Mithilesh K. Das

Lesional tachycardias related to mitral valve surgery.

OBJECTIVESnThe purpose of this study was to define the anatomic distribution of electrically abnormal atrial tissue and mechanisms of atrial tachycardia (AT) after mitral valve (MV) surgery.nnnBACKGROUNDnAtrial tachycardia is a well-recognized long-term complication of MV surgery. Because atrial incisions from repair of congenital heart defects provide a substrate for re-entrant arrhythmias in the late postoperative setting, we hypothesized that atriotomies or cannulation sites during MV surgery also contributed to postoperative arrhythmias.nnnMETHODSnIn 10 patients with prior MV surgery, electroanatomic maps were constructed of 11 tachycardias (6 right atrium [RA], 4 left atrium [LA] and 1 biatrial). Activation and voltage maps were used to identify areas of low voltage, double potentials and conduction block.nnnRESULTSnLesions were present in the lateral wall of the RA (six of seven maps) and in the LA along the septum adjacent to the right pulmonary veins (four of five maps). In 8 of 10 patients, these findings corresponded to atrial incisions or cannulation sites. Arrhythmia mechanisms were identified for 9 of 11 tachycardias. A macro-re-entrant circuit was mapped in six cases, three involving lesions in the lateral wall of the RA and three involving the LA septum and right pulmonary veins. In three of these cases figure-of-eight re-entry was demonstrated, and in the other three a single macro-re-entrant circuit was observed. In three other cases, a focal origin was identified adjacent to abnormal tissue in the RA (two cases) or within a pulmonary vein (one case).nnnCONCLUSIONSnSurgical incisions for MV surgery provide a substrate for atrial arrhythmias. Both macro-re-entrant and focal mechanisms contribute to AT after MV surgery.

Response to Adenosine Differentiates Focal From Macroreentrant Atrial Tachycardia Validation Using Three-Dimensional Electroanatomic Mapping

Background—We previously proposed that adenosine has mechanism-specific effects on atrial tachycardia (AT), such that adenosine terminates AT attributable to triggered activity, transiently suppresses automatic rhythms, and has no effect on macroreentrant AT. This, however, remains controversial, because other studies have reported that adenosine terminates reentrant AT. To clarify this issue, we used 3D electroanatomic mapping to delineate the tachycardia circuit and thereby determine whether the response to adenosine differentiates focal from macroreentrant AT. Methods and Results—We examined the effect of adenosine on 43 ATs in 42 consecutive patients (59±15 years of age; 26 female) who received adenosine during tachycardia and whose mechanism of AT was characterized by pharmacological perturbation, entrainment, 3D electroanatomic mapping, and results of radiofrequency ablation. Eight tachycardias were macroreentrant (noncavotricuspid isthmus-dependent), and 35 ATs were focal (either triggered or automatic). Adenosine administered during AT (at doses sufficient to result in AV block) terminated or transiently suppressed focal AT in 33 of 35 cases, whereas 8 of 8 macroreentrant ATs were adenosine insensitive (P <0.001). Twenty-eight of 35 focal ATs were located along the crista terminalis or tricuspid annulus. Conclusions—The response of AT to adenosine can immediately differentiate atrial tachycardia arising from a focal source from that attributable to macroreentry. This finding can be exploited to facilitate developing a focused, strategic ablative approach at the onset of a procedure.

Emerging indications for cardiac pacing.

Substantial data have been accumulated and indications have been well delineated for pacemaker implantation in the treatment of sinus node dysfunction and heart block. However, many other indications have been proposed for pacemaker implantation. In this review, the authors examine available data regarding pacemaker implantation for new indications: neurally mediated syncope, hypertrophic obstructive cardiomyopathy, congestive heart failure, prevention of atrial fibrillation, and the relative merits of single-chamber and dual-chamber pacemakers.

Muscle sympathetic nerve traffic during spontaneous- versus adenosine-mediated termination of idiopathic right ventricular outflow tract tachycardia

