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A routine change in the automatic capture management algorithm from “adaptive” to “off or monitor” is required to conserve device longevity in a permanent pacemaker with His‐bundle pacing.

Aim The purpose of this study was to explore the possible association between subsequent acute coronary syndrome (ACS) risk and depressive disorder. Methods We used data from the National Health Insurance system of Taiwan to address the research topic. The exposure cohort contained 10 871 patients with new diagnoses of depressive disorders. Each patient was randomly frequency-matched for sex and age with four participants from the general population who did not have any ACS history before the index date (control group). Cox's proportion hazard regression analyses were conducted to estimate the relation between depressive disorders and subsequent ACS risk. Results Among patients with depressive disorders, the overall risk for developing subsequent ACS was significantly higher than that of the control group (adjusted hazard ratio: 1.88, 95% confidence interval: 1.63–2.17). Further analysis revealed that the higher risk was observed in patients who were male, were of older age, or whose diagnosis was combined with other comorbidities. Conclusions The findings from this population-based retrospective cohort study suggest that depressive disorder is associated with an increased subsequent ACS risk.

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)

Summary Dysregulation of plasma lipids is associated with age‐related cardiovascular diseases. L5, the most electronegative subfraction of chromatographically resolved low‐density lipoprotein (LDL), induces endothelial dysfunction, whereas the least electronegative subfraction, L1, does not. In this study, we examined the effects of L5 on endothelial senescence and its underlying mechanisms. C57B6/J mice were intravenously injected with L5 or L1 (2 mg kg−1 day−1) from human plasma. After 4 weeks, nuclear γH2AX deposition and senescence‐associated β‐galactosidase staining indicative of DNA damage and premature senescence, respectively, were increased in the aortic endothelium of L5‐treated but not L1‐treated mice. Similar to that, in Syrian hamsters with elevated serum L5 levels induced by a high‐fat diet, nuclear γH2AX deposition and senescence‐associated β‐galactosidase staining were increased in the aortic endothelium. This phenomenon was blocked in the presence of N‐acetyl‐cysteine (free‐radical scavenger) or caffeine (ATM blocker), as well as in lectin‐like oxidized LDL receptor‐1 (LOX‐1) knockout mice. In cultured human aortic endothelial cells, L5 augmented mitochondrial oxygen consumption and mitochondrial free‐radical production, which led to ATM activation, nuclear γH2AX deposition, Chk2 phosphorylation, and TP53 stabilization. L5 also decreased human telomerase reverse transcriptase (hTERT) protein levels and activity. Pharmacologic or genetic manipulation of the reactive oxygen species (ROS)/ATM/Chk2/TP53 pathway efficiently blocked L5‐induced endothelial senescence. In conclusion, L5 may promote mitochondrial free‐radical production and activate the DNA damage response to induce premature vascular endothelial senescence that leads to atherosclerosis. Novel therapeutic strategies that target L5‐induced endothelial senescence may be used to prevent and treat atherosclerotic vascular disease.

OBJECTIVE Differentiation of the tachycardia originating from the superior vena cava (SVC) or the right superior pulmonary vein (RSPV) is limited by the similar surface P-wave morphology and intraatrial activation pattern during tachycardia. We sought to find a simple method to distinguish between the two tachycardias by analyzing the interatrial conduction time. METHODS Sixteen consecutive patients consisting of 8 with SVC tachycardia and the other 8 with RSPV tachycardia were studied. The interatrial conduction time from the high right atrium (HRA) to the distal coronary sinus (DCS) and the intraatrial conduction time from the HRA to the atrial electrogram at the His bundle region (HIS) were measured during the sinus beat (SR) and during the tachycardia-triggering ectopic atrial premature beat (APB). The differences of interatrial (Delta[HRA-DCS](SR-APB)) and intraatrial (Delta[HRA-HIS](SR-APB)) conduction time between SR and APB were then obtained. RESULTS The mean Delta[HRA-DCS](SR-APB) was 1.0 +/- 5.2 ms (95% confident interval [CI]-3.3-5.3 ms) in SVC tachycardia and 38.5 +/- 8.8 ms (95% CI 31.1-45.9 ms) in RSPV tachycardia. The mean Delta[HRA-HIS](SR-APB) was 1.5 +/- 5.3 ms (95% CI -2.9-5.9 ms) in SVC tachycardia and 19.9 +/- 12.0 ms (95% CI 9.9-29.9 ms) in RSPV tachycardia. The difference of Delta[HRA-DCS](SR-APB) between SVC and RSPV tachycardias was wider than that of Delta[HRA-HIS](SR-APB) (37.5 +/- 9.3 ms vs. 18.4 +/- 15.4 ms, P < 0.01). CONCLUSIONS The wide difference of the interatrial conduction time Delta[HRA-DCS](SR-APB) between SVC and RSPV tachycardias is a useful parameter to distinguish the two tachycardias and may avoid unnecessary atrial transseptal puncture.

