement, may be of limited value. To determine whether hemodynamic improvement alters ventricular late potentials detected by signal-averaged ECG, we studied 27 consecutive patients with dilated heart failure (left ventricular ejection fraction 0.20 +/- 0.06, 15 with coronary artery disease) before and 3 +/- 2 days after tailored vasodilator and diuretic therapy reduced ventricular filling pressures. QRS duration, terminal QRS amplitude (root mean square [RMS]), and low-amplitude (less than 40 microV) signal (LAS) duration were determined by an automated algorithm from the vector magnitude of the QRS high-pass filtered at 25 Hz and at 40 Hz. Despite marked decreases in pulmonary capillary wedge (27 +/- 7 to 16 +/- 5 mm Hg, p less than 0.001) and right atrial (13 +/- 7 to 7 +/- 4 mm Hg, p less than 0.001) pressures and a 20% increase in cardiac output, there was not a significant change in QRS duration, RMS, or LAS. Before and after therapy late potentials, defined as abnormal QRS duration RMS, or LAS, were present in 14 (52%) patients with filtering at 25 Hz and in 22 (81%) patients with filtering at 40 Hz. The signal-averaged ECG after hemodynamic improvement predicted the results during exacerbation of heart failure in all patients. Thus in patients with advanced heart failure the signal-averaged ECG obtained after hemodynamic improvement reflects the findings during exacerbation of heart failure.
Arrhythmias, Cardiac↗
Signal-averaged electrocardiography: diagnostic uses and clinical implications.
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Electrocardiography↗
Prognostic significance of atrial fibrillation in advanced heart failure. A study of 390 patients.
BACKGROUND: Atrial fibrillation is common in advanced heart failure, but its prognostic significance is controversial. METHODS AND RESULTS: We evaluated the relation of atrial rhythm to overall survival and sudden death in 390 consecutive advanced heart failure patients. Etiology of heart failure was coronary artery disease in 177 patients (45%) and nonischemic cardiomyopathy or valvular heart disease in 213 patients (55%). Mean left ventricular ejection fraction was 0.19 +/- 0.07. Seventy-five patients (19%) had paroxysmal (26 patients) or chronic (49 patients) atrial fibrillation. Compared with patients with sinus rhythm, patients with atrial fibrillation did not differ in etiology of heart failure, mean pulmonary capillary wedge pressure on therapy, or embolic events but were more likely to be receiving warfarin and antiarrhythmic drugs and had a slightly higher left ventricular ejection fraction. After a mean follow-up of 236 +/- 303 days, 98 patients died: 56 (57%) died suddenly, and 36 (37%) died of progressive heart failure. Actuarial 1-year overall survival was 68%, and sudden death-free survival was 79%. Actuarial survival was significantly worse for atrial fibrillation than for sinus rhythm patients (52% versus 71%, p = 0.0013). Similarly, sudden death-free survival was significantly worse for atrial fibrillation than for sinus rhythm patients (69% versus 82%, p = 0.0013). By Cox proportional hazards model, pulmonary capillary wedge pressure on therapy, left ventricular ejection fraction, coronary artery disease, and atrial fibrillation were independent risk factors for total mortality and sudden death. For patients who had pulmonary capillary wedge pressure of less than 16 mm Hg on therapy, atrial fibrillation was associated with poorer 1-year survival (44% versus 83%, p = 0.00001); however, in the high pulmonary capillary wedge pressure group, atrial fibrillation did not confer an increased risk (58% versus 57%). CONCLUSIONS: Atrial fibrillation is a marker for increased risk of death, especially in heart failure patients who have lower filling pressures on vasodilator and diuretic therapy. Whether aggressive attempts to maintain sinus rhythm will reduce this risk is unknown.
Actuarial Analysis↗
Comparison of frequency of late potentials in idiopathic dilated cardiomyopathy and ischemic cardiomyopathy with advanced congestive heart failure and their usefulness in predicting sudden death.
