Myocardial Destruction Research Articles

Abnormal Q waves simulating myocardial infarction in diffuse myocardial diseases

Two cases are presented in which deep QS deflections in multiple electrocardiographic leads simulated myocardial infarction. Both patients had diffuse myocardial disease; in one the cause was unknown, and in the other the condition was associated with pseudohypertrophic muscular dystrophy. It is pointed out that diffuse myocardial destruction or replacement from several causes can occasionally give rise to deep, impressive Q-wave changes.

Myocardial Necrosis in Rats: Serum Enzymes, Adrenal Steroid and Histopathological Alterations

Acute infarctoid myocardial necrosis has been produced in virgin rats by injection of isoproterenol. The lesions are essentially identical, both grossly and microscopically, with naturally occurring acute infarcts which we have observed in arteriosclerotic breeder rats. During the establishment of drug-induced necrosis the animals displayed signs of shock and congestive heart failure. Serum transaminases and lactic dehydrogenase levels underwent changes which coincided with the establishment and repair of the myocardial damage. The male rats had a higher mortality rate than the females. The male rats also developed more massive myocardial necrosis and showed a decreased capacity to repair myocardial damage. The adrenal glands became greatly hypertrophied and the thymus became severely involuted coincident with the acute establishment of the myocardial lesion. In vitro studies indicated that changes in adrenal function also accompanied the acute onset of myocardial destruction. The adrenal hypertrophy decreased during recovery from shock and during repair of the lesion.

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.

A study of the influence upon the spatial vectorcardiogram of localized destruction of the myocardium of dog

Superficial myocardial destruction was performed, in acute experiments, on 27 dogs by burning with soldering iron, torch, or electrocautery and by pericardial instillation of formaldehyde. The effect on the QRSsÊ loop of superficial localized myocardial loss was either not detectable or, more often, led to the appearance of a small deformity in the direction predicted by present-day electrocardiographic concepts. Similarly, shifts in S-T vectors and orientation of TsÊ loops, when recorded, were in the predicted direction. The use of a fixative, such as formaldehyde, is suggested as a possible means of producing acute and relatively discrete lesions in the study of the relations between the anatomic site and the electrical activity of cardiac muscle.

A SCIENTIFIC BASIS FOR THE SURGICAL TREATMENT OF CORONARY ARTERY DISEASE IN MAN

AFTER nearly a quarter century of relentless work in the surgical laboratory - against overwhelming odds, due in part to the intrinsic nature of the problem and in part to misleading dogmas in existing medical information, Beck and associates have demonstrated beyond any reasonable doubt that alterations of blood flow with measurable dynamics can be produced in the myocardium of the dog, greatly reducing both the mortality and the myocardial destruction resulting from acute obstruction of a major coronary artery. Some of the specific accomplishments in the surgical laboratory in the study of the coronary circulation, all firsts in the literature on this subject, by Dr. Claude S. Beck and associates are listed as follows: 1. Experimental studies began in 1932 to find direct surgical methods to improve collateral coronary circulation in obstructive diseases of coronary arteries.* 2. Demonstration of arterial extracardiac anastamoses, surgically produced of the caliber of large arterioles

CLINICAL OBSERVATIONS IN CASES OF MASSIVE MYOCARDIAL INFARCTION

MYOCARDIAL infarction is a dramatic episode in the course of coronary artery disease, but it is often thought of in terms of a disease entity with its own course, prognosis and treatment. With the occurrence of myocardial infarction, a new factor is introduced into the course of coronary artery disease with myocardial ischemia, namely, gross and irreparable destruction of a portion of the cardiac muscle. This damage to the myocardium determines the immediate prognosis and the ultimate outcome entirely independently of the degree and progression of coronary arteriosclerosis. Thus, the size of the area of the destroyed muscle is one of the important factors in the prognosis, yet little investigative work has been done in estimation of the size of a myocardial infarct during life. In terms of ordinary clinical thinking, a severe attack of pain with fully developed clinical signs of myocardial infarction is usually considered as evidence of