Hyperestrogenemia and hypotestosteronemia have been observed in association with myocardial infarction (MI) and its risk factors. To determine whether these abnormalities may be prospective for MI, estradiol and testosterone, as well as risk factors for MI, were measured in 55 men undergoing angiography who had not previously had an MI. Testosterone (r=-.36, /"=.008) and free testosterone (r=-A9, P<.001) correlated negatively with the degree of coronary artery disease after controlling for age and body mass index. When the patient group was successively reduced to a final study group of 34 men by excluding the patients with other major disorders, the testosterone and free testosterone correlations persisted (r=-.43, P<.02 and r=-.62, /><.001, respectively). Neither estradiol nor the risk factors, except for T he observations in men of hyperestrogenemia after myocardial infarction (MI), 1 of an association of sex hormones with risk factors for MI, 2 ' 3 and of a concurrence of risk factors for MI in clinical states other than MI and in populations 24 led to the hypothesis that an elevation in the estradiol-to-testosterone ratio or some closely related hormonal alteration may underlie risk factors and that hyperestrogenemia may lead to MI in men. 2 ' 3 Most laboratories studying sex hormones and MI in men have reported a high estradiol level after MI, both acutely 59 and months to years later. 612 Other laboratories have observed a low testosterone level, 1316 and yet others have observed both abnormalities 17 ' 20 after MI. Prospective studies for MI, however, have thus far failed to show an abnormality in the level of either estradiol 2125 or testosterone. 2123 ' 25 The present study investigated whether a hormonal abnormality might be prospective for MI by determining the sex hormone levels in relation to the degree of coronary artery disease (CAD) in men who had not had an MI. The serum estradiol and testosterone levels as well as the levels of risk factors for MI were measured in 55 men undergoing coronary angiography who had not had an MI. Methods PatientsFifty-five male patients undergoing coronary angiography were studied. The patients had been referred to the Cardiac Catheterization Laboratory of Roosevelt Hospital for evaluaReceived September 23, 1993; revision accepted February 10, 1994.From the Department of Medicine, Columbia University College of Physicians and Surgeons, St. Luke's-Roosevelt Hospital Center, New York, NY.Reprint requests to Dr Gerald B. Phillips, Roosevelt Hospital, 428 W 59th St, New York, NY 10019.high-density lipoprotein cholesterol, correlated with the degree of coronary artery disease in the final group. Testosterone correlated negatively with the risk factors fibrinogen, plasminogen activator inhibitor-1, and insulin and positively with high-density lipoprotein cholesterol. The correlations found in this study between testosterone and the degree of coronary artery disease and between testosterone and other risk factors for MI raise the possibility that in men hypote...

Although sex hormones appear to be importantly involved in the development of coronary heart disease, apparently no study has yet reported an alteration in an endogenous sex hormone level in relation to coronary heart disease in women. In an attempt to determine whether any sex hormone abnormality might be a factor in the development of myocardial infarction in women, estradiol and testosterone, as well as sex hormone-binding globulin, insulin, dehydroepiandrosterone sulfate, and risk factors for myocardial infarction, were measured in relation to the degree of coronary artery disease (CAD) in 60 postmenopausal women undergoing coronary angiography. In a multiple-regression analysis with the degree of CAD as the dependent variable and free testosterone (FT), estradiol, age, body mass index, systolic blood pressure, cholesterol, smoking, and insulin as independent variables in the model, only FT (P < .008) and cholesterol (P = .01) were significantly related to the degree of CAD, both positively. To exclude a possible confounding effect due to prior myocardial infarction, the multiple-regression analysis was repeated for the subgroup of 49 patients remaining after excluding the 11 patients who had ever had a myocardial infarction; again only FT (P < .04) and cholesterol (P = .05) were significantly related to the degree of CAD. Neither total testosterone in place of FT nor HDL cholesterol in place of total cholesterol in the model was significantly related to CAD. Sex hormone-binding globulin and dehydroepiandrosterone sulfate, added individually to the model, showed no significant relationship to CAD. These results raise the possibility that in women an elevated FT level may be a risk factor for coronary atherosclerosis.

Both hyperestrogenemia and hypotestosteronemia have been reported in association with myocardial infarction (MI) in men. It was previously observed that the serum testosterone concentration correlated negatively with the degree of coronary artery disease (CAD) in men who had never had a known MI. The present study investigated the relationship of sex hormone levels to the thrombotic component of MI by comparing these levels in 18 men who had had an MI (ie, thrombosis) and 50 men with no history of MI (ie, no thrombosis) whose degree of CAD was in the same range. The mean degree of CAD, age, and body mass index in these two groups was not significantly different. The mean serum estradiol level in the men who had had an MI (38.5 +/- 8.8 pg/mL) was higher (P = .002) than the level in the men who had not had an MI (31.9 +/- 7.1 pg/mL). The mean levels of testosterone, free testosterone, sex hormone-binding globulin, insulin, dehydroepiandrosterone sulfate, cholesterol, HDI, cholesterol, and systolic and diastolic blood pressure did not differ significantly. Estradiol was the only variable measured that showed a significant relationship to MI (P < .003 by multivariate logistic regression). These findings suggest that hyperestrogenemia may be related to the thrombosis of MI.