- Jul 9, 2014
"The association between testosterone-replacement therapy and cardiovascular risk remains unclear with most reports suggesting a neutral or possibly beneficial effect of the hormone in men and women. However, several cardiovascular complications including hypertension, cardiomyopathy, stroke, pulmonary embolism, fatal and nonfatal arrhythmias, and myocardial infarction have been reported with supraphysiologic doses of anabolic steroids. We report a case of an acute ST-segment elevation myocardial infarction in a patient with traditional cardiac risk factors using supraphysiologic doses of supplemental, intramuscular testosterone. In addition, this patient also had polycythemia, likely secondary to high-dose testosterone. The patient underwent successful percutaneous intervention of the right coronary artery. Phlebotomy was used to treat the polycythemia acutely. We suggest that the chronic and recent “stacked” use of intramuscular testosterone as well as the resultant polycythemia and likely increased plasma viscosity may have been contributing factors to this cardiovascular event, in addition to traditional coronary risk factors. Physicians and patients should be aware of the clinical consequences of anabolic steroid abuse."
About this subject in the study:
" His physical examination was remarkable for his muscular appearance and a blood pressure of 190/100. He was in mild distress with no signs of heart failure. His blood chemistry revealed a creatinine of 1.3 mg/dl and elevated liver enzymes (aspartate aminotranferease 86 units/L, and alanine aminotransferase 79 units/L). Hematologic studies noted an hemoglobin of 22 g/dl and hematocrit of 63%. The ejection fraction was 35%. The patient was phlebotomized until his resultant hematocrit was 45%."
"Several case reports describe the deleterious cardiac effects of anabolic steroids including its potentially atherogenic and thrombotic properties. These range from lipid disorders to acute myocardial infarction and sudden cardiac death (Kennedy and Lawrence 1993; Hourigan et al 1998; Fineschi et al 2001; Wysoczanski et al 2008). Thromboembolic phenomenoma, intracardiac and peripherally, have been described (McCarthy et al 2000). Cardiomyopathy, cardiomegaly and biventricular dilatation have been associated with AAS use. Mewis and colleagues (1996) demonstrate a case report of a young bodybuilder with severe coronary artery disease with a two-year history of chronic anabolic steroid use. A case control study of 62 male competitive powerlifters notes a possible increase in premature mortality compared with controls (12.9% versus 3.1%) Parssinen et al 2000). Although difficult to quantitate, the increased risk of cardiac disease may be as high 3-fold among individuals who use AAS (Melchert and Welder 1995; Sullivan et al 1998)."
"Development of an atheromatous plaque perpetuates endothelial dysfunction and promotes platelet aggregation and intracoronary thrombus formation (Ajayi et al 1995; Nieminen et al 1996). AAS may cause a hypercoagulable state, by an increase in production of thromboxane A2 and platelet thromboxane A2 receptor density as well as aggregation responses and a decrease in production of prostaglandins (Ajayi et al 1995). Moreover, a component of endothelial dysfunction has been proposed, which may contribute to abnormal vessel reactivity. However, testosterone in physiologic doses may even be beneficial in patients with angina (English et al 2000), have higher ischemic thresholds and improved quality of life (Malkin et al 2004). Short-term intracoronary administration of testosterone induces coronary artery dilation and increases coronary blood flow in men with established coronary artery disease (Webb et al 1999). Therefore, an interplay of endogenous factors of the patient’s risk profile as well as the testosterone dosing may be issues of whether adverse events occur."
You omitted these findings from the article:
Unfortunately, the data on the use of high dose anabolic steroids in humans are mainly offered as case reports or small studies that lack adequate control groups. In addition, the data available in the literature does not account for the steroid type(s) or dose, as neither may be known. Patients also may be taking concomitant stimulants, such as ephedra, which can confound data and the potential for adverse events.