I right ventricular outflow tract (RVOT) tachycardia is a well-described example of an adrenergically mediated form of ventricular tachycardia (VT).1 The mechanism responsible for RVOT VT is cyclic adenosine monophosphate-mediated triggered activity. A characteristic and identifying feature of this form of VT is termination in response to a bolus dose of adenosine, which is believed to be related to its antiadrenergic effects. This effect of adenosine on RVOT tachycardia may be mediated on at least 2 sites: (1) the cardiac myocyte,2 and (2) the presynaptic postganglionic sympathetic nerve fibers.3 Although continuous intravenous infusion of adenosine increases sympathetic nerve traffic,4 we have previously demonstrated that a bolus of adenosine results in a biphasic response of muscle sympathetic nerve activity (MSNA).3 An initial increase in MSNA is immediately followed by profound sympathetic withdrawal. We therefore sought to determine if adenosine’s antiarrhythmic effects mediated on RVOT VT were solely related to its direct antiadrenergic effects at the cardiac myocyte, or were also temporally related to its potentially synergistic suppressive effects on MSNA, consistent with a presynaptic postganglionic mechanism of action. • • • We studied 3 patients with RVOT tachycardia who were referred for diagnostic cardiac electrophysiologic study and ablation. All subjects gave informed written consent for a protocol approved by the institutional review board. These patients had the repetitive monomorphic form of RVOT tachycardia.5 This phenotype is characterized by frequent ventricular ectopy as well as multiple episodes of spontaneous sustained VT that increase in frequency and duration during infusion of isoproterenol. This permitted collection of multiple data points within each patient. Patient characteristics are listed in Table 1. All patients had sustained VT with left bundle branch block and inferior axis morphology that terminated with an intravenous bolus of adenosine. VT cycle length in these patients was between 360 and 400 ms. Two patients had structurally normal hearts, and the 1 patient with nearly incessant VT had decreased left ventricular function (ejection fraction 35%). Cardiac catheterization and echocardiography in this patient demonstrated no significant coronary artery or valvular disease and the etiology of the cardiomyopathy was believed to be related to the tachycardia. Subjects underwent continuous recording of 12lead electrocardiography, continuous noninvasive blood pressure monitoring (Finapres, Ohmeda, Louisville, Colorado), and monitoring of respiratory cycles and peroneal MSNA. Peripheral sympathetic nerve traffic was measured by direct microneurographic recordings of efferent MSNA as previously described.6 Bursts of MSNA throughout the entire recording were manually marked. The onset (ti) and offset (tf) points of each burst were identified. The area (A) of each burst was calculated as the sum of the voltage (relative to baseline) Vi Vf at all times t within the burst (ti t tf). A baseline recording of 2 minutes was obtained at the beginning of each study. Bursts during the entire recording period were manually annotated and the area A of each burst was calculated as previously described. From this baseline 2-minute recording, the average of all burst areas was calculated, Aavg. For each subsequent portion of the study, the total area of all bursts AT (where AT is the sum of A for each individual burst during time period T) was calculated. The number of normalized bursts occurring during time T is N AT/Aavg. The frequency of normalized bursts is N/T in units of bursts per second. Continuous noninvasive blood pressure was analyzed as systolic, diastolic, and mean pressures (mm Hg) throughout the recordings. Analysis of variance for repeated measures within subjects was used to determine the statistical significance of changes observed before, during, and after episodes of VT. All data were expressed as mean SD. A p value 0.05 was considered statistically significant. Consistent with the adrenergic-mediated mechanism of RVOT tachycardia, all patients demonstrated an increase in ventricular ectopy as well as sustained VT frequency during infusion of isoproterenol (mean dose 1.5 g/min). Sustained VT was also initiated or terminated with programmed stimulation. Antiadrenergic perturbations that terminated VT included adenFrom the Department of Medicine, Division of Cardiology, The New York Hospital–Cornell Medical Center, New York, New York. This study was supported in part by the Mary and David Hoar Fellowship from the New York Academy of Medicine, New York, New York; Grants R01 56139 and M01RR00047 from the National Institutes of Health, Bethesda, Maryland; the John C. Sable Memorial Heart Fund, Henrietta, New York; Maurice and Corinne Greenberg Arrhythmia Research Grant, New York, New York; and the Raymond and Beverly Sackler Foundation, New York, New York. Dr. Lerman’s address is: Division of Cardiology, The New York Hospital–Cornell Medical Center, 525 East 68th Street, Starr 4, New York, New York 10021. E-mail: blerman@mail.med.cornell.edu. Manuscript received June 12, 2002; revised manuscript received and accepted August 14, 2002.

Endocardial detection of repolarization alternans

Repolarization alternans (RPA) is prognostic of sudden cardiac death and is thought to be mechanistically linked to the initiation of ventricular tachyarrhythmias. We sought to determine whether RPA, which is inherently spatially extended, could be measured using a spatially-localized endocardial lead and, if so, whether RPA could be quantified on a beat-to-beat basis. During diagnostic electrophysiological testing, 21 patients (16M, 5F; 62/spl plusmn/16 yr) were evaluated for surface T-wave alternans (TWA) and endocardial RPA (via a right ventricular apex unipolar recording) during 5 min of 550 ms right atrial pacing. Power spectral analysis indicated that 7/21 patients had both surface TWA and endocardial RPA, 8/21 patients had neither, and 6/21 patients had discordant results (71% concordance; p=0.04). Importantly, unlike surface TWA alternans, endocardial RPA was detectable on a beat-to-beat basis. Given the putative mechanistic link between RPA and ventricular arrhythmias, beat-to-beat endocardial RPA detection might be of diagnostic or therapeutic utility.

