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Notes: A 67-year-old man with ischemic cardiomyopathy received an implantable defibrillator for ventricular fibrillation 3 years ago. He now presents with weight loss and an inability to interrogate or establish any telemetric communication with his defibrillator. An abdominal radiograph was obtained (right) that, when compared to a film obtained 5 months earlier (left) illustrated a significant change in the position of the device. Inspection of the manufacturer radiographic

Notes: A 65-year-old man with a history of coronary artery disease underwent coronary artery bypass grafting in 1997 and 1998. He also received a permanent dual chamber pacemaker implantation during the second bypass surgery for complete heart block. He presented a year later to our pacemaker clinic for follow-up. Initial ECG showed ventricular capture by pacemaker atrial output (bottom tracings, left side). When the atrial output was decreased by 0.5V, normal atrial and ventricular pacemaker function was restored (bottom tracings, right side). A chest X-ray revealed an active fixation atrial lead implanted to the right atrium and a passive fixation lead to the ventricle. There was no apparent insulation failure of either lead by X-ray or by impedance measurements. An epicardial pacing lead implanted during bypass surgery for temporary postoperative pacing was not completely removed. The proximity between the retained epicardial wire and the screw of the active fixation atrial lead (arrow) support the hypothesis that the atrial output was conducted by the retained epicardial wire into the ventricles, resulting in unintended ventricular capture by the atrial output. However, we could not exclude the possibility that the atrial lead directly resulted in ventricular capture due to its proximity to the AV grove.

Notes: Unique Properties of Optical Action Potentials. Introduction: Optical mapping with voltage-sensitive dyes has made it possible to record cardiac action potentials with high spatial resolution that is unattainable by conventional techniques. Optically recorded signals possess distinct properties that differ importantly from electrograms recorded with extracellular electrodes or action potentials recorded with microelectrode techniques. Despite the growing application of optical mapping to cardiac electrophysiology, relatively little quantitative information is available regarding the characteristics of optical action potentials recorded from cardiac tissue. Methods and Results: A high-resolution optical mapping system and microelectrode techniques were used to determine the characteristics of guinea pig ventricular action potentials recorded with the voltage-sensitive dye di-4-ANEPPS. The effects of optical magnification, tissue-light interaction, sampling rate, voltage resolution, spatial resolution, and cardiac motion on action potential signal characteristics were determined. The optical action potential signal represents the relative change in transmembrance potential arising from a volume of cells, where the area of a recording site is determined by optical magnification and detector area, and the depth of recording is determined by system optics and the visible light transmission characteristics of cardiac muscle. Using photographic lenses, the depth of tissue contributing to the signal is 〈 250 μm. The action potential plateau and final repolarization can be accurately reconstructed from data digitized at modest sampling rates (450 to 750 Hz), since the frequency content of optical action potentials is band-limited to approximately 150 Hz. However, faster sampling rates are needed to depict the subtle details of the action potential upstroke. In addition to temporal resolution, it is essential to achieve sufficient dynamic range and voltage resolution to accurately represent the time course of membrane potential change. Voltage resolution is inversely related to the square of spatial resolution, hence, there exists an inherent trade-off between increased spatial resolution and diminished voltage resolution. Cardiac motion, which can otherwise limit spatial resolution as well as signal fidelity, can be effectively reduced using mechanical stabilization of the heart without distorting action potential characteristics. Conclusions: Optical mapping with voltage-sensitive dyes provides high-fidelity multisite action potential recording with flexible spatial resolution. When recording cardiac action potentials with voltage-sensitive dyes, the Interdependence of temporal, spatial, and voltage resolutions must be carefully considered.

Notes: T Wave Alternans and Sudden Cardiac Death. Sudden cardiac death remains a preeminent public health problem. Despite advances in preventative treatment for patients known to be at risk, to date we have been able to identify, and thus treat, only a small minority of these patients. Therefore, there is a major need to develop noninvasive diagnostic technologies to identify patients at risk. Recent studies have demonstrated that measurement of microvolt-level T wave alternans is a promising technique for the accurate identification of patients at risk for ventricular arrhythmias and sudden cardiac death. In this article, we review the clinical data establishing the relationship between microvolt T wave alternans and susceptibility to ventricular arrhythmias. We also review the methods and technology that have been developed to measure microvolt levels of T wave alternans noninvasively in broad populations of ambulatory patients. In particular, we examine techniques that permit the accurate measurement of T wave alternans during exercise stress testing.

Notes: Introduction: Although it is well established that alterations in heart rate or activation sequence induce electrical remodeling in the atria, electrical remodeling in the ventricle is poorly understood. Methods and Results: To determine the changes in cellular repolarization that underlie ventricular electrical remodeling caused separately by altered heart rate and activation sequence, optical action potentials were recorded simultaneously from 256 sites spanning the transmural wall of the arterially perfused canine wedge preparation (n = 15) . Action potentials were compared from the same sites under identical conditions [endocardial pacing, cycle length (CL) = 1,000 msec], before and after an intervening 20- to 60-minute period of remodeling induced by (1) rapid pacing (CL = 300 msec) with no change in activation sequence; (2) altered activation sequence (epicardial pacing) with no change in rate; or (3) no change in rate or activation sequence (control). Action potential duration (APD) shortened by 24.8 ± 4.8 msec following a period of rapid heart rate (P 〈 0.05) but prolonged (by 12.7 ± 1.8 msec ) following a period of altered activation sequence (P 〈 0.05) . Hence, even after restoration of baseline heart rate and activation sequence, there were persistent changes in APD from baseline, indicative of electrical remodeling. Moreover, the orientation of the maximum APD gradient across the transmural wall changed more significantly following heart rate remodeling (by 27.7°± 4.9°, P 〈 0.05 ) than following activation sequence remodeling (by 12.3°± 2.4°, P 〈 0.05 ). Conclusion: Persistent changes in ventricular repolarization can be induced by surprisingly short periods of altered rate or activation sequence. In contrast to atrial remodeling, electrical remodeling in the ventricle can result in prolonged APD (with altered activation sequence) or reversal of APD gradient orientation (with rapid rate), suggesting that the nature of ventricular electrical remodeling induced by these two perturbations is different. (J Cardiovasc Electrophysiol, Vol. 14, pp. 394-402, April 2003)

Notes: Prediction of Congenital Long QT Syndrome. Introduction: Previous studies showed that diagnosing congenital long QT syndrome (LQTS) is difficult due to variable penetrance and genetic heterogeneity, especially when subjects from multiple families with diverse mutations are combined. We hypothesized that a combination of clinical and ECG techniques could identify gene carriers within a single family with congenital LQTS. Methods and Results: One hundred one genotyped members of a family with LQTS, including 26 carriers of a HERG mutation, underwent history and ECG analysis. Forty-eight family members also underwent exercise testing with QT and T wave alternans (TWA) analysis and 24-hour Holter monitoring with QT and heart rate variability analysis. A logistic regression model, which included age, gender, QTc, and QTc by age, provided the best prediction of gene carrier status, although there was substantial overlap (78%) of QTc among subjects with and without the mutation. QTc was not helpful as a discriminator in children ≤ 13 years. TWA (observed infrequently) did not add significantly to the model's ability to predict abnormal genotype. Conclusion: Even in this homogeneous LQTS population, the phenotype was so variable that clinical and detailed ECG analyses did not permit an accurate diagnosis of gene carrier status, especially in children. Sustained microvolt TWA was a specific (100%) but insensitive (18%) marker for LQTS. Its ability to predict risk of arrhythmia in this population remains to be determined. Genetic testing serves an essential role in screening for carriers of LQTS.