Raymond D. Pruitt

Left axis deviation induced experimentally in a primate heart

Abstract Production of a septal laceration which interrupts the anterior rami of the left bundle branch in the baboon heart is attended by changes in the spread of excitation into the anterior free wall of the left ventricle. These changes are expressed in the following electrocardiographic alterations: (a) Delay of arrival of excitation at the epicardium of the involved area. Degree of delay ranged from zero at boundaries of the involved area to 20 milliseconds or more at central points. (b) Shift to the left of mean electrical axis in the frontal plane to a degree sufficient to satisfy criteria for clinically significant left axis deviation in the human being. These results are compared with those derived from similar and previously reported studies on dogs, wherein lesser degrees of axis shift were encountered. Species differences in results are believed to depend primarily on differences in the mode of spread of excitation into the ventricular myocardium. These latter differences, in turn, may derive from species peculiarities in the distribution of the major divisions of the left bundle branch, and in the degree to which terminal ramifications of the rapid conduction pathways penetrate the free wall of the left ventricle.

Simulation of Electrocardiogram of Apicolateral Myocardial Infarction by Myocardial Destructive Lesions of Obscure Etiology (Myocardiopathy)

A myocardial destructive process unrelated to occlusive coronary arterial disease has been documented at necropsy in two patients aged 37 years and 23 years at the time of death. In the third patient, 25 years of age, electrocardiographic findings of a transmural lesion of the apicolateral wall of the left ventricle existed in the absence of evidence of impaired myocardial reserve. The nature of myocardial destruction encountered in cases 1 and 2 is compared with that in the case of parchment heart described initially by Osler. The theoretic implications of total loss of R waves in semidirect leads overlying a region of epicardial destruction are noted.

The difficult electrocardiographic diagnosis of myocardial infarction

Summary A review of data on patients suffering from acute pancreatitis provides few instances wherein electrocardiographic evidence of acute myocardial injury or necrosis developed under circumstances in which concomitant coronary insufficiency was not a more likely cause of the myocardial damage. Experimentally induced acute pancreatitis and the intravenous injection of pancreatic enzymes were not attended by electrocardiographic changes of the kind associated with myocardial infarction. Therefore, if a patient suffering from acute pancreatitis develops electrocardiographic changes indicative of acute myocardial infarction, it is likely that a disparity between coronary flow and myocardial need has resulted in myocardial infarction. Intracranial hemorrhage or trauma commonly induces cardiac arrhythmias and changes in T waves, probably by increased vagal stimulation. However, the eletrocardiographic changes described in all except one of the reports reviewed supply only inferential evidence of myocardial injury. Unless other clinical evidence supports existence of myocardial infarction, that diagnosis rests insecurely. Electrocardiographic evidence of confluent myocardial scar rarely is encountered in patients having primary myocardial disease. This conclusion is consonant with the disseminated focal myocardial changes that characterize this type of myocardial disease morphologically. Segmental and T wave changes in acute pericarditis may mimic those of myocardial infarction; the presence of pathologic Q waves, however, is distinctive of infarction. Cor pulmonale, acute or chronic, may simulate posterior myocardial infarction, but only rarely in a degree sufficient to induce sustained justified confusion. A major acute myoccardial infarction may prove difficult of diagnosis when the infarct is transmural but of small circumference, when it is confined to subendocardium, or to the lateral or posterolateral wall of the left ventricle. The nature of electrocardiographic changes induced by such lesions and the basis for their peculiar features are reviewed. Healed myocardial infarcts frequently produce no electrocardiographic changes permitting recognition of the scar. Such scarring almost certainly is responsible for some instances of major shifts in mean electrical axis to the left (left-axis deviation of −30 to −90, S 2 S 3 pattern). However, review of two pathologic studies supports the judgment that uncomplicated left-axis deviation is a perilous sole criterion on which to rest a diagnosis of myocardial infarction.

Electrocardiogram of Bundle-Branch Block in the Bovine Heart

The electrocardiographic consequences of blocking the right or left bundle branch have been recorded in experiments on calves. Block of either bundle was attended by lengthening of QRS interval by approximately 0.02 second and by changes in form of QRS paralleling closely those occurring in canine hearts under comparable circumstances. Significance of this parallelism to concepts of morphology and function of ventricular conduction systems in bovine and canine hearts is considered. Data reported here render problematic the concept of functional continuity of right and left divisions of the specialized ventricular conduction tissue in the bovine heart.

Calcified aneurysm of the left ventricular apex associated with intraventricular block of the left bundle branch type.

Abstract 1. 1. Data are presented on a patient who had a calcified aneurysm of the left ventricle and who had survived for 17 years after the episode of acute myocardial infarction which eventuated in the aneurysm. 2. 2. Electrocardiographic changes were those of intraventricular block of the left bundle branch type combined with anteroseptal myocardial infarction. 3. 3. Correlation between predicted location of the scar as derived electrocardiographically and the site of the lesion as delineated by calcific deposition in the aneurysmal wall was acceptably precise.