Subclinical pulmonary vein narrowing after ablation for atrial fibrillation.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M E Josephson.
Explore the source record for details and available documents.
In atrial tachycardias, catheter ablation using conventional mapping system is associated with high immediate success and low recurrence. Three-dimensional electroanatomical mapping system combined to catheter ablation of atrial tachycardias has reached, in small uncontroled series, success rates of 100%. However, limited data are available about rates of recurrence or complication using this approach. In order to compare both mapping systems, we have conducted a study of 65 consecutive patients (36 women and 29 men) that underwent both electrophysiologic study and catheter ablation for suspected atrial tachycardias. Pre-existing heart disease was noted in 43%, hypertension in 32% and a history of atrial fibrillation of flutter in 52%. Catheter ablation guided by conventional mapping was undertaken in 44 patients and by three-dimensional electroanatomical mapping in 21. Successful ablation was performed in 68% of patients with conventional mapping and in 90% with three-dimensional electroanatomical mapping. No complication and recurrence were observed with the latter approach, while 5 patients had a recurrence and 2 had immediate complication with conventional mapping. Catheter ablation of atrial tachycardias combined with three-dimensional electroanatomical mapping appeared to be effective and safe, however, conventional mapping system still remains a reliable approach that must be considered as the first choice for atrial tachycardias ablation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: The terms counterclockwise (CC) and clockwise (C) atrial flutter (Afl) are used to describe right atrial activation around the tricuspid valve in the left anterior oblique view. The manner in which the left atrium is activated, as reflected by coronary sinus (CS) recordings, has not been systematically evaluated. METHODS AND RESULTS: Nine patients with both CC and C Afl underwent electrophysiological study with CS recordings during both rhythms with the use of a decapolar catheter with the tip placed in the distal CS. Patterns of CS activation during each type of Afl as well as during during sinus rhythm were categorized into 1 of 3 patterns: sequential proximal-to-distal, sequential distal-to-proximal, and fused, indicating activation from different directions. In 7 of 9 patients, the pattern of CS activation in CC Afl and C Afl differed, with a proximal-to-distal pattern in CC Afl and a fused pattern in C Afl. In 2 patients, pacing the high right atrial septum near the presumed site of Bachmann's bundle in sinus rhythm showed a similar fused pattern of CS activation. CONCLUSIONS: These results demonstrate different patterns of CS activation in CC Afl and C Afl in the majority of patients and are consistent with a model in which the left atrium is activated predominantly over Bachmann's bundle during C Afl and over the CS os in CC Afl. These findings may have implications for maintenance of Afl, interpretation of flutter wave morphology on surface ECG, and left atrial mechanical function in Afl.
BACKGROUND: An abnormal signal-averaged ECG (SAECG) is a noninvasive marker of the substrate of sustained ventricular tachycardia after myocardial infarction. We assessed its prognostic ability in patients with asymptomatic unsustained ventricular tachycardia, coronary artery disease, and left ventricular dysfunction. METHODS AND RESULTS: A blinded core laboratory analyzed SAECG tracings from 1925 patients in a multicenter trial. Cox proportional hazards modeling was used to examine individual and joint relations between SAECG variables and arrhythmic death or cardiac arrest (primary end point), cardiac death, and total mortality. We also assessed the prognostic utility of SAECG at different levels of ejection fraction (EF). A filtered QRS duration >114 ms (abnormal SAECG) independently predicted the primary end point and cardiac death, independent of clinical variables, cardioverter-defibrillator implantation, and antiarrhythmic drug therapy. With an abnormal SAECG, the 5-year rates of the primary end point (28% versus 17%, P=0.0001), cardiac death (37% versus 25%, P=0.0001), and total mortality (43% versus 35%, P=0.0001) were significantly higher. The combination of EF <30% and abnormal SAECG identified a particularly high-risk subset that constituted 21% of the total population. Thirty-six percent and 44% of patients with this combination succumbed to arrhythmic and cardiac death, respectively. CONCLUSIONS: SAECG is a powerful predictor of poor outcomes in this population. The noninvasive combination of an abnormal SAECG and reduced EF may have utility in selecting high-risk patients for intervention.
