Testosterone and cardiovascular disease in men

Sixteen of 32 cross-sectional studies found lower levels of testosterone in patients with coronary artery disease compared with healthy controls. Sixteen showed no difference in testosterone levels between cases and controls. In none were high levels of testosterone associated with coronary artery disease. All studies which measured levels of free or bioavailable testosterone found an inverse association with coronary artery disease (reviewed in Alexandersen etal. 1996; Wu and von Eckardstein 2003). None of six longitudinal studies in men showed any significant association between serum levels of testosterone and future coronary artery disease events (reviewed in Alexandersen etal. 1996; Wu and von Eckardstein 2003). With the limitations stated before, this suggests that testosterone plays a neutral or even beneficial role in the pathogenesis of coronary artery disease. This is also supported by the finding of a genetic case-control study, where we did not find any significant association of angiographically assessed coronary artery disease with the CAG repeat polymorphism in exon 1 of the androgen receptor gene (Hersberger and von Eckardstein, unpublished results), which determines testosterone sensitivity (for background information on this polymorphism, see Section 10.8 of this chapter as well as the Chapter 2 on the molecular biology of the androgen receptor).

Data of observational studies suggest that testosterone is a determinant of myocardial mass and may thereby influence the clinical course of heart failure. Also after adjustment for gender differences in body size and weight, men show higher left ventricular mass than women from puberty to the end of life (reviewed by Hayward etal. 2000; 2001; Liu etal. 2003). Moreover, serum levels of testosterone were lower in men with cardiac failure (Kontoleon et al. 2003). The finding that chronic mechanical circulatory support leads to an increase in testosterone levels in men with end-stage cardiac failure (Kontoleon etal. 2003;Noirhomme etal. 1999) is compatible with the aforementioned importance of chronic disease as a cause of male hypogonadism.

In case-control studies, stroke survivors were found to have reduced concentrations of testosterone in both blood and cerebrospinal fluid (Elwan et al. 1990; Jeppesen et al. 1996). Upon ultrasound studies, increased carotid intima media thickness and the presence of carotid plaques (De Pergola 2003 et al.; Fukui 2003 etal.), which are strong risk factors of future stroke (and other cardiovascular events including myocardial infarction), showed an inverse association with serum levels of total or free testosterone.

Peripheral arterial disease is the consequence of atherosclerosis in the aorta and the arteries of the pelvis, the lower and upper extremities. A specific male variant of peripheral artery disease is vasculogenic erectile dysfunction, which is the most frequent cause of erectile dysfunction (see also Chapter 11). Observational studies on the association of testosterone with peripheral arterial disease are scarce. In the Rotterdam study, the presence of aortic calcifications were found to be associated with low total and free testosterone (Hak et al. 2002). With respect to erectile dysfunction, the role of hypotestosteronemia as a source of the vascular variant is difficult to assess since testosterone also affects neurovegetative and psychological aspects of sexual activity. At least, except the small subgroup of men with frank testosterone deficiency (<5%), men with erectile dysfunction were not found to have lower average testosterone levels than matched controls (Jannini et al. 1999; Liu etal. 2003; Lue 2000; Melman etal. 1999).

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