Abstract
Even before the important rôle of phosphocreatine in muscular contraction was recognized, Constabel 1 noted that there was a decreased total creatine content in those human hearts that showed either clinical or post-mortem evidence of damage. Recently Cowan 2 has examined a larger group of hearts, and found that myocardial failure is accompanied by a creatine content that is markedly below normal. Seecof, Linegar and Myers 3 , whose method for determining myocardial creatine we have employed, have also examined a series of human hearts, emphasizing particularly the higher creatine concentration in the left ventricular muscle as compared to the right ventricle.
In our laboratory we have approached from several experimental angles the question of the chemical changes that initiate or accompany heart failure. Since our primary interest is clinical, we have also analyzed muscle from the left ventricle of human hearts, as this material became available from time to time. 4 In Table I we have summarized creatine determinations on 105 additional human hearts. The total creatine has been determined, the total solids, and from this calculated the percentage of creatine on a dry basis. The normal values have been determined in hearts from patients that died a traumatic or surgical death, and in hearts from those who died from an infectious disease, yet showed no gross or microscopic evidence of myocardial involvement. We list the mean value, with the standard deviation from the mean.
In hypertrophied hearts, which have not failed, the values for total creatine are elevated; in those with myocardial change secondary to coronary sclerosis, the averages are low. The creatine content of hearts that have failed is reduced, averaging 30% below normal. Low values were also obtained in hearts that showed microscopic changes, inflammatory or degenerative, from patients that had died of infectious disease.
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