Electrophysiologic testing to identify patients at risk for sudden death.
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Biomedical subjects
Publications and source records attributed to M D Meissner.
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Normal saline (NS) is commonly used as a coronary catheter flush solution. We tested the hypothesis that intracoronary (i.c.) infusions of lactated Ringer's solution (LR) and LR with 5% dextrose (D5LR), both of which contain potassium and calcium, would be associated with less prominent surface ECG changes compared with i.c. infusions of NS. In 34 patients, 10 mL each of NS, LR, and D5LR at 37 degrees C were infused over 5 sec into the left main coronary artery. A 12-lead ECG was recorded before, continuously during, and after each infusion. Blinded ECG analysis revealed T-wave amplitude changes > 0.2 mV in 94%, 12%, and 3% of patients with the use of i.c. NS, D5LR, and LR, respectively (P < 0.0001, NS vs. D5LR or LR). QT prolongation > 40 msec occurred in 88%, 15%, and 18% of patients with i.c. NS, D5LR, and LR, respectively (P < 0.0001, NS vs. D5LR or LR). QT dispersion was increased by > 40 msec in 26% of patients during i.c. NS infusion compared to only 3% of patients with i.c. LR and D5LR infusions (P < 0.01). In conclusion, i.c. NS infusion is associated with more marked repolarization changes as compared with i.c. LR and D5LR infusions. Since such changes may lower arrhythmogenesis thresholds, the routine use of LR as a coronary catheter flush solution should be considered. Cathet. Cardiovasc. Intervent. 48:359-364, 1999.
BACKGROUND: Atrial fibrillation occurs commonly after open-heart surgery and may delay hospital discharge. The purpose of this study was to assess the use of preoperative amiodarone as prophylaxis against atrial fibrillation after cardiac surgery. METHODS: In this double-blind, randomized study, 124 patients were given either oral amiodarone (64 patients) or placebo (60 patients) for a minimum of seven days before elective cardiac surgery. Therapy consisted of 600 mg of amiodarone per day for seven days, then 200 mg per day until the day of discharge from the hospital. The mean (+/-SD) preoperative total dose of amiodarone was 4.8+/-0.96 g over a period of 13+/-7 days. RESULTS: Postoperative atrial fibrillation occurred in 16 of the 64 patients in the amiodarone group (25 percent) and 32 of the 60 patients in the placebo group (53 percent) (P=0.003). Patients in the amiodarone group were hospitalized for significantly fewer days than were patients in the placebo group (6.5+/-2.6 vs. 7.9+/-4.3 days, P=0.04). Nonfatal postoperative complications occurred in eight amiodarone-treated patients (12 percent) and in six patients receiving placebo (10 percent, P=0.78). Fatal postoperative complications occurred in three patients who received amiodarone (5 percent) and in two who received placebo (3 percent, P= 1.00). Total hospitalization costs were significantly less for the amiodarone group than for the placebo group ($18,375+/-$13,863 vs. $26,491+/-$23,837, P=0.03). CONCLUSIONS: Preoperative oral amiodarone in patients undergoing complex cardiac surgery is well tolerated and significantly reduces the incidence of postoperative atrial fibrillation and the duration and cost of hospitalization.
