Making QT correction simple is complicated.
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Biomedical subjects
Publications and source records attributed to N G Boyle.
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The purpose of this study was to assess whether in patients with syncope and heart failure due to nonischemic cardiomyopathy, treatment with an implantable cardioverter-defibrillator (ICD) compared with conventional medical therapy is associated with a reduction in sudden death and total mortality. Patients with advanced heart failure who have syncope have been shown to be at high risk for sudden death. Further risk stratification has been difficult in patients with nonischemic cardiomyopathy in whom inducibility on electrophysiologic study is not predictive of future risk. Of 639 consecutive patients with nonischemic cardiomyopathy referred for heart transplantation, 147 patients with history of syncope and no prior history of sustained ventricular tachycardia or cardiac arrest were identified. Outcomes were compared for the 25 patients managed with an ICD and 122 patients managed with conventional medical therapy. There were no differences in the baseline variables in the 2 groups of patients, including age, ejection fraction, and medical treatments for heart failure, but patients receiving an ICD were more likely to have had nonsustained ventricular tachycardia (56% vs. 15%, p = 0.001). During a mean follow-up of 22 months, there were 31 deaths, 18 sudden, in patients treated with conventional therapy, whereas there were 2 deaths, none sudden, in patients treated with an ICD. An appropriate shock occurred in 40% of the ICD patients. Actuarial survival at 2 years was 84.9% with ICD therapy and 66.9% with conventional therapy (p = 0.04). Thus, in patients with nonischemic cardiomyopathy and syncope, therapy with an ICD is associated with a reduction in sudden death and an improvement in overall survival.
Failure to detect ventricular tachycardia and/or ventricular fibrillation by implantable cardioverter defibrillators (ICDs) is a rare but serious problem. We report a case of failure to detect an episode of induced ventricular tachycardia by a dual chamber ICD, due to abbreviation of ventricular detection window secondary to programmed pacing parameters and a rate-smoothing algorithm. In this patient, the intradevice interaction was corrected by programming rate-smoothing off. This report highlights the potentially lethal consequences of critical timing relationships among the pacing function, arrhythmia detection, and the characteristics of the arrhythmia when using a modern dual chamber ICD. Physicians responsible for patients with ICDs must be aware of such interactions.
Three cases of twiddler's syndrome in patients with an abdominally implanted cardioverter defibrillator (ICD) and an endocardial lead system are reported. The condition was detected when an increase in pacing threshold or lead impedance was noted at routine follow-up. Successful revision was possible in all patients; however, a recurrence in one patient necessitated removal of the device. Elderly female patients with some degree of obesity appear most susceptible. Minimizing pocket size and suturing of the device to the fascia should decrease the chance of developing this problem.
Junctional rhythm is commonly observed during radiofrequency catheter ablation of the fast or slow pathways of atrioventricular nodal reentrant tachycardia (AVNRT). However, the origin of these beats remains unclear. We analyzed the retrograde atrial activation sequence of 16 patients (mean +/- SD: 41.2 +/- 18.9 years old) undergoing catheter ablation for typical AVNRT with detailed catheter mapping of the triangle of Koch. The earliest atrial activations were concordant during tachycardia and junctional rhythm in only 5 of 16 patients. The findings suggest that junctional rhythm is unlikely to represent direct stimulation of the atrioventricular (AV) node via a discrete slow pathway but rather results from enhanced automaticity from > or =1 sites in the AV nodal transitional zone. The ensuing atrial activation pattern results from anisotropic spread from these sites. In addition, these data imply that the original concept of the AV node comprising 2 anatomically defined pathways may not be valid, and that a functionally defined pathway model may be a more accurate representation.
BACKGROUND: Atrial dysrhythmia patients have exaggerated intra-atrial conduction delays and prolonged relative refractoriness in response to atrial premature depolarizations (APDs). Furthermore, atrial fibrillation (AF) is more readily inducible by APDs from the high right atrium (HRA) than the coronary sinus (CS). In this study, we postulated that site-specific intra-atrial conduction delays can explain why AF is initiated more from the HRA than from the CS. METHODS AND RESULTS: We examined 17 patients (age, 49 +/- 22 years) without a history of atrial flutter, AF, or structural heart disease. Programmed stimulation was carried out from the HRA and distal CS, and bipolar recordings were made at the HRA, His bundle, posterior triangle of Koch, and CS. More prolongations in conduction and relative refractoriness in all intra-atrial sites were observed during HRA than CS APDs. AF was induced in 8 patients after HRA and not CS stimulation. During HRA stimulation, patients with AF inducibility exhibited significant prolongation of conduction to the posterior triangle of Koch and marked broadening of the posterior triangle of Koch electrogram compared with CS stimulation. In patients without AF inducibility, the posterior triangle of Koch electrogram width was the same during HRA and CS stimulation. CONCLUSIONS: The existence of site-dependent intra-atrial conduction delays and site-dependent dispersion of refractoriness appears to be a common property of the atrial myocardium and does not necessarily forecast AF inducibility. However, the presence of nonuniform anisotropic characteristics of the posterior triangle of Koch may be critical for AF induction.
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Explore the source record for details and available documents.
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BACKGROUND: The ability to image the coronary arteries noninvasively would represent an advance in patient care. We have developed a magnetic resonance (MR) angiographic technique that allows the acquisition of complete images of coronary flow within a single breath-hold. By this method, the feasibility of noninvasive MR coronary angiography was evaluated in 25 subjects, including 19 healthy adult volunteers and six patients after diagnostic coronary angiography. METHODS AND RESULTS: Noninvasive MR coronary angiography was performed with a fat-suppressed ECG-gated gradient-echo sequence with k-space segmentation. Overlapping transverse sections were initially used to image coronary flow, with oblique images obtained after identification of proximal anatomy. The left main coronary artery was seen in 24 subjects (96%), with a mean diameter of 4.8 mm (range, 3.4-6.2 mm) and average length of 10 mm (range, 8-14 mm). The left anterior descending coronary artery was seen in 100% of subjects, with a mean proximal diameter of 3.6 mm (range, 2.6-4.3 mm) and for an average length of 44 mm (range, 28-93 mm). The left circumflex coronary artery was seen in 76% of subjects, with a mean proximal diameter of 3.5 mm (range, 2.6-4.3 mm) and for an average length of 25 mm (range, 9-42 mm). The right coronary artery was also identified in 100% of subjects, with a mean proximal diameter of 3.7 mm (range, 2.7-5.1 mm) and for an average length of 58 mm (range, 24-122 mm). Quantitative angiography of normal proximal segments demonstrated a good correlation with MR-determined lumen diameters (r = 0.86, p < 0.002). Occluded vessels in patients with coronary artery disease displayed an absence of flow signal distal to the occlusion, whereas vessels with significant angiographic stenoses demonstrated signal loss corresponding to the area of the stenosis, with visualization of the more distal vessel. CONCLUSIONS: Breath-hold MR coronary angiography provides visualization of the major epicardial vessels. In the future, MR coronary angiography may provide a noninvasive means for the evaluation of patients with known or suspected coronary artery disease.