scope:

Summary

1. Evaluation of the clinical course, indices of the severity of infarction, and hemodynamic changes in patients admitted with chest pain at the Johns Hopkins Hospital has been made in relation to smoking intensity as determined by measurements of carboxyhemoglobin and thicyanate on admission. Smoking has been evaluated as an indication of CO exposure because it is the principal source of such exposure in Baltimore.

2. Among 140 confirmed cases of myocardial infarction recent or current smokers had evidence of larger infarcts than non-smokers with ex-smokers intermediate. This difference could not be explained by differences in sex, age and race in the three groups.

3. When age is taken into account, the recent smokers had higher mortality than the non-smokers or ex-smokers.

4. Hemodynamic function was relatively good in recent smokers, despite their larger infarcts, perhaps due to catecholamine release associated with smoking.

5. These results are consistent with both an acute and chronic effect on the myocardium of long-term low-level exposures to CO, but clearly cannot be related to that factor by itself. Other constituents of cigarette smoke may be of equal or greater importance in these effects than CO.

6. Because of the relative importance of smoking as a source of CO exposure in the general population, it is unlikely that research on the effects of low-level CO exposure in man can be carried further by this type of study. A more promising group to study would be large groups occupationally exposed to CO alone, in whom the role of cigarette smoking could be assessed independently of CO exposure.