BACKGROUND: The diagnostic criteria for panic disorder include symptoms commonly experienced by patients with paroxysmal supraventricular tachycardia (PSVT). Since electrocardiographic documentation of PSVT can be elusive, symptoms may be ascribed to other conditions. OBJECTIVE: To systematically evaluate the potential for PSVT to simulate panic disorder. METHODS: A retrospective survey of 107 consecutive patients with reentrant PSVT was conducted. Objective and subjective assessments of PSVT symptomatology were made, including the application of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), panic disorder criteria. RESULTS: The criteria for panic disorder according to DSM-IV were fulfilled by 67% of patients. Paroxysmal supraventricular tachycardia was unrecognized after initial medical evaluation in 59 patients (55%), including 13 (41%) of 32 patients with ventricular preexcitation by electrocardiogram, and remained unrecognized for a median of 3.3 years. Prior to eventual identification of PSVT, physicians (nonpsychiatrists) attributed symptoms to panic, anxiety, or stress in 32 (54%) of the 59 patients. When PSVT was unrecognized, women were more likely than men to have symptoms ascribed to psychiatric origins (65% vs 32%, respectively; P < .04). Paroxysmal supraventricular tachycardia was detected in only 6 (9%) of 64 patients undergoing Holter monitoring vs 8 (47%) of 17 patients who wore an event monitor (P < .001). During a 20-month median follow-up, electrophysiologically guided therapy (ablation in 81% of patients) resolved symptoms in 86% of patients; only 4% continued to meet DSM-IV panic disorder criteria without evidence of PSVT recurrence. CONCLUSIONS: The clinical characteristics of patients with PSVT referred for electrophysiologically guided therapy can mimic panic disorder. Diagnosis of PSVT is often delayed by inappropriate rhythm detection techniques (Holter instead of event monitoring) and failure to recognize ventricular preexcitation on the sinus electrocardiogram; symptoms due to unrecognized PSVT are often ascribed to psychiatric conditions.
Despite the advent of dual chamber ICDs, differentiation of VT (SMVT) with 1:1 VA conduction will remain a challenge. In this study, VA conduction capability and prevalence of inducible sustained monomorphic (SM) VT with 1:1 VA conduction was assessed in 305 ICD recipients. SMVT with a mean cycle length (CL) of 304 +/- 61 ms was induced in 161 (53%) patients. Twenty-six percent of the patients maintained 1:1 VA conduction to CL < or = 400 ms during incremental ventricular pacing, regardless of presenting tachyarrhythmia or presence of inducible SMVT. Among ten patients who had inducible SMVT with possible 1:1 VA conduction (based on SMVT CL comparable to the shortest CL associated with 1:1 retrograde conduction during ventricular pacing), all seven with available intracardiac tracings had documented 1:1 VA conduction during the induced SMVT--representing 4.4% of the patients with inducible SMVT (95% CI 1.2%-7.6%), and 2.3% of the entire ICD cohort (95% CI 0.6%-4.0%). We conclude that about one-fifth of ICD recipients possess 1:1 VA conduction to CL < or = 400 ms and that inducible SMVT with 1:1 VA conduction can be demonstrated in a small but nonnegligible proportion of ICD recipients. These data are relevant to the design of tachyarrhythmia-discrimination algorithms for dual chamber ICDs.
INTRODUCTION: Implantable cardioverter defibrillators (ICDs) are occasionally used in presumed high-risk patients with electrocardiographically undocumented syncope, although the incidence of ventricular tachyarrhythmias in this population is not well defined. METHODS AND RESULTS: We studied 33 consecutive patients receiving an ICD (67% nonthoracotomy and 70% tiered therapy) after electrophysiologic testing for unmonitored "syncope" (n = 29) or "near-syncope" (n = 4). Atherosclerotic heart disease was present in 24 (73%); mean left ventricular ejection fraction (LVEF) was 0.39 +/- 0.15; and sustained monomorphic ventricular tachycardia (SMVT) was inducible in 18 (55%). Over a median follow-up of 17 months (range 4 to 61), 12 patients (36%) received > or = 1 appropriate ICD discharge triggered by SMVT (cycle length 230 to 375 msec) in 10 and ventricular flutter or fibrillation in 2--without concomitant antiarrhythmic medication in 8 of 12 cases. Inducible SMVT and LVEF < or = 0.35 were statistically significant, independent predictors of an appropriate ICD discharge (P < 0.02 and P < 0.03, respectively). Estimated 1-year cumulative survival free of appropriate discharge was 34% versus 87%, respectively, in patients with versus without inducible SMVT (P < 0.02), and 18% versus 56%, respectively, in patients with LVEF < or = 0.35 versus LVEF > 0.35 (P < 0.03). CONCLUSION: In this highly select, multicenter population of ICD recipients with electrocardiographically undocumented syncope, a substantial incidence of appropriate device discharges was observed, particularly in patients with inducible SMVT and LVEF < or = 0.35. These findings support the notion that, in patients with LV dysfunction and inducible SMVT, ventricular tachyarrhythmias are likely to account for episodes of syncope or near-syncope.
