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Methadone and QT Prolongation. Background: Methadone is associated with QTc prolongation and sudden death in susceptible patients. We sought to investigate whether there is a gender-based difference in susceptibility to methadone-associated QTc prolongation in heroin-dependent patients receiving a low-dose treatment regimen. Methods: A cross-sectional assessment of dose and gender effects was performed in 283 patients (229 males, 54 females) who received a 12-lead ECG for QTc measurement 59 days (interquartile range: 36-288 days) after methadone treatment. To determine the effects of methadone over time, a subset of 150 participants (126 men, 24 women) who underwent a 12-lead ECG before and 37 days (interquartile range: 32-44 days) after methadone treatment were selected. Results: In the cross-sectional study, a significant dose-dependent interaction between methadone and QTc (r = 0.201, P = 0.0007) was observed in individuals receiving a median methadone dose of 40 mg/day (interquartile range: 30-60 mg/day). The methadone-QTc correlation was significant in males (r = 0.210, P = 0.0014) but not in females (r = 0.164, P = 0.2363). The longitudinal assessment of methadone's effects over a 6-month period showed that 60.7% of individuals experienced an increase in QTc compared to baseline data. The adjusted QTc significantly increased from 418.5 to 426.9 milliseconds in males (P < 0.0001), compared to an insignificant change in females (437.7 milliseconds vs 441.1 milliseconds, P = 0.468). Conclusions: Low-dose methadone therapy shows dose-dependent QTc prolongation and is associated with significant QTc lengthening within 6 months of treatment initiation. Men are more susceptible than women to low-dose methadone-associated QTc prolongation. (J Cardiovasc Electrophysiol, Vol. 23, pp. 527-533, May 2012) [ABSTRACT FROM AUTHOR]

Abstract: Atrial fibrillation (AF), the most common cardiac arrhythmia, is frequently accompanied by atrial interstitial fibrosis. Angiotensin II (Ang II) dependent signaling pathways have been implicated in interstitial fibrosis during the development of AF. However, Ang II could be further degraded by angiotensin converting enzyme II (ACE2). We examined expression of ACE2 in the fibrillating atria of pigs and its involvement in fibrotic pathogenesis during AF. Nine adult pigs underwent continuous rapid atrial pacing to induce sustained AF and six pigs were sham controls (i.e., sinus rhythm; SR). In the histological examinations, extensive accumulation of extracellular matrix in the interstitial space of the atria, as evidenced by Masson’s trichrome stain, were found in fibrillating atria. The relative amount of collagen type I in the atria with AF was significantly increased as compared with that in the SR. Local ACE activity in the fibrillating atria was also markedly higher than that in the SR subjects. ACE2 gene and protein expression in the AF subjects were significantly decreased compared with those in the SR subjects, whereas expression of mitogen-activated/ERK kinase 1/2 (MEK1/2), extracellular signal-regulated protein kinase 2 (ERK2), and activated ERK2 were significantly greater in the AF subjects. We propose that decreasing ACE2 expression during AF may affect the Ang II-dependent signaling pathway. In addition, our results suggest that atrial fibrosis in AF may be induced by antagonistic regulation between ACE and ACE2 expression. [Copyright &y& Elsevier]

