Abnormal hormone levels in men with coronary artery disease.

Zumoff, Barnett; Troxler, Raymond G.; O’Connor, John F.; Rosenfeld, Robert; Kream, Jacob; Levin, Joseph; Hickman, James R.; Sloan, Adrianne; Walker, William E.; Cook, R L; Fukushima, David K.

doi:10.1161/01.atv.2.1.58

Cited by 70 publications

(22 citation statements)

References 29 publications

(8 reference statements)

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“…Two previous studies measured testosterone in men with and without CAD who had not had an MI; one found the mean level of testosterone low in the men with CAD 29 and one found it normal. 30 It appears that no previous studies have measured testosterone in relation to the degree of CAD in men who had not had an MI.…”

Section: Discussionmentioning

confidence: 99%

The association of hypotestosteronemia with coronary artery disease in men.

Phillips

Pinkernell

Jing

1994

Arterioscler Thromb

359

177

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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...

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Section: Discussionmentioning

confidence: 99%

The association of hypotestosteronemia with coronary artery disease in men.

Phillips

Pinkernell

Jing

1994

Arterioscler Thromb

359

177

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“…On the other hand, other groups did not confirm these findings using coronary angiography in two male samples (119,120). Retrospective studies have examined whether myocardial infarction survivors were characterized by reduced DHEA-S levels compared with healthy controls (115,116,118). Two of these studies demonstrated that DHEA-S levels were lower in myocardial infarction survivors compared with healthy controls (115,116), while the third one found the opposite (116).…”

Section: Cardiovascular Diseasementioning

confidence: 97%

“…Several studies have identified plasma DHEA or DHEA-S as being cardioprotective (113)(114)(115)(116)(117)(118). In both men and women, elevated DHEA-S levels were associated with retarded progression of atherosclerosis measured by coronary artery angiography (113), ultrasound carotid wall thickness (117) and pulse wave velocity aorta calcification (114).…”

Section: Cardiovascular Diseasementioning

confidence: 99%

Dehydroepiandrosterone, obesity and cardiovascular disease risk: a review of human studies

Tchernof

Labrie

2004

European Journal of Endocrinology

152

100

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The age-related decline in serum dehydroepiandrosterone (DHEA) and its sulfated ester (DHEA-S) has suggested that a relative deficiency of these steroids may be causally related to the development of chronic diseases generally associated with aging, including insulin resistance, obesity, cardiovascular disease, cancer, reductions of the immune defense, depression and a general deterioration in the sensation of well-being. The numerous studies which have focused on the link between DHEA and cardiovascular disease have generally been inconsistent, generating much debate and controversy on this issue. The present article is an analysis of studies on the relationship between endogenous DHEA or DHEA-S, obesity and cardiovascular disease risk, as well as DHEA treatment studies. Elevated plasma levels of free DHEA are associated with reduced obesity in both men and women, and with smaller abdominal body fat accumulations in men. However, contradictory results have been reported regarding the relationships between the sulfate ester DHEA-S and adiposity. Age differences in the populations studied may have been a confounding factor in these associations. On the other hand, DHEA-S level is not a predictor of cardiovascular disease endpoints in women, and appears to be a relatively weak one in men. DHEA intervention studies suggest that the effects of DHEA on serum lipids are, at best, modest or non-significant. The uncertainty as to whether endogenous and exogenous DHEA should be considered cardioprotective is related to discrepancies in the literature on this topic. Several studies may have been plagued by methodological problems such as low power, unreliable analytical methods, confounding factors or other differences in the populations studied. As a consequence, the original reports demonstrating dramatic effects of either endogenous or exogenous DHEA on cardiovascular disease risk have never been replicated. We propose that the effects of DHEA on cardiovascular disease risk (either favorable or unfavorable) should be considered to be much more modest than previously believed.