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Tachycardia discrimination in future implantable cardioverter defibrillators (ICDs) is likely to be enhanced by the addition of an atrial sensing/pacing lead. However, differentiation of sinus tachycardia (ST) from ventricular tachycardia (VT) with 1:1 VA conduction will remain problematic. We assessed the use of the AV interval as a potential criterion for correctly differentiating ST from VT. Incremental V pacing at the right ventricular (RV) apex served as a "VT" model in each of 41 patients with 1:1 VA conduction to pacing cycle lengths < or = 450 msec. High right atrial and RV apical electrograms during normal sinus rhythm (NSR) and during incremental V pacing were digitized (simulating ICD sensing). From these signals, AV interval versus pacing cycle length plots were computer generated to identify crossover cycle lengths, each defined as the cycle length at which the AV interval during V pacing equals the AV interval during NSR. At cycle lengths longer than the crossover value, the AV interval during "VT" exceeds the AV interval during NSR. In contrast, the AV interval during ST is physiologically shorter than the AV interval during NSR. Thus, ST can be readily differentiated from "VT" over a range of cycle lengths greater than the crossover value. The overall mean calculated crossover cycle length was 371 +/- 52 msec. In 11 patients paced multiple times, each crossover cycle length was reproducible (mean coefficient of variation was 1.2% +/- 0.9% per patient). AV intervals measured at the RV apex were also analyzed with incremental V pacing during catecholamine stimulation (isoproterenol, n = 5) and during alternate site "VT" (RV outflow tract [n = 8] and left ventricle [n = 2]). In all these cases, the new "VT" plots of AV interval versus pacing cycle length coincided with or fell to the left of those obtained during control RV apical pacing and recording (i.e., these AV interval values crossed the NSR baseline at cycle lengths < or = the crossover cycle length). Thus, the cycle length range for recognizable differentiation of ST from "VT" remained valid. The data suggest that the described AV interval criterion relying on the crossover cycle length: (1) is a promising approach to improve differentiation of ST from relatively slow VTs with 1:1 VA conduction, and (2) can readily be automated in future dual chamber ICDs, given its computational simplicity.
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OBJECTIVE: To test the hypothesis that female prevalence is greater than expected among reported cases of torsades de pointes associated with cardiovascular drugs that prolong cardiac repolarization. DATA SOURCES: A MEDLINE search of the English-language literature for the period of 1980 through 1992, using the terms torsade de pointes, polymorphic ventricular tachycardia, atypical ventricular tachycardia, proarrhythmia, and drug-induced ventricular tachycardia, supplemented by pertinent references (dating back to 1964) from the reviewed articles and by personal communications with researchers involved in this field. STUDY SELECTION: Ninety-three articles were identified describing at least one case of polymorphic ventricular tachycardia (with gender specified) associated with quinidine, procainamide hydrochloride, disopyramide, amiodarone, sotalol hydrochloride, bepridil hydrochloride, or prenylamine. A total of 332 patients were included in the analysis following application of prospectively defined criteria (eg, corrected QT [QTc] interval of 0.45 second or greater while receiving drug). DATA EXTRACTION: Clinical and electrocardiographic descriptors were extracted for analysis. Expected female prevalence for torsades de pointes associated with quinidine, procainamide, disopyramide, and aminodarone was conservatively estimated from gender-specific data reported for antiarrhythmic drug prescriptions in 1986, as derived from the National Disease and Therapeutic Index, a large pharmaceutical database; expected female prevalence for torsades de pointes associated with sotalol, bepridil, and prenylamine was assumed to be 50% or less since these agents are prescribed for male-predominant cardiovascular conditions. RESULTS: Women made up 70% (95% confidence interval, 64% to 75%) of the 332 reported cases of cardiovascular-drug-related torsades de pointes, and a female prevalence exceeding 50% was observed in 20 (83%) of 24 studies having at least four included cases. When analyzed according to various descriptors, women still constituted the majority (range, 51% to 94% of torsades de pointes cases), irrespective of the presence or absence of underlying coronary artery or rheumatic heart disease, left ventricular dysfunction, type of underlying arrhythmia, hypokalemia, hypomagnesemia, bradycardia, concomitant digoxin treatment, or level of QTc at baseline or while receiving drug. When cases of torsades de pointes were analyzed by individual drug, observed female prevalence was always greater than expected, representing a statistically significant difference (P < .05) for all agents except procainamide. CONCLUSIONS: These findings strongly suggest that women are more prone than men to develop torsades de pointes during administration of cardiovascular drugs that prolong cardiac repolarization. The pathophysiological basis for, and therapeutic implications of, this gender disparity should be further investigated.