TSAI, C.-T., et al.: Distinct Clinical Features in the Recipients of the Implantable Cardioverter Defibrillator in Taiwan: A Multicenter Registry Study. Little information about the ICD is available from the Asian Pacific region. The purpose of this study was to characterize the clinical features in ICD patients in Taiwan and to compare these features with those in patients in the Western populations, mainly the Canadian Implantable Defibrillator Study (CIDS), the Antiarrhythmics versus Implantable Defibrillator (AVID) trial, and the Cardiac Arrest Study Hamburg (CASH) trial. From February 1995 to October 2001, 101 ICDs were implanted in 92 patients (78 [84%] men) in 12 hospitals. Clinical presentations included sudden cardiac death due to VF/VT in 35 (38%) patients, syncopal VT in 25 (27%), drug refractory nonsyncopal VT in 27 (29%), and unexplained syncope with inducible sustained VT/VF in 5 (6%). The mean age was significantly younger than that in CIDS or AVID (59 ± 16 vs 63 ± 9 years in CIDS, P = 0.02; vs 65 ± 11 years in AVID, P < 0.001), but was comparable to that in CASH (59 ± 16 vs 58 ± 11 years in CASH, P = 0.75). The mean LVEF was significantly higher than that in CIDS or AVID (48 ± 19% vs 34 ± 15% in CIDS, P < 0.001; vs 32 ± 13% in AVID, P < 0.001), but was comparable to that in CASH (48 ± 19 vs 46 ± 19% in CIDS, P = 0.83). The ICD patients in the current study also showed a higher incidence of normal heart (23 vs 4% in CIDS, P < 0.001; vs 3% in AVID, P < 0.001; vs 9% in CASH, P < 0.001) and cardiomyopathy (41% vs 10% in CIDS, P < 0.001; vs 15% in AVID, P < 0.001; vs 11% in CASH, P < 0.001), but a lower incidence of coronary artery disease (29% vs 83% in CIDS, P < 0.001; vs 82% in AVID, P < 0.001; vs 73% in CASH, P < 0.001). During a mean follow-up of 28 ± 24 months, 13 (14%) patients died. Older age was the only factor associated with poorer survival after ICD implantation. Forty-seven (51%) patients received appropriate ICD discharges during follow-up. History of prior myocardial infarction was the only factor associated with an earlier first appropriate ICD discharge and LVEF < 0.35 the only factor associated with subsequent poorer survival after the first ICD discharge. In conclusion, this study demonstrated many distinct clinical features in our ICD population that were different from those in the Western populations. (PACE 2003; 26:2083–2090). [ABSTRACT FROM AUTHOR]

Introduction: Heart rate turbulence is a powerful de novo risk predictor for patients surviving acute myocardial infarction. However, little is known about its underlying physiologic mechanism. Methods and Results: Hypothesizing that heart rate turbulence is barorceptor reflex related, we studied heart rate and blood pressure fluctuations at rest and after systematically introduced ventricular premature beats in 16 patients without structural heart disease (10 men and 6 women; mean age 45 ± 17 years) before and after sequential sympathetic (esmolol 4-mg bolus followed by 120 µg/kg/min intravenously), parasympatbetic (atropine 0.04 mg/kg intravenously), and combined autonomic blockade (esmolol plus atropine). Turbulence onset (%) and turbulence slope (msec/beat) were averaged from 10 respective ventricular premature beats. Spontaneous baroreflex sensitivity (msec/mmHg) was calculated from 5 minutes of sinus rhythm recording. The results showed that turbulence slope decreased after atropine (0.71 ± 0.50 msec/beat vs 5.17 ± 3.96 msec/beat at baseline; P < 0.01) and combined autonomic blockade (1.23 ± 1.02 msec/beat; P < 0.01) but was unchanged after esmolol (4.53 ± 3.30 msec/beat; P > 0.05). Turbulence onset increased after atropine (0.32% ± 0.35% vs -0.45 ± 0.94 at baseline; P < 0.05) and combined sympathetic and parasympathetic blockade (0.58% ± 0.86%; P < 0.05) but was unchanged after esmolol (-0.62% ± 1.33%; P > 0.05). Turbulence slope was positively correlated with baroreflex sensitivity at baseline (r = 0.78, P < 0.01) and after esmolol (r = 0.8, P < 0.01), but dissociated after atropine (r = 0.16, P > 0.05) and combined autonomic blockade (r = 0.31, P > 0.05). Turbulence onset was negatively correlated with baroreflex sensitivity at baseline (r = -0.61, P < 0.05), after esmolol (r = -0.80, P < 0.01), and after atropine (r = -0.53, P < 0.05). Conclusion: Heart rate turbulence of turbulence onset and turbulence slope is critically vagal dependent and highly correlated with spontaneous baroreflex sensitivity, which underscores its clinical importance in cardiovascular risk stratification. [ABSTRACT FROM AUTHOR]

