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Biomedical subjects

L A Saxon

Publications and source records attributed to L A Saxon.

51 records · Page 3Linked to original sources

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↗

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↗

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↗

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↗

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.

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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↗

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↗

Permanent pacemaker placement in chronic atrial fibrillation associated with intermittent AV block and cerebral symptoms.

We examined the hypothesis that a greater than or equal to 2 second pause detected on 24-hour Holter monitoring in patients with persistent atrial fibrillation and complaints of syncope or dizziness lacked sufficient specificity to warrant implantation of a permanent pacemaker. We retrospectively reviewed cases from our 24-hour electrocardiographic (Holter) monitoring data base. A total of 411 consecutive Holter monitoring records demonstrating persistent atrial fibrillation obtained during a 5-year period (1982 to 1987) were examined. One hundred and five (26%) patients had cerebral symptoms (dizziness or syncope) as a primary indication for monitoring 80 (76%) patients were identified with documented ventricular pauses of greater than or equal to 2 seconds. Three hundred and six patients (74%) underwent 24-hour monitoring without cerebral symptoms as an indication and 209 (68%) patients had greater than or equal to 2-second pauses. Clinical information was available in 164 (50 symptomatic and 114 asymptomatic) patients. There were no significant differences in the clinical or Holter findings between the two groups. Of the 50 symptomatic patients, 15 (30%) underwent permanent pacemaker placement and the remaining 35 (70%) were managed conservatively during a mean follow-up of 23 +/- 5 months. Eleven of 15 paced (73%) and 31 of 35 (89%) nonpaced patients experienced resolution of their cerebral symptoms (NS). The sensitivity of Holter monitoring in detecting pauses of greater than or equal to 2 seconds in patients with cerebral symptoms was high (76%), but the specificity (32%) and positive predictive values (28%) were low.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Significance of the clinical presentation in ventricular tachycardia/fibrillation.

We examined the hypothesis that clinical presentation in patients with sustained ventricular tachycardia/fibrillation (VT/VF) predicts clinical, electrophysiologic (EP) findings and long-term outcome. We included in the study 121 consecutive patients seen in our EP laboratory with documented and inducible sustained VT/VF. Patients were categorized into three groups according to their clinical presentation: (1) cardiac arrest (CA)-53 patients; (2) syncope (S)-20 patients; (3) palpitations/dizziness (P)-48 patients. There were no significant differences in age, sex, or prevalence of underlying heart disease between groups. The left ventricular ejection fraction (LVEF) was significantly lower for patients with CA (mean +/- S.D.; 31 +/- 14%) or S (30 +/- 11%) when compared with P (39 +/- 15%) (p less than 0.05). Induction of VT/VF required a more aggressive stimulation protocol (three extrastimuli) in patients with CA (53%) when compared with patients with S (30%) or P (29%) (p less than 0.05). The cycle length of the induced VT was shorter for CA (239 +/- 64 msec) patients as compared with the S (294 +/- 67 msec) or the P (319 +/- 94 msec) patients (p less than 0.01). Polymorphic VT or VF was induced in 28% of CA patients, in 9% of S patients, and in 12% of P patients (p less than 0.05). There were significantly more sudden deaths observed during the 4-year follow-up interval in patients presenting with CA compared to the P group (p less than 0.05). The 4-year survival was 67 +/- 8% for P, 45 +/- 15% for S, and 45 +/- 10% for CA patients (N.S.).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Depressed central respiratory drive causing weaning failure. Its reversal with doxapram.

A patient failed to wean from mechanical ventilation. Her problem was unique in that she had a depressed central drive to breathe manifested by hypopnea when removed from the ventilator. After excluding the known problems that impair successful weaning, we empirically administered three separate infusions of doxapram, a respiratory stimulant. These infusions produced a dramatic improvement in spontaneous ventilation and led to successful weaning and hospital discharge.

Doxapram↗