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September 1965

Massive Pulmonary EmbolismV. Evolution of Electrocardiographic and Enzyme Changes in Survivors

Author Affiliations

From the Department of Surgery, University of Maryland School of Medicine. Pangborn Fellow in peripheral vascular disease (Dr. Just-Viera) and Research Fellow in Cardiology, National Institutes of Health (Dr. Gonzalez).

Arch Surg. 1965;91(3):497-503. doi:10.1001/archsurg.1965.01320150127024

RECOGNITION of the growing importance and increasing frequency of pulmonary embolism has centered attention on these aspects of thromboembolism: diagnosis, differentiation from and contribution to myocardial infarction, and evolution and prognosis.

Awareness of thromboembolism is essential for its diagnosis. The electrocardiogram (ECG) and serial x-rays are useful aids, but the presence of small clots in the pulmonary artery remains difficult to establish conclusively. Wacker and co-workers1 described a potentially useful triad for the diagnosis of pulmonary embolism: (1) an increase in serum lactic acid dehydrogenase (SLDH) levels within 24 hours after the embolic episode; (2) normal levels of serum glutamic oxalacetic transaminase (SGOT); and (3) an increase in serum bilirubin levels.

The present report describes the evolution of electrocardiographic changes following nonlethal pulmonary embolism in dogs, relates such changes to variation in SLDH and SGOT levels following embolism, and presents the electrocardiograph patterns observed after embolization of animals with

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