Dilated Cardiomyopathy after Sequential Therapy with Abirate | 45510

Oncology & Cancer Case Reports

ISSN - 2471-8556


Dilated Cardiomyopathy after Sequential Therapy with Abiraterone and Enzalutamide

Freeman B, Wang J

Background: Newer agents targeting the androgen signaling pathway, including abiraterone acetate (Zytiga) and enzalutamide (Xtandi), have led to survival improvements in the management of metastatic castration resistant prostate cancer (mCRPC). However, the short and long term impact of these agents on cardiovascular risk remains unclear. We present a case of non-ischemic cardiomyopathy after sequential therapy with abiraterone and enzalutamide.

Case report: An 81-year-old gentleman with a past medical history of mCRPC presented to medical oncology clinic with complaints of new onset of orthopnea and exertional dyspnea. Four weeks prior to this visit, he was started on enzalutamide 160 mg daily, after his disease progression following five months of abiraterone therapy. Clinical examination was consistent with heart failure. His 12 lead EKG revealed sinus tachycardia with a ventricular rate of 106, without acute ST-T wave changes. His cardiac enzymes were within normal limits. The Natriuretic peptides B-type (BNP) was 1,200 pg/mL. A 2D echocardiograph revealed diffuse hypokinesis with a left ventricle ejection fraction of 25% without regional wall motion abnormalities noted. A myocardial perfusion (MIBI) stress scan showed a dilated left ventricle with global hypokinesis. Left ventricle ejection fraction was calculated at 27%, diastolic volume at 208 mL, and end systolic volume at 152 mL. There were no focal perfusion defects. The overall clinical diagnosis was consistent with cardiomyopathy.

Conclusion: Urologists and medical oncologists should consider the cardiac side effects of the new generation androgen signaling axis targeting agents with the aim of maximizing both quality of life and survival in patients with mCRPC. Further research on the impact of novel endocrine therapies is needed to assess the risk of cardiovascular disease and the extent to which these therapies decrease the cardio-protective effects of testosterone.

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