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T H Everett

Publications and source records attributed to T H Everett.

6 recordsLinked to original sources

Assessment of global atrial fibrillation organization to optimize timing of atrial defibrillation.

BACKGROUND: We hypothesized that frequency domain analysis of a wide bipolar interatrial electrogram describes the global organization of atrial fibrillation (AF) and should vary over time. By timing shocks to periods of high organization of AF, cardioversion efficacy should improve. METHODS AND RESULTS: A total of 15 dogs (weight, 28.2+/-3.4 kg) were rapidly paced for 48 to 72 hours to induce AF. Coil electrodes with a surface area of 1.80 cm(2) were then placed in the left and right atria to form a wide bipole. Wide bipolar electrograms were digitally filtered, and a fast Fourier transform was performed over a sliding 2-s window every 0.5 s. The organization index (OI) was calculated as the ratio of the area of the dominant peak and its harmonics to the total area of the magnitude spectrum. The atrial defibrillation threshold (ADFT(50)) was determined using a 3-ms/3-ms biphasic shock and an up-down-up protocol. Additional shocks with higher and lower energies were delivered in a random sequence to develop a distribution curve. The OI varied over time, with a mean of 0.42+/-0.03, a maximum of 0.65+/-0.07, and a minimum of 0.20+/-0.06. The OI changed rapidly, with durations of high organization (OI>0.5) ranging from 1 to 5 s. The ADFT(50) for QRS complex-synchronized shocks was 183+/-56 V, versus 142+/-49 V for shocks synchronized to an OI>0.5 (P<0.001). The distribution curve shifted leftward when shocks were synchronized to an OI>0.5. CONCLUSIONS: AF signals show a high degree of variability. Shock efficacy is increased when shocks are delivered during periods of high AF organization as determined by the OI method.

Algorithms↗

The effects of atrial electrical remodeling on atrial defibrillation thresholds.

Electrical remodeling of atrial fibrillation may account for the increase in atrial defibrillation thresholds over time. The aim of this study was to examine the time course of electrical remodeling and the benefit of early defibrillation on the defibrillation threshold. Twenty-six mongrel dogs weighing 27.6 +/- 3.3 kg were induced into AF by repeated high output burst atrial pacing. Eight dogs were paced for multiple time periods of 5, 20, 40, and 60 minutes. Five dogs each had burst pacingfor 4 hours and 8 hours, and eight dogs were paced at a high rate (640 beats/min) for 48 hours. Biphasic atrial defibrillation shocks with a pulse width of 3/3 ms synchronized to the left apical electrogram were delivered to coil electrode catheters positioned in the lateral left and right atria. Defibrillation voltage was increased from 50 V in 20- to 30-V steps until defibrillation was successful. As the pacing period increased, a decrease in atrial fibrillation cycle lengths and atrial effective refractory period was not observed before 8 hours. Similarly, the defibrillation threshold did not change significantly until the 8-hour pacing period was reached. The defibrillation thresholds were 69 +/- 28 V for 5 minutes, 64 +/- 20 V for 20 minutes, 99 +/- 85 V for 40 minutes, 78 +/- 51 V for 60 minutes, 78 +/- 38 V for 4 hours, 124 +/- 33 V for 8 hours, and 133 +/- 32 V for 48 hours (mean +/- SD) (P < 0.05). Atrial electrical remodeling in a rapid atrial pacing canine model is not observed until after 4 hours of burst atrial pacing. The atrial defibrillation threshold increases with increasing duration of burst atrial pacing, and follows a similar time course to other parameters of electrical remodeling.

Animals↗

Role of calcium in acute hyperthermic myocardial injury.

INTRODUCTION: We hypothesized that intracellular calcium overload may play an important role in heat-induced myocardial injury. This postulate was investigated using a model of isolated guinea pig papillary muscle in which resting tension was measured as an indirect indicator of cytosolic free-calcium concentration and the fluorescence changes of Fluo-3 AM dye was measured as a direct indicator of cytosolic free-calcium concentration. METHODS AND RESULTS: Excised guinea pig right ventricular papillary muscles were attached to a force transducer in a high-flow tissue bath and superfused with Tyrode's solution at 37 degrees +/- 0.5 degrees C. The temperature was rapidly changed to between 38.0 degrees and 56.0 degrees C for 60 seconds and then returned to 37.0 degrees C. Hyperthermia caused a reversible increase in resting tension at temperatures between 45 degrees and 50 degrees C and irreversible contracture at > or =50 degrees C. Rapid cooling contracture experiments and experiments measuring fluorescence of myocytes loaded with 5 microM Fluo-3 AM dye demonstrated that the hyperthermia-induced rise in resting tension was likely due to an increase in intracellular calcium content. Inhibition of the sarcoplasmic reticulum calcium pump with 20 microM thapsigargin resulted in irreversible contracture of the papillary muscles at temperatures between 45 degrees and 50 degrees C and significant increases in Fluo-3 fluorescence at 48 degrees C. Blockade of sarcolemmal calcium channels with 0.5 mM cadmium or 40 microM verapamil did not attenuate the heat-induced increase in resting tension and Fluo-3 fluorescence. CONCLUSION: Hyperthermia causes an increase in resting tension of cardiac muscle that most likely is mediated by a calcium channel-independent increase in calcium permeability of the sarcolemmal membrane and/or release of stored intracellular calcium.

