Harold Ensign Bennet Pardee.

Harold Ensign Bennet Pardee (1886–1973) (Fig. 1) was born in New York City on December 11, 1886, the son of Dr. Ensign Bennet Pardee and Clare Burton Pardee.1, 2 He received his A.B. degree from Columbia College in 1906, at the age of 18, and his M.D. from the College of Physicians and Surgeons in 1909. During three years of postgraduate training at The New York Hospital, he became interested in diseases of the heart under the guidance of Lewis A. Conner and of Horatio Burt Williams, who introduced one of the earliest string galvanometers (the electrocardiograph) into American practice. Pardee began working in the Medical Clinic of The New York Hospital in 1912. He served in the Army Medical Corps during the First World War and spent time at Colchester in the United Kingdom at the heart hospital established by Thomas Lewis to deal with the prevalent problem of “soldier’s heart.” Pardee is best known for his pioneering research on the electrocardiographic (ECG) recognition and characterization of myocardial infarction and ischemia. “An electrocardiographic sign of coronary artery obstruction” was published in the Archives of Internal Medicine in 1920,3 at a time when there was increasing interest in the role of the ECG in the evaluation of coronary occlusion. In 1918, Fred Smith in Chicago had reported ECG repolarization changes that accompanied ligation of the coronary arteries in dogs.4 The following year, James B. Herrick, also from Chicago, published a paper in which T-wave inversion in a 42-year-old physician, studied 6 weeks and also 6 months after clinical coronary occlusion, was noted to be similar to the experimental findings of Smith.5 Pardee’s 1920 paper is historically important because it contained the first clear description of the typical evolution of ECG findings in myocardial infarction in humans. He made several significant observations in this paper. Perhaps most notable is Pardee’s clear description of transient ST-segment elevation during the acute phase of infarction, which he described as a takeoff of the T wave from the descending R wave, well above the ECG baseline. Paul Dudley White later called this finding “Pardee’s sign.” The main emphasis of Pardee’s paper, however, was on the evolution of more persistent symmetric T-wave inversion with a shortened ST segment during the later phases of infarction, as previously observed by Smith and by Herrick.4, 5 Pardee believed the finding was characteristic of old thrombosis, and he called this ECG abnormality the “coronary T wave.”3 Today, this T-wave inversion would be interpreted as chronic localized ischemia. His paper also included a careful review of a series of about 1,000 ECGs, presumably assembled from hospital and patient records. Within this group he identified four additional cases of the “coronary T wave,” and in each case the patient had a history consistent with coronary artery disease. Pardee was working only with the three standard limb leads. In this paper, he erroneously attributed the axis shift associated with localized necrosis (as a result of what would now be considered pathologic Q waves) to ventricular hypertrophy secondary to infarction. During the subsequent two decades, Pardee made periodic contributions to the literature on ECG recognition of the varied manifestations of coronary artery disease. He dedicated the first edition of his text, Clinical Aspects of the Electrocardiogram, published in 1924, to Horatio Williams.6 This book was well received, and new editions appeared in 1928, 1933, and 1941. Summarizing progress in the ECG recognition of coronary occlusion in the third edition, Pardee observed that “if records are taken soon enough and are taken frequently, a special series of changes will be found in about 90 per cent of patients suffering from this condition.” He noted that soon after occlusion, the part of the curve that is most strikingly affected Clin. Cardiol. 28, 396–398 (2005)