Clinical consequences of electrocardiographic artifact mimicking ventricular tachycardia.
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Biomedical subjects
Publications and source records attributed to F Morady.
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Two hundred patients with atrial fibrillation underwent transthoracic cardioversion using adhesive electrodes positioned at the apex and right infraclavicular area, and the apex electrode was randomly selected to serve as the cathode or anode. The mean defibrillation energy requirement with the cathodal configuration was significantly lower than with the anodal configuration.
BACKGROUND: High-intensity focused ultrasound has been applied to internal organs from outside the body to ablate tissue. No published study has assessed the feasibility of ablating cardiac tissue within the beating heart by use of this type of therapeutic ultrasound. The purpose of this study was to determine whether high-intensity focused ultrasound can be used to ablate the atrioventricular (AV) junction within the beating heart. METHODS AND RESULTS: Ten dogs were anesthetized and underwent a thoracotomy. The heart was covered with a polyvinyl chloride membrane. The thorax above the membrane was perfused with degassed water, which functioned as a coupling medium for the ultrasound. A 7.0-MHz diagnostic ultrasound probe was affixed to a spherically focused 1.4-MHz high-intensity focused ultrasound transducer with a 1.1x8.3-mm focal zone 63.5 mm from the ablation transducer. The diagnostic ultrasound probe was calibrated such that the location of the focal zone of the ablation transducer was identifiable on the 2-dimensional ultrasound image. Target sites were identified with the diagnostic ultrasound. The maximum ultrasound intensity for ablation (2.8 kW/cm2) was delivered to the AV junction only during electrical diastole and for a total of 30 seconds. Complete AV block was achieved in each of the 10 dogs with 6.5+/-5.6 (range, 3 to 21) 30-second applications of therapeutic ultrasound. Gross inspection showed that the mean lesion volume was 124+/-143 mm3, with a depth of 6.7+/-3.6 mm, a length of 5.7+/-2.5 mm, and a width of 4.7+/-1.8 mm. Four hours after the dogs were killed, histopathological study demonstrated a well-demarcated area of necrosis and early inflammation. CONCLUSIONS: High-intensity focused ultrasound produces well-demarcated lesions and appears to be a feasible energy source to create complete AV block within the beating heart without damaging the overlying or underlying cardiac tissue. This energy source may allow for a noninvasive approach to ablation of cardiac arrhythmias.
BACKGROUND: Atrial fibrillation cannot always be converted to sinus rhythm by transthoracic electrical cardioversion. We examined the effect of ibutilide, a class III antiarrhythmic agent, on the energy requirement for atrial defibrillation and assessed the value of this agent in facilitating cardioversion in patients with atrial fibrillation that is resistant to conventional transthoracic cardioversion. METHODS: One hundred patients who had had atrial fibrillation for a mean (+/-SD) of 117+/-201 days were randomly assigned to undergo transthoracic cardioversion with or without pretreatment with 1 mg of ibutilide. We designed a step-up protocol in which shocks at 50, 100, 200, 300, and 360 J were used for transthoracic cardioversion. If transthoracic cardioversion was unsuccessful in a patient who had not received ibutilide pretreatment, ibutilide was administered and transthoracic cardioversion attempted again. RESULTS: Conversion to sinus rhythm occurred in 36 of 50 patients who had not received ibutilide (72 percent) and in all 50 patients who had received ibutilide (100 percent, P<0.001). In all 14 patients in whom transthoracic cardioversion alone failed, sinus rhythm was restored when cardioversion was attempted again after the administration of ibutilide. Pretreatment with ibutilide was associated with a reduction in the mean energy required for defibrillation (166+/-80 J, as compared with 228+/-93 J without pretreatment; P<0.001). Sustained polymorphic ventricular tachycardia occurred in 2 of the 64 patients who received ibutilide (3 percent), both of whom had an ejection fraction of 0.20 or less. The rates of freedom from atrial fibrillation after six months of follow-up were similar in the two randomized groups. CONCLUSIONS: The efficacy of transthoracic cardioversion for converting atrial fibrillation to sinus rhythm was enhanced by pretreatment with ibutilide. However, use of this drug should be avoided in patients with very low ejection fractions.