This report describes a patient who underwent implantation of an atriobiventricular pacemaker following AV junction ablation and insertion of a temporary right ventricular (RV) pacemaker. During implantation, intermittent loss of sinus P wave tracking occurred when the three permanent leads were connected to the generator. Analysis of marker annotation disclosed intermittent abnormal ventricular sensing that reinitiated postventricular atrial blanking and caused failure of P wave tracking. This phenomenon disappeared after removing the temporary RV lead, but not by turning off the temporary pacemaker. We assume that mechanical contact between the temporary and the permanent RV leads is the underlying mechanism.

Ablation of Atypical Atrial Flutter. Subeustachian isthmus-dependent typical atrial flutter has been well studied. We demonstrate a case with atypical atrial fiutter involving only the base of the right atrium around the inferior vena cava. Entrainment pacing and mapping studies documented a distinct circuit traversing the subeustachian isthmus, propagating through the posterobasal right atrium, and skirting the inferior vena cava. Successful radiofrequency ablation of the arrhythmia was accomplished by creating a linear lesion at the subeustachian isthmus. Mapping of the inferior vena cava region and the demonstration of concealed entrainment are essential steps in establishing the mechanism of the atypical atrial flutter.

Bipolar leads are most commonly used in the current practice of pacemaker therapy. In our study of 124 patients implanted with Guidant/Cardiac Pacemakers (CPI) Vigor dual chamber pacemakers, 5 patients had unexpectedly abrupt increases in bipolar lead impedance and pacing threshold 2 weeks to 18 months postimplantation without changes in sensing function. With the lead configuration reprogrammed to unipolar, the lead impedance and pacing threshold were restored to appropriate ranges. The changes in bipolar lead parameters can be caused by the CPI's "Quick Connect" (QC1) header lead system incorporated in these pacemakers.

We report on a rare case of anomalous origin of left coronary artery from the noncoronary sinus of Valsalva. Intraaortic intravascular ultrasound study identified the origin of the left coronary artery and facilitated subsequent selective coronary angiography of the artery.

Radial artery punctures for diagnostic coronary angiography or coronary balloon angioplasty were performed in 211 patients with a success rate of 98% (207 patients). In the four failed transradial accesses, the procedure was accomplished via the transfemoral route. Major local vascular complications included one arteriovenous fistula, one pseudoaneurysm, and one ischemic contracture of the right hand. Reduced radial pulses were noted in 25 (12%) patients at follow-up without ischemic manifestations. Transradial diagnostic coronary angiography was successfully completed in 184 (98%) of 187 patients. The technical success for balloon angioplasty was obtained in 73 (97%) of 75 patients. Clinical success was observed in 68 (91%) patients; balloon angioplasty resulted in one nonfatal myocardial infarction and four late deaths (3 cardiac and 1 stroke). We believe that transradial catheterization for diagnostic coronary angiography and balloon angioplasty in our relatively small built Chinese population is a safe and practical alternative approach. Cathet. Cardiovasc. Diagn. 40:159–163, 1997. © 1997 Wiley-Liss, Inc.

Unroofed coronary sinus, a rare congenital anomaly first described by Raghib and colleagues1 in 1965, is a result of an embryologic error involving imperfect or complete failure of development of the left atriovenous fold, which is manifested as a focal (fenestration or partial unroofing of the coronary sinus) or complete absence of the coronary sinus septum. Before the era of echocardiography, precise diagnosis of this anomaly was possible only during surgical procedure or at autopsy. Since the advent of the echocardiography, several studies have reported the usefulness of two-dimensional transthoracic and transesophageal echocardiography in the diagnosis of unroofed coronary sinus. We describe the intracardiac echocardiographic delineation of partially unroofed coronary sinus and persistent left superior vena cava in a patient with atrioventricular nodal reentrant tachycardia. Incidental finding of the dilated coronary sinus during radio frequency ablation of the tachycardia led to the diagnosis of this unusual anomaly.