VIII. I'll \i;m AcoLooY 565 



which in;i>' l)c cilhcr primary or sccoiidarx' to, or (luitc iii(|('|)('ii(|ciit of, ii 

 primary disease process. 



1. Heart Disease 



\'oS('Isanj>;, Shute, and Shute'^"'" report that intensive tocopherol therapy 

 usually ameliorates or abolishes the clinical signs and symptoms (anginal 

 pain, exertional dyspnoea, fatiguahility, lowered exercise tolerance) of coro- 

 nary, rheumatic, and hypeitensive heart disease, and also hastens the reso- 

 hition of coronary throml)i and the recovery of damaged cardiac tissue. 

 These effects are attributed to a pharmacologic action of a-tocopherol in 

 decreasing the oxygen requirement of cardiac muscle, in helping to resolve 

 and also in preventing intravascular thrombi, and in improving the func- 

 tional state of the capillary bed. Although, as they point out, there is con- 

 siderable experimental evidence to support such postulations, there are 

 also certain etiologic and other differences between cardiac disease in man 

 and the experimentally induced lesions of vitamin E deficiency. Clinical 

 reports""'^ which might be considered as supporting these claims record a 

 total of 109 cases of heart disease, of which 40 were regarded as being bene- 

 fited to a variable degree by tocopherol therapy. On the other hand, another 

 series of clinical reports, ^^"^^ representing observations on a total of 252 



« A. li. Vogelsang, E. V. Shute, and W. E. Shute, Med. Record 160, 21 , 163, 279 (1947) ; 



161, 83, 155 (1948). 

 ' W. E. Shute, E. V. Shute, and A. B. Vogelsang, Med. Record 160, 91, 230 (1947); 



Ann. Internal Med. 30, 1004 (1949). 



8 W. E. Shute, Summary 1, 13 (1949); 3, 19 (1951). 



9 W. E. Shute and E. V. Shute, Summarij 2, 3 (1950). 



'« A. L. Pascoe and W. E. Shute, Summari/ 1, 50 (1949). 



" M. B. Molotchick, Med. Record 160, 11 (1947). 



'- L. Pin, Contribution to the Study of the Physiological and Therapeutic Properties 



of Vitamin E. Maurice Lavergne, Paris, 1947. 

 >3 K. P. Ball, Lancet, I, 116 (1948). 



'* C. N. J. Gram and V. Schmidt, Nord. Med. 37, 82 (1948). 

 '» X. Agadjanian, J. Med. Paris 68, 29 (1948); Summary 3, 50 (1951). 

 ''' J. Dedichen, Xord. Med. 41, 324 (1949). 

 '" S. Baer, W. I. Heine, and D. B. Gelfond, Am. J. Med. Sci. 215, .542 (1948); Ann. 



X. y. Acad. Sci. 52, 412 (1949). 

 " H. Levy and E. P. Boas, Ann. Internal Med. 28, 1117 (1948). 

 '' D. II. Makinson, S. Oleesky, and R. V. Stone, Lancet I, 102 (1948). 

 2" G. L. Baum and W. Stein, Wisconsin Med. J. 48, 315 (1949). 

 -' C. K. Donegan, A. L. Messer, E. S. Orgain, and J. M. Ruffin, Am. J. .Med. Sci. 



217, 294 (1949). 

 " II. Eiehert, Southern .Med. J. 42, 717 (1949). 

 2' J. Travell, S. H. Rinzler, H. Bakst, Z. II. Benjamin, and .\. L. Hohl), Ann. X. Y. 



Acad Sci. 52, 345 (1949). 

 2^ H. P. Rush, Calif. .Med. 71, 381 (1949). 

 " I. S. Ravin and K. H. Katz, Xew Engl. J. Med. 240, 331 (1949). 