BACKGROUND: Conversion of chronic atrial fibrillation (AF) is associated with atrial stunning, but the short-term effect of a brief episode of AF on left atrial appendage (LAA) emptying velocity is unknown. The purpose of this study was to determine whether a short episode of AF affects left atrial function and whether verapamil modifies this effect. METHODS AND RESULTS: The subjects of this study were 19 patients without structural heart disease undergoing an electrophysiology procedure. In 13 patients, LAA emptying velocity was measured by transesophageal echocardiography in the setting of pharmacological autonomic blockade before, during, and after a short episode of AF. During sinus rhythm, the baseline LAA emptying velocity was measured 5 times and averaged. AF was then induced by rapid right atrial pacing. After either spontaneous or electrical conversion, LAA emptying velocity was measured immediately on resumption of sinus rhythm and every minute thereafter. The mean duration of AF was 15.3+/-3.8 minutes. The mean baseline emptying velocity was 70+/-20 cm/s. The first post-AF emptying velocity was 63+/-20 cm/s (P=0.02 versus baseline emptying velocity). The post-AF emptying velocity returned to the baseline emptying velocity value after 3.0 minutes. The mean percent reduction in post-AF emptying velocity was 9.7+/-21% (range, 15% increase to 56% decrease). A second group of 6 patients were pretreated with verapamil (0.1-mg/kg IV bolus followed by an infusion of 0.005 mg. kg-1. min-1). In these patients, the first post-AF emptying velocity, 58+/-14 cm/s, was not significantly different from the pre-AF emptying velocity, 60+/-13 cm/s (P=0.08). CONCLUSIONS: In humans, several minutes of AF may be sufficient to induce atrial contractile dysfunction after cardioversion. When atrial contractile dysfunction occurs, there is recovery of AF within several minutes. AF-induced contractile dysfunction is attenuated by verapamil and may be at least partially mediated by cellular calcium overload.
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Tumor necrosis factor-alpha (TNF-alpha) has been implicated in the pathogenesis of congestive heart failure and may be associated with an increase in mortality. A recent in vitro study showed that amiodarone decreases TNF-alpha production by human blood mononuclear cells in response to lipopolysaccharide. However, no previous clinical studies have determined the effect of chronic amiodarone therapy on TNF-alpha levels. Thus, the purpose of this study was to determine whether amiodarone affects TNF-alpha levels in patients with ischemic and nonischemic cardiomyopathy. TNF-alpha levels were analyzed by an enzyme-linked immunoassay using plasma samples at baseline, 1, and 2 years of follow-up in New York Heart Association class III patients (n = 40 in each of the placebo and amiodarone groups, mean ejection fraction 0.25+/-0.09) who were randomized in the Congestive Heart Failure-Survival Trial of Antiarrhythmic Therapy, a multicenter, double-blind, placebo-controlled study in which the effect of amiodarone on survival was investigated. TNF-alpha levels were elevated in both groups of patients at baseline, 6.6+/-3.1 and 7.7+/-5.3 pg/ml in the amiodarone and placebo groups, respectively (p = 0.3). There were no significant differences in demographic or clinical variables between the 2 groups. Amiodarone treatment was associated with a significant increase in TNF-alpha levels in patients with ischemic cardiomyopathy, 12.7+/-12.5 and 6.8+/-3.7 pg/ml in the amiodarone and placebo groups, respectively (p = 0.03) at 1 year. No change in TNF-alpha levels was observed in patients with nonischemic cardiomyopathy. In contrast to the in vitro data, amiodarone treatment is associated with an increase in TNF-alpha levels in patients with ischemic cardiomyopathy. This increase is not associated with an adverse effect on survival.
The purpose of this study was to determine the ability of physicians to differentiate atrial flutter from atrial fibrillation on a surface electrocardiogram (ECG). A questionnaire containing three 12-lead ECGs was mailed to 689 physicians, with multiple-choice questions asking whether the rhythm on each ECG was atrial flutter or atrial fibrillation. ECG 1 showed atrial fibrillation with prominent atrial activity (>0.2 mV) in lead V1; ECG 2 displayed atrial fibrillation with prominent atrial activity (>0.2 mV) in leads III and V1; and ECG 3 displayed atrial flutter. Overall, ECG1 was correctly identified as atrial fibrillation by 79% of physicians, ECG 2 was correctly identified as atrial fibrillation by 31%, and ECG 3 was correctly identified as atrial flutter by 90%. Cardiology fellows and cardiologists correctly identified ECG 1 more often than house officers and internists (95% vs 63%; P < or = .01). ECG 2 was correctly identified by 26% of cardiology fellows and cardiologists and by 37% of house officers and internists (P = .10). ECG 3 was correctly identified by 91% of cardiology fellows and cardiologists and by 82% of house officers and internists (P = .06). In conclusion, atrial fibrillation is frequently misdiagnosed as atrial flutter. Misdiagnosis of atrial fibrillation occurs more often when atrial activity is prominent on an ECG in more than one lead.