Signal-averaged electrocardiograms were obtained in 62 consecutive patients with advanced congestive heart failure (CHF) undergoing evaluation for possible heart transplantation to determine if late potentials: (1) provide unique information compared to assessment of ventricular ectopic activity on ambulatory electrocardiogram, and (2) identify a subgroup of CHF patients with higher sudden death risk. Patients with a history of cardiac arrest or sustained ventricular tachycardia were excluded. CHF was due to old myocardial infarction in 40 patients and idiopathic dilated cardiomyopathy in 22 patients. Late potentials were present in 16 of 40 (40%) patients with old infarction but in only 3 of 22 (14%) patients with nonischemic CHF (p = 0.03). Twenty-four-hour ambulatory electrocardiograms were obtained in 34 patients (55%). Total ventricular ectopic activity and repetitive forms of ectopy were similar in patients with and without late potentials. Nine patients died suddenly, 9 had nonsudden death, 15 underwent heart transplantation and 29 were alive and well after a mean follow-up of 218 +/- 154 days. At 1 year, the actuarial risk of death was 37% and of sudden death was 20%. Sudden death risk was 12% in patients with late potentials versus 21% in those without (p = 0.73). Thus, the incidence of the arrhythmia substrate producing late potentials depends on the CHF etiology. The signal-averaged electrocardiogram and ambulatory electrocardiogram provide independent information for possible risk assessment in CHF. However, late potentials are poor predictors of sudden death risk when CHF is advanced, possibly due to the heterogeneity of causes of sudden death--ventricular tachycardia being only 1 of many possible mechanisms.
Arrhythmias, Cardiac↗
Delayed presentation of cardiac perforation after apparently successful catheter ablation for incessant ventricular tachycardia.
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Aged↗
Facilitation of ventricular tachycardia initiation by procainamide during programmed ventricular stimulation in patients with heart failure.
Antiarrhythmic drugs occasionally facilitate, rather than prevent, ventricular tachycardia. The purpose of this study was to assess the incidence of procainamide facilitation of ventricular tachycardia initiation during programmed electrical stimulation in patients with no history of spontaneous sustained ventricular tachycardia but who are at high risk. Twenty patients with advanced heart failure (mean left ventricular ejection fraction 0.19 +/- 0.09) and nonsustained ventricular tachycardia and in whom sustained ventricular tachycardia was not inducible by programmed electrical stimulation in the basal state were studied. Six patients had coronary artery disease, 13 had idiopathic dilated cardiomyopathy, and 1 had valvular heart disease. All patients received programmed stimulation from the right ventricular apex with one to three extra-stimuli before and after the intravenous infusion of 10 mg/kg of procainamide (serum level 6.6 +/- 2.4 mcg/l). In two patients (10%) sustained monomorphic ventricular tachycardia was initiated only after the administration of procainamide. One of these patients later died in ventricular tachycardia during hyperkalemia. Of the noninducible patients, during a follow-up period of 6 +/- 5 months, two died suddenly and one developed symptomatic ventricular tachycardia. Thus, procainamide can unmask potential reentry circuits in some patients who have not had spontaneous sustained ventricular tachycardia. In patients with heart failure, this risk, as assessed by programmed stimulation after a single dose of procainamide, appears to be low.
Adult↗
Treatment of catecholamine-sensitive right ventricular tachycardia by endocardial catheter ablation.
Endocardial catheter ablation with direct current high voltage shocks was performed in a patient with recurrent syncope due to a catecholamine-sensitive ventricular tachycardia that was drug refractory and occurred in the absence of identifiable heart disease. Pace mapping and catheter activation mapping of the spontaneous and isoproterenol-induced ventricular tachycardia located the tachycardia origin in the right ventricular outflow tract. Ablation dramatically reduced spontaneous ventricular tachycardia and ectopic activity (from 50,000 to less than 100 ectopic beats/24 h). The patient has remained symptom free and without ventricular tachycardia recurrence for 3 years. These observations and review of previous studies suggest that catheter mapping can easily locate the arrhythmia focus in the right ventricular outflow tract and that catheter ablation can be performed at low risk. Catheter ablation is a viable option for the treatment of right ventricular catecholamine-sensitive tachycardias that are unresponsive to antiarrhythmic drugs.
Adult↗