BACKGROUND: Resetting has been used to characterize reentrant circuits causing clinical tachycardias. METHODS AND RESULTS: To determine the mechanisms of resetting, sustained ventricular tachycardia was induced in dogs with 4-day-old myocardial infarctions by programmed stimulation. Premature stimulation was accomplished from multiple regions within reentrant circuits; resetting curves were constructed and compared with activation maps. Monotonically increasing responses, or a "mixed" response (increasing portion preceded by a flat portion), occurred. All reentrant circuits had a fully excitable gap. Interval-dependent conduction delay and concealed retrograde penetration led to increased resetting response curves. CONCLUSIONS: Multiple mechanisms revealed by mapping cause resetting of reentrant circuits.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVE: To test the potential of gene transfer approaches to enhance cardiac chronotropy in a porcine system as a model of the human heart. METHODS: Plasmids encoding either the human beta(2) adrenergic receptor or control constructs were injected into the right atria of native Yorkshire pig hearts. Percutaneous electrophysiological recording catheters equipped with 33 gauge circular injection needles were positioned in the mid-lateral right atrium. At the site of the earliest atrial potential the circular injection needles were rotated into the myocardium and the beta(2) adrenergic receptor (n = 6) or control plasmid constructs (n = 5) were injected. RESULTS: Injection of the beta(2) adrenergic receptor construct significantly enhanced chronotropy compared with control injections. The average (SD) heart rate of the pigs was 108 (16) beats/min before injection. Two days after injection with control plasmids the heart rate was 127 (25) beats/min (NS compared with preinjection rates). After injection with plasmid encoding the beta(2) adrenergic receptor the heart rate increased by 50% to 163 (33) beats/min (p < 0.05 compared with preinjection and postinjection control rates). CONCLUSIONS: The present studies showed in a large animal model that local targeting of gene expression may be a feasible modality to regulate cardiac pacemaking activity. In addition, these investigations provide an experimental basis for developing future clinical gene transfer approaches to upregulate heart rate and modulate cardiac conduction.
Sudden cardiac death, which accounts for approximately 350,000 deaths each year, is a major health care problem. Antiarrhythmic drugs have not been reliable in preventing sudden cardiac death. Although beta-blockers, angiotensin-converting enzyme inhibitors, and revascularization play a role in prevention of sudden cardiac death, the development and subsequent refinement of the implantable cardioverter-defibrillator has made the most important contribution to its management. Several randomized, controlled trials have demonstrated improved survival in patients resuscitated from cardiac arrest. Two recent trials also suggest a role for primary prevention in selected patients with coronary artery disease, ventricular dysfunction, and nonsustained ventricular tachycardia in whom sustained ventricular tachycardia is induced. Further technological refinements and development of new, more sensitive risk stratifiers with a higher positive predictive value for sudden cardiac death will expand the indications for this life-saving therapy.
Explore the source record for details and available documents.
OBJECTIVES: We sought to evaluate the utility of excluding myocardial infarction (MI) in patients presenting to the emergency department (ED) with atrial fibrillation (AF) and to identify predictors of MI in this group. BACKGROUND: Patients with AF are frequently admitted to the hospital, in part, to exclude an associated MI. There are no prospective data on unselected patients to support this common practice. METHODS: We conducted a prospective cohort study of all patients who presented to a single-center ED with the primary diagnosis of AF. RESULTS: Of a total of 255 patients, 190 (75%) were admitted to the hospital, and 109 of them underwent a standard "rule-out MI" protocol. Of these 109 patients, six (5.5%) were identified as having an acute MI at the time of admission. Chest pain was present in 39% of patients, with a sensitivity and specificity for the occurrence of MI of 100% and 65%, respectively. ST segment elevation or depression was present in 43% of patients, with a sensitivity and specificity of 100% and 51%. The presence of either major ST segment depression (>2 mm) or elevation on the admission electrocardiogram (ECG) was present in 6%, with a sensitivity of 100% and a specificity of 99%. The resulting positive and negative predictive values were 86% (95% confidence interval [CI] 42% to 99%) and 100% (95% CI 96% to 100%), respectively. Use of this criterion would have reduced the number of rule-out MIs in our study group by 94%, with no loss of sensitivity. CONCLUSIONS: Chest pain and ST segment depression are extremely common findings in patients presenting to the ED with AF and have limited power to predict MI. In contrast, ECG evidence of ST segment elevation or depression >2 mm appears to be a reliable discriminator of which patients are at risk for MI. Patients without significant ST segment changes are at very low risk for MI and may not require performance of the rule-out MI protocol or hospital admission if clinically stable.
