Severe Coronary Heart Disease after Anabolic Steroid Cycle
Severe Coronary Heart Disease after Anabolic Steroid Cycle
Anabolic steroids are frequently abused, thus increasingthe risk of cardiovascular disease, despite the known unfavorable influence on lipid profiles.
We report on a young bodybuilder who presented with ventricular tachycardia as the first manifestation of severe underlying coronary heart disease.
Coronary angiogram revealed severe stenotic lesions in the right coronary artery and the left descending coronarym-tery. and hypokinetic regions corresponded to posterolateraland anterior myocardial infarctions. This young patient had a history without any coronary risk factors, but with a 2-year abuse of the anabolic steroid stanazolol.
No report publishedso tar has shown possible atherogenic consequences of longtermabuse of stanazolol.
Key words: anabolic steroids. stanazolol, coronary heart disease,myocardial infarction
Introduction Anabolic steroids are frequently abused by professional athletes and bodybuilders who seek a competitive advantage in sports which require strength and increased muscle mass. Besides the known virilizing and hepatotoxic effects. many studies of bodybuilders and weight lifters using anabolic steroids have revealed profound reductions of all high-densitylipoprotein (HDL) subfractions accompanied by elevated low-density lipoprotein (LDL) levels.'.'
Synthetic androgens, such as the 17-a-alkylated steroid stanazolol, appear to producea greater lowering of the HDL LDL-ratios than does testosterone!
Therefore, anabolic steroid use and resultant unfavorable lipid profiles may increase the risk of cardiovascular disease. Several reports illustrate an alarming cardiotoxic potentialof these steroids.
We report the case of a young patient taking winstrol aka Stanozolol for 2 years, who presented with ventricular tachycardia as the manifestation of severe underlying coronary heart disease(CHD).
The case suggests a causal relationship to anabolic steroid abuse and, to our knowledge, is the first published report which shows the possible atherogenic consequences of long-term anabolic steroid use.
tA 28-year-old man was admitted to hospital with ventricular tachycardia at a heart rate of 1 SO beat min. The patient was in stable condition and the tachycardia was converted into sinusrhythm by administration of 50 mg ajmalin.
The patienthad never been in hospital before and had never complained of palpitations, angina, or other cardiac symptoms.
He was referred to our hospital for further diagnostic studies and therapy. On admission, there were no abnormal physical findings.The electrocardiogram recorded at sinus rhythm disclosed aQlSlll pattern, R reduction in VI-VI, and T-wave inversions in VJ-V~ and in 11,111, and aVE The echocardiogram found a dilated left ventricle with diffuse hypokinesia and fractional shortening of 25% with 67 mm end-diastolic diameter.
Coronaryangiography revealed severe CHD with stenotic lesions in the right coronary artery and the typical pattern of a recanalizedthrombus in the left anterior descending artery (Figs. I, 2).Ventriculogram revealed akinetic myocardium in the anterolateral,apical, septal, and posterior-inferior region of the leftventricle compatible with myocardial infarctions in those regions.
This was confirmed by an apical lack of perfusion and inferior reduced perfusion in 'O1thallium myocardium scintigraphyat rest. In electrophysiologic studies, ventricular tachycardiaswith two different morphologies could be casily induced.Serial drug testing of class 1 and III antiarrhythmicdrugs showed a partial suppression only with amiodarone,which did not alter even after successful percutaneous translumindcoronary angioplasty of the right coronary artery. The patient was discharged with 200 mg amiodarone in additionto antianginal therapy including aspirin.
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The patient had no coronary risk factors such as a history ofsmoking, hypertension, diabetes, or a positive thmily history.Six months prior to admission he had discontinued stanazolol (winstrol) which had consisted of a weekly dose of 280 mg over 2 years;he had been taking this steroid to increase his muscle mass forbodybuilding.
On admission, total cholesterol was 2 I9 mg/dland triglycerides were I40 mg/dl. All other laboratory studieswere within normal limits, including cardiac enzymes andelectrolytes. The lipoprotein profile showed an HDL of 47tng/dl, an LDL of I63 nigldl; very low-density lipoprotein was9 nig/dl. The HDL/LDL ratio was calculated at 3.4. Lipoprotein(a)was normal.
The TPHA test and other serologicalstudies for potential underlying infectious diseases were negative.No abnormalities of coagulation and of the tibrinolysissystems were detected.DiscussionA young bodybuilder presented with ventricular tachycardiaas the firs1 manifestation of severe underlying CHD.Electrocardiographic recordings and angiographic studies disclosedsigns of myocardial infarction with anterior and inferior-posteriordistribution.
The patient had no coronary risk factors.but he had a 2-year history of oral intake of the anabolicsteroid stanazolol, which he had discontinued 6 months priorto admission.McNutt ef d4 have described the case of a weight lifterwho took anabolic drugs for 6 weeks. This patient sufferedlrorn myocardial infarction with subsequent normal coronaryangiography, and the authors speculated that the altered lipoproteinswith severe hypercholesterinemia on admissioncaused coronary vasospasni leading to myocardial infarction.FIG. 2 Coronary angiograni in the LAO 60" position: the proxinialpart ofthe left anterior descending artery shows the typical pattern ofrecanalized thrombus as ectatic, irregularly shaped vessel walls miintracoronary defects with local retention of iiijectcd dye.In contrast, we report the case of a patient whose angiogrnmshowed severe atherosclerotic signs after long-term anabolicdrug abuse.The deleterious effect of anabolic drugs on the lipoproteinprofile, subsequently leading to an increased atherogenic risk,has been well documented in some studies. -i, '-')
Consequently,increments of LDL and lowering of HDL are correlatedpositively with the risk of CHD.'"Most investigators have observed a significant reduction ofHDL and increase of the LDL fraction after regulx applicationof stanazolol over 2-3 months in bodybuilders and weightlifters.',? Similar tendencies of lipoproteins were seen in poslmenopausalwomen receiving an anabolic androgenic steroidfor o~teoporosis.~Our patient had a long-term steroid abuse of 2 years, undthere are no studies published so far that report the eifects of'such a long drug exposure on the lipoprotein prolile. Webb rtu1. I found that the alterations in HDL and LDL tiietabolismswere reversible after cessation of the drug, independent of thenumber of months the patient was off the drug or the ultercdLDUHDL ratio achieved by the treatment. Hence, our patientshowed only a slightly altered lipid electrophoresis, and the totalcholesterol and triglyceride levels were also within normallimits.
The latter finding is consistent with the results of allstudies cited above in which cholesterol-triglyceride levelswere not influenced by the stanazolol treatment. probably becauseof its ability to effect a marked increase in the hepatictriglyceride lipase activity facilitating HDL catabolism.xIt may well be that the duration of steroid intake is an importantfactor for the development of atherosclerosis,' I althoughin our case we do not know when the myocardial infarctiontook place. A contributory fact might be that the eftectof weight training itself, independent of use of anabolic