OBJECTIVES: This study was undertaken to characterize the outcome of survivors of ventricular fibrillation with no or minimal structural heart disease who received an implantable cardioverter-defibrillator. BACKGROUND: The prognosis among survivors of ventricular fibrillation with minimal or no structural cardiac abnormalities remains unclear. Since the advent of implantable cardioverter-defibrillators, this question takes on added importance. METHODS: This 10-center retrospective study provided information on 28 survivors of ventricular fibrillation (mean age 42 years) with minimal or no structural abnormalities who were treated with an implantable cardioverter-defibrillator. RESULTS: Ventricular tachyarrhythmias (polymorphic in all but one patient) were induced during baseline programmed stimulation in 39% of patients. During a median 30.6-month follow-up period after implantable cardioverter-defibrillator implantation, there were no cardiac deaths and two noncardiac deaths. Sixteen patients experienced 36 shock episodes (total 88 shocks). The majority of shocks were classified as "indeterminate"; one patient received 47 "spurious" shocks during one shock episode and each of four patients received one "appropriate" shock. Ventricular arrhythmias were not inducible in any of these latter four patients. CONCLUSIONS: Survivors of ventricular fibrillation with minimal or no structural cardiac abnormalities receiving an implantable cardioverter-defibrillator have an excellent 3-year survival rate. The occurrence, albeit infrequent, of appropriate implantable cardioverter-defibrillator shocks in this group suggests that these patients have a potential risk of recurrent cardiac arrest whose fatal outcome may be avoided by implantable cardioverter-defibrillator therapy.
The effect of ibutilide, a new Class III antiarrhythmic agent, upon acute onset atrial fibrillation was investigated in a closed-chest canine model of acute left ventricular (LV) dysfunction. Twenty-four anesthetized mongrel dogs, mean weight 24.9 +/- 4 kg were subjected to coronary artery microsphere embolization and volume loading, followed by attempted induction of atrial fibrillation (AF) by rapid atrial pacing. Acute ischemic LV dysfunction was successfully induced by embolization in all dogs, and caused significant (P < 0.02) decreases in LV systolic pressure, peak + dp/dt (and -dp/dt), stroke volume, and RR interval; whereas LV end diastolic pressure and QTc significantly increased. Sustained AF (> or = 30 min) was successfully induced in 15 of 24 dogs (62%) and unsustained AF (< 30 min) was induced in the remainder (38%). At 30 minutes after induction of sustained AF, 15 dogs were randomized to intravenous ibutilide (0.15 mg/kg, given as a 0.075 mg/kg bolus, followed by 0.075 mg/kg infusion over 1 hour; n = 7) or placebo (saline; n = 8). There were no statistically significant differences between the ibutilide and the placebo groups with respect to mean LV systolic pressure, LV end diastolic pressure, LV dp/dt, RR interval, or QTc interval during AF prior to infusion. All seven dogs receiving ibutilide converted to sinus rhythm after a median of 3 minutes (range 0.5-26 min), while only three of eight placebo dogs (P < 0.03) converted to sinus rhythm after a median duration of 30 minutes (range 15-60 min) (P < 0.04 for difference in time to conversion).(ABSTRACT TRUNCATED AT 250 WORDS)
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