Explore the source record for details and available documents.
We describe the case of a 32-year-old woman with palpitations and atrial fibrillation (AF) as the only documented arrhythmia. The patient underwent electrophysiologic study and was found to have inducible AV nodal reentrant tachycardia (AVNRT). During a prolonged episode of AVNRT, AF developed in both atria, but AVNRT persisted. Dissociation of the atria during AVNRT is evidence that the atrium is not necessary in AVNRT. This case also illustrates the utility of an electrophysiologic study in locating a potentially curable arrhythmia as the primary cause of AF in young patients.
BACKGROUND: Empirical antiarrhythmic therapy has not reduced mortality among patients with coronary artery disease and asymptomatic ventricular arrhythmias. Previous studies have suggested that antiarrhythmic therapy guided by electrophysiologic testing might reduce the risk of sudden death. METHODS: We conducted a randomized, controlled trial to test the hypothesis that electrophysiologically guided antiarrhythmic therapy would reduce the risk of sudden death among patients with coronary artery disease, a left ventricular ejection fraction of 40 percent or less, and asymptomatic, unsustained ventricular tachycardia. Patients in whom sustained ventricular tachyarrhythmias were induced by programmed stimulation were randomly assigned to receive either antiarrhythmic therapy, including drugs and implantable defibrillators, as indicated by the results of electrophysiologic testing, or no antiarrhythmic therapy. Angiotensin-converting-enzyme inhibitors and beta-adrenergic-blocking agents were administered if the patients could tolerate them. RESULTS: A total of 704 patients with inducible, sustained ventricular tachyarrhythmias were randomly assigned to treatment groups. Five-year Kaplan-Meier estimates of the incidence of the primary end point of cardiac arrest or death from arrhythmia were 25 percent among those receiving electrophysiologically guided therapy and 32 percent among the patients assigned to no antiarrhythmic therapy (relative risk, 0.73; 95 percent confidence interval, 0.53 to 0.99), representing a reduction in risk of 27 percent). The five-year estimates of overall mortality were 42 percent and 48 percent, respectively (relative risk, 0.80; 95 percent confidence interval, 0.64 to 1.01). The risk of cardiac arrest or death from arrhythmia among the patients who received treatment with defibrillators was significantly lower than that among the patients discharged without receiving defibrillator treatment (relative risk, 0.24; 95 percent confidence interval, 0.13 to 0.45; P<0.001). Neither the rate of cardiac arrest or death from arrhythmia nor the overall mortality rate was lower among the patients assigned to electrophysiologically guided therapy and treated with antiarrhythmic drugs than among the patients assigned to no antiarrhythmic therapy. CONCLUSIONS: Electrophysiologically guided antiarrhythmic therapy with implantable defibrillators, but not with antiarrhythmic drugs, reduces the risk of sudden death in high-risk patients with coronary disease.
Rhythm disturbances can range from the harmless to the life-threatening, and treatment varies accordingly, from watchful waiting to emergency intervention. Traditional antiarrhythmic medications have largely been supplanted by newer agents; pharmacologic therapy is giving way to device-based treatment, including pacemakers, defibrillators, and catheter ablation.