Steroids and Cardiovascular System

A common reason given for many of the cardiovascular problems associated with steroid use is thrombosis formation. Dickerman, et.,al (1996) found that Protein S levels decrease with elevated androgen levels, thus allowing for an increase in the activity of the coagulation system and subsequent thrombus formation. A review by Vanberg and Atar (2010) concluded that AAS confer an enhanced pro-thrombotic state, most prominently through an activation of platelet aggregability. However a reduction in serum Lp (a) levels through ASS may reduce the cardiovascular risk so this area still needs further study.

An increase in blood pressure has also been blamed for many cardiac problems attributed to steroids. Although few studies have shown any increase in blood pressure Kuipers et al. (1991) found an increase in diastolic blood pressure from 74 to 86mm Hg due to ten weeks of self administration of High-dose ASS. They also found that levels returned to normal approximately 6 weeks after cessation of drug administration. However Hartgens et al.(2003) did not find any increase in blood-pressure following 16 weeks of self-administration of ASS. This is in line with the majority of literature. It’s worth noting that self-administration could be a factor in this and other studies. There is no monitoring of the subjects under these conditions which could lead to changes in results through lack of compliance from the subjects. This could result in a high level of variance in this study and studies similar.  On analysing the cardiac effects of ASS on strength athletes Urhausen et.,al (2004) concluded that their results showed that increases in blood pressure with ASS use is small and transient. No definitive conclusions can yet be made on wither ASS negatively effects blood pressure following long term use or otherwise.

Furthermore no firm conclusions have been made on the role of ASS on left ventricular hypertrophy. There is a common belief that in some strength trained athletes left ventricular hypertrophy can result from training alone but it has proved not to be the case in almost all well-conducted trials. Many trials exploring the cardiac effects of ASS are done on animals, which has resulted in some ambiguity. Even though the results are yet to be noted in humans the investigations appear to correlate with the animal studies. A study on the effect of ASS with or without growth hormone (GH) on left ventricular dimensions on power athletes was conducted by Karila, et al. (2003). They found a significant association between left ventricular mass and ASS dose (r=0.54 P<0.015) and concluded that use of ASS is associated with concentric remodelling of LV.  Other studies have failed to find any change in LV size. Thompson, P.D et al. (1992) tested 12 steroid users against 11 non-users under scientific parameters and found that no significant difference in left ventricular diastolic cavity diameter (57 ± 3 vs. 56 ± 5 mm), septal thickness (10 ± 2 vs. 9 ± 1 mm), posterior wall thickness (8 ± 1 vs. 8 ± 1 mm) and myocardial mass (149 ± 27 vs. 135 ± 21 g). Hartgens et al.,(2003) therefore concluded that it must then be assumed that heart structure and function will not change after a period of four months of ASS use by an athlete. However a study done since by Hussan et al. (2009) found through echocardiographic results that bodybuilders who use steroids have smaller LV dimension with thicker walls, impaired diastolic function, as well as higher peak systolic strain rate compared to non-users.

Figure 4: (Hussan et al. (2009)

The end systolic dimensions (ESD) were significantly smaller in group 1 (2.6 ± 0.29), as compared to group 2 (2.9 ± 0.11) and group 3 (3.06 ± 0.08), at P < 0.0001.
The end diastolic dimensions (EDD) were significantly smaller in group 1 (4.6 ± 0.3), as compared to group 2 (5 ± 0.1) and group 3 (5.06 ± 0.08), at P = 0.0004.
In the same figures, interventricular septal dimensions (IVS) were significantly thicker in group 1 (1.06 ± 0.08), as compared to group 2 (0.8 ± 0.07) and group 3 (0.76 ± 0.11), at P = 0.007.
Left ventricular posterior wall (LVPW) was significantly thicker in group 1(1.07 ± 0.09), as compared to group 2 (0.88 ± 0.08) and group 3 (0.8 ± 0.11), at P = 0.009.
Left ventricular ejection fraction (LV EF) was significantly higher in group 1 (72 ± 8), as compared to group 2 (60 ± 0.7) and group 3 (61 ± 1.3), at P < 0.001.
Left ventricular mass was significantly bigger in group 1(212 ± 12), as compared to group 2 (165 ± 3) and group 3 (163 ± 2.5), at P < 0.001.
After correction of LV mass to the body surface area, corrected LV mass is still significantly higher in group 1(129 ± 15) as compared to group 2 (97 ± 2) and group 3 (96 ± 1.5) at P < 0.05, whereas it showed no change between groups 2 and 3, P = 0.23. NA, Hussan et al. (2009)
 
They hypothesised that all users of supraphysiologic doses of ASS experienced impaired diastolic function which may be due to the decreased compliance caused by LV hypertrophy or secondary to myocardial ischemia as AAS use had been associated with pro-atherogenic effect. In addition Urhausen et al. (1989) found an increase in the LV posterior wall (P < 0.01) and septum thickness (ns) resulted in increased LV wall thickness:diameter (P < 0.01) and LV muscle mass:volume (P < 0.05). LV can occur for endurance training alone which makes the results in body-building subjects more noticeable. Further study into LV hypertrophy in endurance athletes abusing AAS would be useful as there is currently a lack of knowledge in this area.

 A review by Di Paolo et.,al (2007) analysed four sudden deaths that occurred in bodybuilders on ASS. All four deaths were attributed to heart failures and all had similar findings on analysis: coronary atherosclerosis causing significant luminal narrowing, pulmonary thromboembolism, coronary and endocavitary thrombi, inflammatory infiltrates, myocardial damage and small vessel disease. The most interesting finding is the prominence in all four cases of small vessel disease. Small arteriolar vessels were thickened and showed intimal hyperplasia. This could play a role in causing chronic ischemic damage and arrhythmogenic potential (Di Paolo et.,al (2007). Although very rare, sudden death as a consequence of cardiac trauma is still a risk factor for athletes taking ASS.

End of steroids and cardiovascular system