Thomas F. Fitzgerald's research while affiliated with Baystate Medical Center and other places
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Publications (6)
Digitalis and Ventricular Tachycardia. Digoxin was used to treat a patient with an adenosine-sensitive ventricular arrhythmia. The patient had an exercise-induced ventricular tachycardia that was evaluated electrophysiologically and displayed characteristics of a triggered arrhythmia. The tachycardia was terminated reproducibly with 12 mg of intrav...
Premature atrial stimuli delivered during the relative refractory or "vulnerable" period exhibit increased local stimulus-response latency and may occasionally induce atrial arrhythmias. The use of adenosine to treat supraventricular tachycardias may also provoke atrial arrhythmias. In this study we investigated the effects of adenosine on the late...
Ventricular premature stimuli were used to demonstrate adenosine-mediated decreases in the retrograde refractoriness of accessory atrioventricular connections. This response is consistent with the concept that accessory atrioventricular connections have electrophysiologic properties that are similar to those of atrial myocardium.
Intravenous adenosine produced slight decreases in conduction times for premature atrial complexes but proportionally greater shortening of the functional refractory period. Decreased wavelength may provide a basis for transient atrial fibrillation, which is sometimes observed after adenosine administration.
Several forms of antitachycardia pacing have been used successfully for terminating cardiac arrhythmias, and implantable devices now incorporate a tier of overdrive pacing for treating of ventricular tachycardia (VT). No consensus exists regarding the optimal mode of pacing therapy. Accordingly, a prospective, randomized, crossover study of antitac...
Citations
... The ADA levels reflect cellular immune functionality (25) and are also closely associated with CVDs (26-28). Adenosine, a degradation product of ATP, has been attributed to exert different effects on heart: a protective agent for reperfusion heart on one hand (29-31) and a harmful agent for induction of some heart diseases such as atrial fibrillation and atrial flutter on the other hand (32)(33)(34). The induction of atrial fibrillation by adenosine has been well recognized and the possible underlying mechanisms include sympathoexcitatory effects, direct stimulatory effects on pulmonary vein tissue and the shortening of atrial action potential duration (32). ...
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... It was concluded that, although reflex activation of the sympathetic nervous system with a rapid increase in catecholamine levels may potentially contribute to a decrease in refractoriness, this may also result from a direct effect of adenosine, similarly as observed in working atrial myocytes. 2 Our case is unique in that the AP conduction was most likely dependent on adenosine and was unmasked independently of any alteration in AV node conduction potentially resulting from the drug. Whether this phenomenon could have been demonstrated after the previous procedure is unknown, as adenosine was not administered at that time. ...
... Even though the time elapsed for delivery of 3 pulses with 30 ms duration would be shorter that the reported action potential duration recorded in vitro in swine ventricle at physiological temperatures (> 100 ms; Roscher et al., 2001), it is possible that the in vivo conditions, such as transient myocardial ischemia and increased catecholamine release, resulting from the interruption of cardiac pumping during VF, may have resulted in action potential shortening (Christé et al., 2006;Hoeker et al., 2014). In this case, it is likely that defibrillatory pulses would reach some cells during the relative refractory period (vulnerable period), which would favor arrhythmia reinitiation (Corbisiero et al., 1999), thus masking or even reverting the beneficial effect of multidirectional defibrillation. These observations point out the importance of using short shocks for efficient multidirectional defibrillation. ...