Introduction: The slope of the power spectrum in heart rate variability (HRV) reflects the fractal or scaling behavior in HR dynamics and recently was confirmed as an independent predictor of postmyocardial infarction survival. Whether or not the new measurement in HRV foresees the functional evolution in patients with advanced congestive heart failure treated by β blockers is unclear. Methods and Results: Sequential 24-hour Holter ECG recordings were obtained at baseline, and 1 and 3 months after addition of atenolol therapy for advanced congestive heart failure in 10 patients. The slope and intercept of the regression line of power-law behavior, the short- and intermediate-term of detrended fluctuated analysis (DFA), the approximate entropy (ApEn), and the standard frequency spectra of the 24-hour HRV were compared sequentially as well as with those in 12 age-matched normal controls. The results showed that the slope (-1.70 ± 0.45 vs -1.22 ± 0.21; P < 0.05) and the intercept (5.11 ± 0.46 vs 5.62 ± 0.24; P < 0.05) of the regression line of power-law behavior and the short-term DFA (for 4 to 11 heats) (0.78 ± 0.18 vs 1.13 ± 0.21; P < 0.05) increased after 3 months of atenolol treatment However, the change in intermediate-term DFA (>11 beats) and ApEn was not apparent (1.24 ± 0.21 vs 1.22 ± 0.15 and 1.34 ± 0.14 vs 1.36 ± 0.11; both P > 0.05). The evolution of the slope or intercept of the regression line of the HRV power spectrum did not correlate with the echocardiographic or clinical cardiac function, or with the frequency spectral components of the HRV (P > 0.05). Conclusion: Additional beta-blocker therapy upregulated the fractal behavior control of the HRV in patients with advanced congestive heart failure. The improvement was independent of subjective and objective global cardiac performance. [ABSTRACT FROM AUTHOR]

Introduction: The funny current (If) contributes to phase IV spontaneous depolarization in cardiac pacemaker tissue. Enhanced If activity in myocardial tissue may lead to increased automaticity and therefore tachyarrhythmia. We measured the amount of If activity in the messenger ribonucleic acid (mRNA) in human atrial tissue and correlated the mRNA amount to left atrial filling pressure and atrial fibrillation (AF). Methods and Results: A total of 34 patients undergoing open heart surgery were included (15 men and 19 women, aged 55 ± 10 years). Atrial tissue was obtained from the right atrial free wall, the right atrial appendage, the left atrial free wall, and the left atrial appendage, respectively. The mRNA amount of the If channel was measured by reverse transcription polymerase chain reaction and was normalized to the mRNA levels of glyceraldehyde 3-phosphate dehydrogenase. We found that the If channel mRNA was present at ail the atrial sampling sites. A higher left atrial filling pressure, an indicator of congestive bean failure, was associated with a higher If mRNA level (r² = 0.446, P < 0.01 by linear regression). We also found that the mRNA amount was significantly higher in patients with AF than in patients without AF (1.68 ± 0.49 vs 1.27 ± 0.43; P < 0.05). Age, sex, right atrial filling pressure, left atrial dimension, and left ventricular ejection fraction had no significant effect on the mRNA level. conclusion: The mRNA of the If channel is present in the free-wall area and appendage area from both atria. Increased left atrial filling pressure and clinical AF are associated with increased If mRNA level. [ABSTRACT FROM AUTHOR]

General anesthesia is sometimes required during radiofrequency catheter ablation (RFCA) of various tachyarrhythmias because of an anticipated prolonged procedure and the need to ensure stability during critical ablation. In this study, we examine the feasibility of using propofol anesthesia for RFCA procedure. There were 150 patients (78 male, 72 female; mean age 30 years, range 4-96 years) in the study. Electrophysiologic study was performed before and during propofol infusion in the initial 20 patients and was performed only during propofol infusion in the remaining 130 patients. In the initial 20 patients, propofol infusion increased the sinus rate and facilitated AV nodal conduction. The accessory pathway effective refractory period, as well as the sinus node recovery time, atrial effective refractory period, and ventricular effective refractory period were not significantly changed. There were 152 tachyarrhythmias in 150 patients (24 atrial flutter, 31 AV nodal reentrant tachycardia, 68 AV reciprocating tachycardia, 12 ventricular tachycardia, and 17 atrial tachycardia). Most (148/152) tachycardias remained inducible after anesthesia and RFCA was performed uneventfully. However, in four of the seven pediatric patients with ectopic atrial tachycardia, the tachycardia terminated after propofol infusion and could not be induced by isoproterenol infusion. Consequently, RFCA could not be performed. Intravenous propofol anesthesia is feasible during RFCA for most tachyarrhythmias except for ectopic atrial tachycardia in... [ABSTRACT FROM AUTHOR]

