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IN MEMORIAM In Memoriam: Albert L. Waldo, MD, PhD (Hon) (1936–2023) G. Neal Kay, MD,* Ken Okumura, MD, PhD, FHRS,† Judith A. Mackall, MD, FHRS,‡ Andrew E. Epstein, MD, FHRSx From the *Electrophysiology Section, University of Alabama at Birmingham, Birmingham, Alabama, † Division of Cardiology, Saiseikai Kumamoto Hospital, Kumamoto, Japan, ‡ Electrophysiology Section, University Hospitals of Cleveland Medical Center, Case Western Reserve University, Cleveland, Ohio, and x Electrophysiology Section, Cardiovascular Division, University of Pennsylvania, Philadelphia, Pennsylvania. On August 17, 2023, the electrophysiology community lost a pioneer whose contributions are hard to overstate. Albert L. Waldo, MD, PhD (Hon), was a true genius who took obser- vations from the bedside and generated profound insights into the underlying mechanism of atrial flutter, supraventric- ular tachycardia, and ventricular tachycardia (VT). Dr Waldo was born in Bronx, NY. He was the son of Jew- ish immigrants, and his father was a Julliard-trained conductor and music teacher and his mother a homemaker. After receiving his MD degree from the SUNY Downstate University College of Medicine in 1962 with subsequent training at Kings County Hospital, Brooklyn, NY, where he was chief resident, and Johns Hopkins University School of Medicine, Baltimore, MD, he came to Columbia Univer- sity, New York City, NY, for a fellowship in cardiology. There he met his mentor Brian Hoffman, MD, and began in- traoperative recording of electrograms. In 1972 he joined the University of Alabama at Birmingham (UAB) and in 1986 was recruited to University Hospitals of Cleveland to estab- lish the Cardiac Electrophysiology Section. Before leaving New York, he married Rosin Torres, his amazing wife and dear friend to many. At UAB Dr Waldo developed a canine sterile pericarditis model to understand the mechanism of postoperative atrial arrhythmias, pioneered multisite mapping in this model as well as in humans undergoing open heart surgery, estab- lished antitachycardia pacing as a means to terminate arrhythmias, and most importantly described transient entrainment. Stemming from his observations of rapid atrial pacing using temporary epicardial pacing electrodes during postoperative atrial flutter,1 Dr Waldo demonstrated that overdrive pacing at a critically rapid rate could terminate atrial flutter. He showed that pacing at progressively faster rates from the high right atrium could accelerate the atrial rate to that of the pacing rate without interrupting this arrhythmia. However, his sentinel observation was that at pacing rates sufficient to interrupt atrial flutter by pacing from the high right atrium, there was an abrupt change from a negative to a positive P-wave morphology associated with a decrease in activation time to the posterior-inferior left atrial electrode recording site. These initial observations led him to coin the term “transient entrainment of a tachy- cardia.” 2,3 The critical insights leading to our understanding of tran- sient entrainment came from Dr Waldo’s observations of rapid pacing during VT. His breakthrough observation was from a patient with postoperative VT with 1:1 retrograde atrial activation. By pacing the atrium at a rate faster than the spontaneous VT rate, he showed that the ventricular rate could be accelerated to the atrial pacing rate associated with the shortening of the QRS duration. This suggested that transient entrainment of a tachycardia occurs when each antidromic wavefront from the pacing impulse resets the tachycardia to the pacing rate while colliding with the Address reprint requests and correspondence: Dr Andrew E. Epstein, Electrophysiology Section, Cardiovascular Division, Hospital of the University of Pennsylvania – Pavilion, One Convention Avenue, Level 2, City Side, Philadelphia, PA 19104. E-mail address: andrew.epstein@ pennmedicine.upenn.edu. 1547-5271/$-see front matter Published by Elsevier Inc. on behalf of Heart Rhythm Society. https://doi.org/10.1016/j.hrthm.2023.09.008

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