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OBJECTIVE: To study the association of the fragmented QRS complex versus the Q wave with myocardial scar and viability. BACKGROUND: A prior study has suggested that the fragmented QRS complex on an electrocardiogram (ECG) is a highly sensitive and specific marker of myocardial scar as detected by regional perfusion abnormalities on a nuclear stress test. There is no external validation of this data. METHODS: We correlated the ECG and nuclear perfusion images of 460 consecutive patients with known or suspected coronary artery disease. The presence of fragmented QRS or Q waves in two contiguous ECG leads was correlated with major coronary artery distributions on nuclear perfusion imaging. RESULTS: For the 1842 evaluated territories, the fragmented QRS complex was not superior to the Q wave in detecting fixed or mixed myocardial defects. The fragmented QRS complex was associated with worse sensitivity (1.7%) in comparison to the Q wave (31.7%) for identifying myocardial scar. The fragmented QRS complex carried a higher false positive rate in patients with normal perfusion scans (15.8%, 221 segments), in comparison to Q waves (1.4%, 17 segments). CONCLUSION: In our study population, both the fragmented QRS and Q wave had poor sensitivity and specificity in detecting fixed or mixed myocardial scar. Larger studies are needed to evaluate fragmented QRS as a surrogate of myocardial scar before it can be incorporated into clinical practice.

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BACKGROUND: The role of coronary perfusion in the maintenance of atrial fibrillation (AF) electrical sources that anchor to the posterior (wall of the) left atrium (PLA) has been incompletely investigated. We hypothesized that the PLA-pulmonary vein region is perfused by branches originating from both the right and left coronary arteries. OBJECTIVE: The purpose of this study was to evaluate whether branches originating from the right and left coronary arteries could serve as conduits to chemically ablate restricted PLA regions. METHODS: In Langendorff-perfused sheep hearts, the right anterior and left anterior atrial arteries (RAAA and LAAA) and the branches of the left circumflex artery (LCX) were identified as main coronary artery branches perfusing the atria. During sustained AF, 20-mL boluses of cold Tyrode's solution (4°C) was injected into each artery to determine changes in dominant frequency. The injection that yielded the largest dominant frequency decrease indicated the coronary branch to be subsequently perfused with ethanol. Ethanol was selectively injected into the LAAA (n = 4), LCX (n = 4), or RAAA (n = 1). RESULTS: Six of nine AF cases rapidly terminated upon ethanol perfusion. In those hearts and in eight additional preparations (n = 17), Congo red and Evans blue was subsequently perfused into the remaining atrial branches. The perfusion territories were classified as triple-vessel PLA perfusion (n = 4), LAAA-dominant PLA perfusion (n = 5), balanced double-vessel PLA perfusion (n = 5), and LCX or RAAA dominant (n = 3). CONCLUSION: PLA coronary perfusion relies on a variable contribution of right and left coronary branches. Regional irrigation of ethanol in well-delineated PLA perfusion territories enabled ablation of high-frequency sites during AF.

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BACKGROUND: Left atrial appendage (LAA) isolation is rare and may be associated with impaired transport function and thromboembolism. OBJECTIVE: The purpose of this study was to determine the mechanisms of inadvertent isolation of the LAA during atrial fibrillation (AF) ablation. METHODS: This study consisted of 11 patients (ejection fraction 0.43 +/- 0.18, left atrial diameter 51 +/- 8 mm) with persistent AF who had LAA conduction block during a procedure for AF (n = 8) or atrial tachycardia (AT) (n = 3). RESULTS: LAA conduction block occurred during ablation at the Bachmann bundle region in 6 patients, mitral isthmus in 3, LAA base in 2, and coronary sinus in 1. The mean distance from the ablation site to the LAA base was 5.0 +/- 1.9 cm. LAA isolation was transient in all 6 patients in whom LAA conduction was monitored and was permanent in the 4 patients in whom conduction was not monitored during energy delivery. The remaining patient was noted to have LAA isolation during a redo procedure before any ablation. Nine of (82%) the 11 patients have remained arrhythmia-free without antiarrhythmic drugs at mean follow-up of 6 +/- 7 months, and all have continued taking warfarin. CONCLUSION: Electrical isolation of the LAA may occur during ablation of persistent AF and AT even when the ablation site is remote from the LAA. This likely is due to disruption of the Bachmann bundle and its leftward extension, which courses along the anterior left atrium and bifurcates to surround the LAA. Monitoring of LAA conduction during ablation of persistent AF or AT is important in avoiding permanent LAA isolation.

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Breathing is regulated by a central neural oscillator that produces rhythmic output to the respiratory muscles. Pathological disturbances in rhythm (dysrhythmias) are observed in the breathing pattern of children and adults with neurological and cardiopulmonary diseases. The mechanisms responsible for genesis of respiratory dysrhythmias are poorly understood. The present studies take a novel approach to this problem. The basic postulate is that the rhythm of the respiratory oscillator can be altered by a variety of stimuli. When the oscillator recovers its rhythm after such perturbations, its phase may be reset relative to the original rhythm. The amount of phase resetting is dependent upon stimulus parameters and the level of respiratory drive. The long-range hypothesis is that respiratory dysrhythmias can be induced by stimuli that impinge upon or arise within the respiratory oscillator with certain combinations of strength and timing relative to the respiratory cycle. Animal studies were performed in anesthetized or decerebrate preparations. Neural respiratory rhythmicity is represented by phrenic nerve activity, allowing use of open-loop experimental conditions which avoid negative chemical feedback associated with changes in ventilation.In animal experiments, respiratory dysrhythmias can be induced by stimuli having specific combinations of strength and timing. Newborn animals readily exhibit spontaneous dysrhythmias which become more prominent at lower respiratory drives. In human subjects, swallowing was studied as a physiological perturbation of respiratory rhythm, causing a pattern of phase resetting that is characterized topologically as type 0. Computational studies of the Bonhoeffer-van der Pol (BvP) equations, whose qualitative behavior is representative of many excitable systems, supports a unified interpretation of these experimental findings. Rhythmicity is observed when the BvP model exhibits recurrent periods of excitation alternating with refractory periods. The same system can be perturbed to a state in which amplitude of oscillation is attenuated or abolished. We have characterized critical perturbations which induce transitions between these two states, giving rise to patterns of dysrhythmic activity that are similar to those seen in the experiments. We illustrate the importance of noise in initiation and termination of rhythm, comparable to normal respiratory rhythm intermixed with spontaneous dysrhythmias. In the BvP system the incidence and duration of dysrhythmia is shown to be strongly influenced by the level of noise. These studies should lead to greater understanding of rhythmicity and integrative responses of the respiratory control system, and provide insight into disturbances in control mechanisms that cause apnea and aspiration in clinical disease states. (c) 1995 American Institute of Physics.