Acute Disease↗

Frequency domain algorithm for quantifying atrial fibrillation organization to increase defibrillation efficacy.

We hypothesized that frequency domain analysis of an interatrial atrial fibrillation (AF) electrogram would show a correlation of the variance of the signal and the amplitude of harmonic peaks with the periodicity and morphology (organization) of the AF signal and defibrillation efficacy. We sought to develop an algorithm that would provide a high-resolution measurement of the changes in the spatiotemporal organization of AF. AF was initiated with burst atrial pacing in ten dogs. The atrial defibrillation threshold (ADFT50) was determined, and defibrillation was repeated at the ADFT50. Bipolar electrograms from the shocking electrodes were acquired immediately preshock, digitally filtered, and a FFT was performed. The organization index (OI) was calculated as the ratio of the area under the first four harmonic peaks to the total area of the spectrum. For a 4-s window, the mean OI was 0.505 +/- 0.087 for successful shocks, versus 0.352 +/- 0.068 for unsuccessful shocks (p < 0.001). Receiver operator characteristic (ROC) curve analysis was used to determine the optimal sampling window for predicting successful shocks. The area of the ROC curve was 0.8 for a 1-s window, and improved to 0.9 for a 4-s window. We conclude that the spectrum of an AF signal contains information relating to its organization, and can be used in predicting a successful defibrillation.

Algorithms↗

Electrical, morphological, and ultrastructural remodeling and reverse remodeling in a canine model of chronic atrial fibrillation.

BACKGROUND: In patients with recurrent persistent atrial fibrillation (AF), vulnerability to AF persists indefinitely despite presumed completion of reverse electrical remodeling within days of return to normal sinus rhythm. Atrial electrical and anatomic remodeling and reverse remodeling were studied in a canine model of chronic AF. METHODS AND RESULTS: Chronic AF was induced in 8 dogs by creating moderate mitral regurgitation and rapidly pacing the right atrium at 640 bpm for >8 weeks. Measurements performed at baseline, after establishment of chronic AF, and then at 4 hours and again at 7 to 14 days after cardioversion to sinus rhythm included atrial effective refractory periods, AF cycle lengths, left atrial dimensions, premature atrial contraction (PAC) frequency, and atrial vulnerability to atrial extrastimuli. After establishing chronic AF, atrial effective refractory period shortening, increases in spontaneous PAC frequency, increases in left atrial size with loss of contractility, and multiple ultrastructural abnormalities were demonstrated. Complete reverse electrical remodeling and decreases in PACs were observed after 7 to 14 days of sinus rhythm, but there was no resolution of anatomic and ultrastructural abnormalities. Occurrence of spontaneous AF paralleled PAC frequency, but vulnerability to AF induction persisted (75% immediately after conversion versus 63% at 4 hours and 50% at 7 to 14 days) despite reverse electrical remodeling. CONCLUSIONS: After conversion from chronic AF to sinus rhythm in this canine model, electrical remodeling occurs rapidly. However, gross and ultrastructural anatomic changes persist, as does vulnerability to induced AF. Vulnerability to AF initiation 7 to 14 days after cardioversion is more dependent on persisting structural abnormalities than on electrophysiological abnormalities.

Animals↗

Morphological and physiological characteristics of discontinuous linear atrial ablations during atrial pacing and atrial fibrillation.

INTRODUCTION: Linear atrial ablations are thought to be necessary to accomplish successful catheter ablation of atrial fibrillation. In order to investigate the conduction characteristics of atrial myocardium in regions of linear lesion discontinuity (gaps), we performed activation sequence mapping in gap regions during atrial pacing and atrial fibrillation. METHODS AND RESULTS: In seven dogs, a linear epicardial ablation was created on the right atrial free wall with a discontinuous segment (gap) in the mid-portion of the lesion. A plaque electrode was used to measure conduction across the gap. Conduction was assessed during (1) atrial pacing from the edge of the plaque electrode during sinus rhythm, and (2) during atrial fibrillation. After each series of measurements, the lesion gap was decreased by creating additional radiofrequency ablations and repeat conduction maps were obtained. The process was repeated until conduction block was observed during atrial pacing. Gap lengths ranged from 0 to 25 mm. During atrial pacing, gaps as narrow as 2 mm demonstrated normal conduction and gaps as large as 5 mm demonstrated block during pacing. Although conduction block was never present across gaps greater than 5 mm, the ability to predict conduction block as a function of gap width was difficult for lesions < or = 5 mm due to a significant degree of overlap between normal conduction and conduction block in this gap range. During atrial fibrillation, 1/175 (0.6%) mapped wavelets conducted across gaps that demonstrated block during pacing; whereas, 411/600 (68.5%; P < 0.0001) wavelets conducted across gaps that did not demonstrate block during pacing (P = NS compared to preablation measurements). Histologically normal atrial myocytes were observed within gaps exhibiting conduction block. CONCLUSIONS: Visible gaps > 5 mm rarely demonstrate conduction block during atrial pacing and atrial fibrillation; whereas, gaps < or = 5 mm in length may demonstrate block. Lesion gaps that do not demonstrate conduction block during atrial pacing have no higher rate of functional conduction block during atrial fibrillation than fibrillating atria without ablation lesions.

Animals↗