OBJECTIVE: The purpose of this study is to review the clinical course of persistent junctional reciprocating tachycardia (PJRT) in 21 patients spanning a wide age range to examine the electrophysiologic characteristics of the conduction system in these patients with PJRT, particularly in regards to its incessant nature and to evaluate the long-term response to radiofrequency ablation. BACKGROUND: Persistent junctional reciprocating tachycardia is uncommon, occurring in 1% of patients with supraventricular tachycardia. Its presentation, course and treatment are incompletely characterized. METHODS: The clinical, electrocardiographic, electrophysiologic and echocardiographic data of 21 patients with PJRT were reviewed. RESULTS: In 9 of these 21 patients, the mean tachycardia cycle length increased significantly (p < 0.0001) as the patients grew, from a mean tachycardia cycle length of 308+/-64 ms in the patients less than 2 years, 414+/-57 ms in the patients between 2 years and 5 years, to 445+/-57 ms in the patients greater than 5 years, primarily due to slowing of retrograde conduction in the accessory pathway. Persistent junctional reciprocating tachycardia was associated with impaired ventricular function in 11, improving spontaneously in 4 and, after successful ablation of the accessory pathway, in 7. All patients except one were uncontrolled on one or more medications. Ablation of the accessory pathway was successful in 19 of 21 patients. CONCLUSIONS: We conclude that PJRT is characterized by an onset in early childhood and by an age-related prolongation of the tachycardia cycle length mediated primarily through conduction delay in the concealed, retrogradely conducting accessory pathway. Ablation of the accessory pathway provides definitive treatment for PJRT.
OBJECTIVE: The purpose of this study was to determine if the atrial response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction during paroxysmal supraventricular tachycardia is a useful diagnostic maneuver in the electrophysiology laboratory. BACKGROUND: Despite various maneuvers, it can be difficult to differentiate atrial tachycardia from other forms of paroxysmal supraventricular tachycardia. METHODS: The response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction was studied during four types of tachycardia: 1) atrioventricular nodal reentry (n = 102), 2) orthodromic reciprocating tachycardia (n = 43), 3) atrial tachycardia (n = 19) and 4) atrial tachycardia simulated by demand atrial pacing in patients with inducible atrioventricular nodal reentry or orthodromic reciprocating tachycardia (n = 32). The electrogram sequence upon cessation of ventricular pacing was, categorized as "atrial-ventricular" (A-V) or "atrial-atrial-ventricular" (A-A-V). RESULTS: The A-V response was observed in all cases of atrioventricular nodal reentrant and orthodromic reciprocating tachycardia. In contrast, the A-A-V response was observed in all cases of atrial tachycardia and simulated atrial tachycardia, even in the presence of dual atrioventricular nodal pathways or a concealed accessory atrioventricular pathway. CONCLUSIONS: In conclusion, an A-A-V response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction is highly sensitive and specific for the identification of atrial tachycardia in the electrophysiology laboratory.
OBJECTIVES: The purpose of this study was to determine the outcome of patients with nonischemic dilated cardiomyopathy, unexplained syncope and a negative electrophysiology test who are treated with an implantable defibrillator. BACKGROUND: Patients with nonischemic cardiomyopathy and unexplained syncope may be at high risk for sudden cardiac death, and they are sometimes treated with an implantable defibrillator. METHODS: This study prospectively determined the outcome of 14 consecutive patients who had a nonischemic cardiomyopathy, unexplained syncope and a negative electrophysiology test and who underwent defibrillator implantation (Syncope Group). Nineteen consecutive patients with a nonischemic cardiomyopathy and a cardiac arrest who were treated with a defibrillator (Arrest Group) served as a control group. RESULTS: Seven of 14 patients (50%) in the Syncope Group received appropriate shocks for ventricular arrhythmias during a mean follow-up of 24+/-13 months, compared with 8 of 19 patients (42%) in the Arrest Group during a mean follow-up of 45+/-40 months (p = 0.1). The mean duration from device implantation until the first appropriate shock was 32+/-7 months (95% confidence interval [CI], 18 to 45 months) in the Syncope Group compared to 72+/-12 months (95% CI, 48 to 96 months) in the Arrest Group (p = 0.1). Among patients who received appropriate shocks, the mean time from defibrillator implantation to the first appropriate shock was 10+/-14 months in the Syncope Group, compared with 48+/-47 months in the Arrest Group (p = 0.06). Recurrent syncope was always associated with ventricular tachyarrhythmias. CONCLUSIONS: The high incidence of appropriate defibrillator shocks and the association of recurrent syncope with ventricular arrhythmias support the treatment of patients with nonischemic cardiomyopathy, unexplained syncope and a negative electrophysiology test with an implantable defibrillator.
