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The mortality of a group of Canadians who survived myocardial infarction for at least three months was compared with the mortality of medically selected lives insured in Canada at standard rates. The results were expressed as the ratio of the actual deaths incurred in the infarction group to the deaths expected according to the insured table. There were 120 men, approximately 25 in each decade from the fourth to the eighth inclusive, with no condition other than coronary disease which might affect survival. The severity and number of infarcts did not influence selection.Calculating from the date of entry into the study the mortality ratio after 10 years was 530%. Calculating from the date of first infarction, the mortality ratio from 0 to five years was 980%, from six to 10 years 510% and after 10 years 320%. The mortality ratio was greatest in the fourth decade, 9400%, and decreased progressively: fifth, 2400%; sixth, 1300%; seventh, 400%; eighth, 230%. In the younger groups the high mortality ratios were due to the small number of expected deaths at young ages, not to an increase in the absolute number of actual deaths. In each age group the mortality ratio decreased with time but remained substantially increased even after 10 years. The mortality experience of this coronary group was worse than that of more rigidly selected, insured coronary groups.

Male and female death rates from all the major forms of cardiovascular disease were approximately equal until about 1920. Since that time the male:female ratio in fatal ischemic heart disease (IHD) has risen dramatically, but some closely related diseases such as cerebrovascular disease and uncomplicated angina pectoris have maintained sex ratios close to unity. It is difficult to reconcile this divergent trend in the sex ratio of IHD with a simple stenotic-thrombotic view of myocardial infarction (MI) and it is suggested that the modern epidemic of MI in men may be the result of a disorder of muscle metabolism ("vulnerable myocardium") superimposed on a relatively stable background of stenotic-thrombotic arterial disease. The proposed mechanism would also help to explain the selective action of some modern "coronary risk factors" (such as cigarette smoking and physical inactivity) which increase the risk of MI but have little or no effect on the risk of developing cerebrovascular disease or uncomplicated angina pectoris.