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“…6810 ' 11 In contrast, plasma estrogens are elevated in individuals who have symptoms of CHD without angiographically demonstrable evidence of vascular occlusion. 9 Moreover, individuals with hypergonadotrophic hypergonadism (Klinefelters syndrome, 47 XXY) and plasma estrogen levels at least as high as in men with CHD do not experience death rates greater than that predicted for the general population. 12 Additionally, plasma estradiol levels of cases and controls were identical during longitudinal evaluation of low risk and high risk males who subsequently did or did not develop CHD.…”

mentioning

confidence: 99%

“…12 Additionally, plasma estradiol levels of cases and controls were identical during longitudinal evaluation of low risk and high risk males who subsequently did or did not develop CHD. 13 These latter studies in males indicated that hyperestrogenemia may not be a uniform risk factor for CHD because many hyperestrogenemic individuals 9 ' 12>13 do not experience increased episodes of CHD compared to males with normal plasma estrogen content. Moreover, the suggested protective effect of estrogen in females 1 " 5 as opposed to its apparent absence in males 6 ' 8 ' 10 ' 11 implies complex effects of estrogens in CHD that may be genderspecific.…”

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confidence: 99%

Estrogen-mediated cytoplasmic and nuclear distribution of rat cardiovascular estrogen receptors.

Lin

Shain

1985

Arteriosclerosis

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We used either the synthetic estrogen R2858 (moxestrol) or estradiol-17(3 to characterize estrogen receptors in cytoplasmic (R2858) and nuclear (estradiol-17B) preparations from rat aorta and myocardium. Relative steroid specificity studies showed that only estrogens were effective inhibitors of R2858 or estradiol-171) binding to aortic and myocardial estrogen receptors, whereas androgens, progestins, and cortisol were ineffective inhibitors. Low ionic strength sucrose density gradient analyses showed that myocardial estrogen receptors that localized in the cytoplasmic fraction migrated as macromolecules with sedimentation coefficients of 8S to 9S. In contrast, two binding components of sedimentation coefficients 8S to 9S and 10S to 11S were characteristic of the estrogen receptors localized in aortic cytoplasmic preparations. High ionic strength sucrose density gradient analysis showed that aortic and myocardial estrogen receptors localized in the nuclear fraction migrated as macromolecules with sedimentation coefficients of 4S to 6S. Saturation analyses showed that aortic and myocardial cytoplasmic preparations from intact young mature male rats contained 50.6 ± 12.9 (mean ± SD) and 51.0 ± 14.1 fmol receptor/mg DNA, respectively. The respective R2858 dissociation constants were 0.42 and 0.15 nM. Estrogen receptors could not be demonstrated in nuclear preparations from cardiovasculature of intact males. Estradiol-17(3 injection of intact young mature male rats caused "depletion" of aortic and myocardial cytoplasmic fraction estrogen receptors and resulted in the appearance of 51.9 ± 21.0 and 36.9 ± 9.5 fmol receptor/mg DNA in the corresponding nuclear fractions. The respective estradiol-17(3 dissociation constants were 1.56 and 0.71 nM. Increased estrogen receptor content of cardiovascular nuclear fractions of estradiol-17(3 injected male rats correlated well with the concomitant decreased cytoplasmic fraction receptor content. The ability of estradiol-17(3 to affect localization of cardiovascular estrogen receptors between cytoplasmic and nuclear fractions suggests these estrogen receptors are physiologically functional and indicates that estrogen may directly regulate cardiovascular cell function. (Arteriosclerosis 5:668-677, November/December 1985)T he higher incidence of coronary heart disease (CHD) in postmenopausal women as compared to premenopausal individuals 12 and in oral contraceptive users as compared to nonusers 23 and the decreased mortality of estrogen-only users as compared to nonusers 2 -"• 5 has suggested a possible Received December 17,1984; revision accepted July 10,1985. etiologic role for estrogens in CHD. This impression is supported by reports of higher plasma estrogen content in males who survived a myocardial infarction 6 " 11 or have documented coronary artery occlusion in the absence of an infarction. 8 ' 9 These clinical observations have led some investigators to conclude that hyperestrogenemia is an additional risk factor for CHD in males. 6810

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Abnormal hormone levels in men with coronary artery disease.

Cited by 70 publications

References 29 publications

The association of hypotestosteronemia with coronary artery disease in men.

The association of hypotestosteronemia with coronary artery disease in men.

Dehydroepiandrosterone, obesity and cardiovascular disease risk: a review of human studies

Estrogen-mediated cytoplasmic and nuclear distribution of rat cardiovascular estrogen receptors.

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