Ventricular relaxation is an important determinant of ventricular filling; impaired relaxation may decrease cardiac output and stroke volume. Relaxation has been shown to occur more quickly following beats with an increased extent of systolic fiber shortening. Since cardiac output and stroke volume are greater during atrioventricular (AV) sequential pacing than during ventricular pacing at identical heart rates, we reasoned that AV sequential pacing would improve relaxation. To assess this hypothesis we studied 21 dogs with chronic (1-3 months) complete heart block (CHB) induced by radiofrequency catheter ablation of the His bundle. Bight and left heart pressures, thermodilution cardiac output, and single plane ventriculography were recorded during baseline rhythm (CHBJ, and WI, and AV sequential pacing at a heart rate greater than the sinus rate. None had ventriculoatrial conduction. During AV sequential pacing, the AV interval was set at 150 msec. Cardiac output and stroke volume were significantly increased in the AV sequential compared to the VVI pacing mode. Left ventricular pressures, maximal positive and negative dP/dt, and the time constant (T) of isovolumic pressure decay were not different in the two modes. We conclude that despite increased stroke volume in the AV sequential pacing mode, relaxation is unchanged. We believe the lack of change in relaxation is due to nonuniform ventricular activation when depolarization is initiated at the right ventricular apex. [ABSTRACT FROM AUTHOR]

Percutaneous endocardial electrode catheter ablation using stored direct current (DC) electrical energy was performed in five patients with recurrent ventricular tachycardia (VT) refractory to many antiarrhythmic drugs, including amiodarone. All had prior myocardial infarction and poor left ventricular function with ejection fractions ranging from 20% to 40%. Endocardial catheter and pace mappings were used to localize the earliest site of activation during VT. Under general anesthesia, two to six shocks with 200 to 300 joules DC energy per shock were delivered to the localized sites. Immediate complications included ventricular fibrillation in one patient, transient QRS complex widening in two patients, transient complete AV block with persistent first-degree AV block in one patient, and transient asystole in two patients. None had inducible VT immediately following ablation, or 4 to 6 days later; none had evidence of intracardiac clot by two-dimensional (2D) echocardiography on the third to fifth day. Peak creatine kinase ranged from 189 lo 1610 IU/L with 9% to 18% MB fraction. During a follow-up of 6 to 30 months, three patients had no recurrence of VT. Two patients had recurrent VT with a slower rate, which was controlled with antiarrhythmic drugs. None had worsening congestive heart failure. Two patients died of nonarrhythmic causes. We conclude that nonsurgical endocardial ablation of VT with an electrode catheter is effective for the treatment of refractory VT in selected patients with coronary artery disease. [ABSTRACT FROM AUTHOR]

Approach. Radiofrequency catheter ablation of the atrioventricular junction is usually achieved from either the right or left atrioventricular junction. We describe a new approach in which the atrioventricular junction was successfully ablated from the supravalvular region of the noncoronary cusp of the aortic valve in an unusual patient in whom conventional approaches were unsuccessful. [ABSTRACT FROM AUTHOR]

A healthy 37-year-o!cl male presented with a history of frequent palpitations and sustained wide QRS complex tachycardia with a right bundle branch block and left axis morphology. Serial electrophysiological studies revealed two inducible tachycardias, which were shown to represent atrioventricular nodal reentrant tachycardia and idiopathic left ventricular tachycardia. Transformation from one tachycardia to the other occurred spontaneously as well as following atria! or ventricular pacing. Radiofrequency catheter ablation of the slow atrioventricular nodal pathway resulted in cure of atrioventricular nodal reentrant tachycardia and the prevention of spontaneous recurrence of ventricular tachycardia, suggesting a role of atrioventricular nodal reentrant tachycardia in triggering the clinical episodes of ventricular tachycardia. The patient has remained asymptomatic without antiarrhythmic therapy for 8 months. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 56-year-old male with a thrombotic occlusion in the distal superior vena cava (SVC) by a pacemaker lead. Three years following pacemaker placement for sick sinus syndrome the patient developed facial edema, dyspnea and syncope. Complete resolution for the SVC syndrome was achieved by percutaneous venoplasty.

Presents a letter to the editor about the use of routine echocardiography after uncomplicated radiofrequency catheter ablation of supraventricular tachyarrhythmias.

Presents a letter to the editor in response to the article "Undesirable mode switching with a dual chamber rate responsive pacemaker," by M.R. Pitney, et al, which appeared in a 1993 issue of the periodical "PACE."