BACKGROUND: The effect of general anesthesia on defibrillation efficacy in humans is not known. The purpose of this study was to determine the effect of general anesthesia on the defibrillation energy requirements in patients undergoing implantation of a pectoral defibrillator. METHODS AND RESULTS: Nineteen consecutive patients who underwent defibrillator implantation under general anesthesia were prospectively compared to 16 consecutive patients who underwent defibrillator implantation by the same physicians, using similar devices, at another hospital under conscious sedation. Pre-discharge testing was performed 1.4 +/- 1.0 days after implant using sedation in both groups. The defibrillation energy requirement was determined using the same predefined step-down protocol (15, 10, 8, 5, 3, 1 J) at the time of implantation and during pre-discharge testing. The clinical characteristics of the patients were similar between groups. There was no significant difference in the mean implant defibrillation energy requirement compared to the mean pre-discharge defibrillation energy requirement in either the general anesthesia group (8.5 +/- 4.7 vs. 8.4 +/- 3.4 J; p = 0.9) or in the conscious sedation group (9.4 +/- 3.9 vs. 9.0 +/- 3.8 J; p = 0.7). CONCLUSIONS: When compared to conscious sedation, general anesthesia with mechanical ventilation has no significant effect on defibrillation efficacy in patients undergoing defibrillator implantation.
Prior studies have demonstrated that sympathetic tone may influence the effects of adenosine on His-Purkinje automaticity, and that enhanced vagal tone may influence its effects on the sinus node. However, the interaction between autonomic tone and the effects of adenosine on the sinus node in humans remains unknown. Therefore, this study was designed to investigate the interaction between different states of autonomic tone and the bradycardiac response of the sinus node to adenosine. In 11 patients without structural heart disease who underwent a clinically indicated electrophysiology procedure, the sinus cycle length was measured before and after a 12-mg bolus of adenosine in the baseline state, during an infusion of 2 mcg/min of isoproterenol, after the administration of 0.2 mg/kg of propranolol, and again after the administration of 0.04 mg/kg of atropine. Adenosine significantly lengthened the sinus cycle length in the baseline state (760 +/- 165 vs 909 +/- 188 ms, P < 0.05), during isoproterenol infusion (516 +/- 67 vs 766 +/- 146 ms, P < 0.05), after propranolol (850 +/- 153 vs 914 +/- 143 ms, P < 0.05) and after the combination of propranolol and atropine (662 +/- 76 vs 801 +/- 121 ms, P < 0.05). The degree of lengthening in sinus cycle length was significantly greater (P < 0.05) during isoproterenol infusion (253 +/- 157 ms, or 51% +/- 40%) than in the baseline state (149 +/- 85 ms, or 20% +/- 12%), after propranolol (68 +/- 53 ms, or 8% +/- 8%), and after propranolol and atropine (140 +/- 110 ms, or 21% +/- 18%). The negative chronotropic effect of adenosine is influenced by autonomic tone. The effect of adenosine on the sinus node is accentuated by beta-adrenergic stimulation and unaffected by beta-adrenergic blockade or combined beta-adrenergic and cholinergic blockade.