Significance of sustained monomorphic ventricular tachycardia induced with short coupling intervals in patients with ischemic cardiomyopathy.

P ventricular stimulation has emerged as an important tool for identifying patients at risk for sudden cardiac death, especially in those with coronary artery disease, left ventricular dysfunction, and nonsustained ventricular tachycardia (VT). Most induction protocols include programmed stimulation with up to triple ventricular extrastimuli at 2 cycle lengths from 2 right ventricular sites. Because of concerns regarding specificity, many electrophysiology laboratories and multicenter trials like the Multicenter Automatic Defibrillator Implantation Trial (MADIT) preclude stimulation at coupling intervals 200 to 180 ms. To determine the specificity of a protocol that permitted the introduction of ventricular extrastimuli at coupling intervals 200 ms, we evaluated patients with coronary artery disease and left ventricular dysfunction undergoing electrophysiologic study for nonsustained VT, and compared the annualized event rates (sustained VT or ventricular fibrillation [VF] requiring implantable cardioverterdefibrillator [ICD] therapy) in patients in whom sustained monomorphic VT or VF was induced with coupling intervals 200 ms with those in whom at least 1 coupling interval was 200 ms. A similar analysis was also performed comparing coupling intervals 180 ms or 180 ms. • • • The study population was derived from 298 consecutive patients with ischemic cardiomyopathy (ejection fraction 40%) and nonsustained VT (lasting for 3 beats and 30 seconds at a rate 100 beats/min) who were evaluated for inducibility of sustained ventricular tachyarrhythmias. After giving written informed consent, patients underwent electrophysiologic study after an overnight fast. Quadripolar catheters were advanced under fluoroscopic guidance to the high right atrium, His bundle position, and right ventricular apex, and to the right ventricular outflow tract if VT was not induced from the right ventricular apex. Bipolar intracardiac electrograms were filtered at 30 to 500 Hz and recorded on optical disk. Ventricular stimulation was performed at 4 times diastolic threshold using a pulse width of 2 ms, and extrastimuli were introduced until refractoriness was reached. Electrophysiologic study included the introduction of up to 3 extrastimuli at 2 right ventricular sites delivered during 2 drive cycle lengths. Extrastimuli were delivered using an iterative protocol. For example, during delivery of triple ventricular extrastimuli, a second extrastimulus (S3) was routinely decremented after the third extrastimulus (S4) failed to capture. When both extrastimuli subsequently captured the ventricles, S4 was once again decremented. This iterative process was repeated until S3 achieved refractoriness. This sequence was then duplicated using all 3 extrastimuli and was completed when the first extrastimulus reached absolute refractoriness. If sustained monomorphic VT was not inducible with up to triple ventricular extrastimuli from 2 right ventricular sites, isoproterenol was infused (in contrast to MADIT and the Multicenter Unsustained Tachycardia Trial [MUSTT]). The isoproterenol dose was titrated to increase the baseline heart rate by 20% to 25%, and programmed stimulation was repeated from the right ventricular outflow tract. Positive end points for induction included sustained monomorphic VT regardless of cycle length or polymorphic VT/VF (induced with single or double extrastimuli). All inducible patients received an ICD. Appropriate device therapy (antitachycardia therapy or shock) was confirmed during ICD interrogation at 3to 6-month intervals or immediately after a defibrillator discharge. Comparison of group means was performed using the paired t test or Mann-Whitney test as appropriate (SPSS for Windows, 9.0, SPSS Inc., Chicago, Illinois). In addition, Kaplan-Meier survival analysis was performed to ascertain differences in time to first arrhythmic event requiring device therapy (antitachycardia therapy or shock). For all comparisons, a p value 0.05 was required to reject the null hypothesis. One hundred seven patients received an ICD for either sustained monomorphic VT (101 patients) or polymorphic VT/VF induced with single or double ventricular extrastimuli (6 patients). Two patients died due to nonarrhythmic causes within the first 3 months of ICD implant and 3 patients were lost to follow-up. The mean age was 67 11 years and 86 patients (84%) were men. Seventy-three patients (72%) required triple ventricular extrastimuli for induction. From the Department of Medicine, Division of Cardiology, New York Hospital-Cornell University Medical Center, New York, New York. This work was supported in part by Grant RO1 HL-56139 from the National Institutes of Health, Bethesda, Maryland, and grants from the American Heart Association Grand-in-Aid, New York Affiliate, the Maurice and Corinne Greenberg Arrhythmia Research Grant, and the Raymond and Beverly Sackler Foundation, New York, New York. Dr. Lerman’s address is: Division of Cardiology, The New York HospitalCornell Medical Center, 525 East 68th Street, Starr 409, New York, New York 10021. E-mail: blerman@med.cornell.edu. Manuscript received August 13, 2001; revised manuscript received and accepted January 7, 2002.