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INTRODUCTION: The relationship between temperature at the electrode-tissue interface and the loss of AV and ventriculoatrial (VA) conduction is not established, and the optimal target temperature for the slow pathway approach to radiofrequency ablation of AV nodal reentrant tachycardia (AVNRT) is unknown. Therefore, the purpose of this study was to compare target temperatures of 48 degrees C and 60 degrees C during the slow pathway approach to ablation of AVNRT. METHODS AND RESULTS: The study included 138 patients undergoing ablation for AVNRT. Patients undergoing slow pathway ablation using closed-loop temperature monitoring were randomly assigned to a target temperature of either 48 degrees C or 60 degrees C. The primary success rates were 76% in the patients assigned to 48 degrees C and 100% in the patients assigned to 60 degrees C (P < 0.01). The ablation procedure duration (33 +/- 31 min vs 26 +/- 28 min; P = 0.2), fluoroscopic time (25 +/- 15 min vs 24 +/- 16 min; P = 0.5), and mean number of applications (9.3 +/- 6.5 vs 7.8 +/- 8.1; P = 0.3) were similar in patients assigned to 48 degrees and 60 degrees C, respectively. The mean temperature (46.1 degrees +/- 24.8 degrees C vs 48.7 +/- 3.2 degrees C; P < 0.01), the temperature associated with junctional ectopy (48.1 degrees +/- 2.0 degrees C vs 53.5 degrees +/- 3.5 degrees C, P < 0.0001), and the frequency of VA block during junctional ectopy (24.6% vs 37.2%; P < 0.0001) were less in the patients assigned to 48 degrees C compared to 60 degrees C. The frequency of transient or permanent AV block was similar in each group (2.8% vs 3.6%; P = 0.2). In the 60 degrees C group, only 12% of applications achieved an electrode temperature of 60 degrees C. During follow-up of 9.9 +/- 4.2 months, there was one recurrence of AVNRT in the 48 degrees C group and none in the 60 degrees C group. CONCLUSIONS: Compared to 48 degrees C, a target temperature of 60 degrees C during radiofrequency slow pathway ablation is associated with a higher primary success rate and a higher incidence of VA block during junctional ectopy induced by the radiofrequency energy. AV block is not more common with the higher target temperature, but only if VA conduction is aggressively monitored during applications of radiofrequency energy.
INTRODUCTION: The purpose of our study was to evaluate the effect of repeated cardioversion with an implantable atrial defibrillator on the clinical outcome of patients with atrial fibrillation. METHODS AND RESULTS: The effects of the implantable atrial defibrillator on the total duration of atrial fibrillation, number of atrial fibrillation recurrences, and left atrial size were evaluated prospectively in 16 patients with atrial fibrillation (13 men and 3 women; mean age 58 +/- 11 years). Seven patients had no cardiovascular disease, 5 patients had hypertension, 3 patients had coronary heart disease, and 1 patient had congenital heart disease. Eight patients had paroxysmal atrial fibrillation for a mean duration of 80 +/- 61 months, and eight patients had persistent atrial fibrillation for a mean duration of 68 +/- 119 months. Except for one patient who received digoxin throughout the study, all patients received the same Class I or III antiarrhythmic agent throughout the study. The implantable atrial defibrillator successfully converted 50 (93%) of 54 spontaneous episodes of atrial fibrillation in 12 patients. During the initial 3 months of clinical follow-up, the atrial defibrillator documented 261 +/- 270 hours of atrial fibrillation compared with 126 +/- 172 hours (P = 0.01) during the subsequent 3 months. The left atrial size decreased from 4.4 +/- 0.7 cm at the time of atrial defibrillator implantation to 4.1 +/- 0.6 cm (P = 0.02) 6 months later. The number of atrial fibrillation recurrences did not change. These findings were observed in the absence of changes in drug therapy. No complications were observed. CONCLUSION: Restoration and maintenance of sinus rhythm in patients with atrial fibrillation by repeated cardioversion with an implantable atrial defibrillator was associated with a reduction in the total arrhythmia duration and a reduction in left atrial size. These results suggest that maintenance of sinus rhythm with the atrial defibrillator may reverse the remodeling process associated with atrial fibrillation.
INTRODUCTION: The postpacing interval (PPI) has been used to discriminate bystander sites from critical sites within a ventricular tachycardia (VT) reentry circuit, with a PPI that is similar to the VT cycle length (CL) being indicative of a site within the reentry circuit. The purpose of this study was to assess the clinical value of the PPI for identifying effective target sites for ablation of VT at sites of concealed entrainment in patients with prior myocardial infarction. METHODS AND RESULTS: In 24 patients with coronary artery disease and a past history of myocardial infarction, 36 VTs with a mean CL of 483+/-80 msec (+/- SD) were mapped and targeted for radiofrequency (RF) ablation. The only criterion used to select target sites for ablation was concealed entrainment. In a post hoc analysis, the PPI was measured at 47 ineffective and 26 effective ablation sites. The mean PPI-VTCL difference at the 26 effective sites (114+/-137 msec) did not differ significantly from the mean at the 47 ineffective sites (177+/-161 msec; P = 0.1). The sensitivity of a PPI-VTCL difference < or = 30 msec for identifying an effective ablation site was 46%, the specificity 64%, the positive predictive value 41%, and the negative predictive value 68%. CONCLUSION: The PPI-VTCL difference is not useful for discriminating between sites of concealed entrainment that are within or outside of a VT reentry circuit in patients with prior infarction. Therefore, in patients with prior infarction, the PPI is not clinically useful for identifying sites of concealed entrainment at which RF ablation should or should not be attempted.