Abstract:
:The severe teratogenic side effects of thalidomide led to its well-publicized withdrawal in the 1970s, but as it is cautiously being reintroduced into clinical use, new adverse effects are being described. A 65-year-old male with multiple myeloma received chemotherapy which included cyclophosphamide, thalidomide and dexamethasone. Whilst on this treatment he experienced severe chest pain leading to an acute hospital admission complicated by significant bradycardia with sinus pauses of 7 s, necessitating temporary right ventricular pacing. Despite correction of the bradycardia with temporary pacing, he experienced further episodes of chest pain, during which an ECG (with the pacemaker briefly switched off) showed ST elevation in the inferior leads along with runs of non-sustained ventricular tachycardia. Emergency coronary angiography demonstrated unobstructed coronary arteries. Due to ST elevation in the absence of flow-limiting coronary disease his presentation was presumed to be due to intermittent coronary artery spasm. He was started on sustained-release nifedipine without any beta-blockers and further thalidomide therapy was omitted. On this pharmacological therapy, over a period of 24 months, there were no further recurrences of any cardiac symptoms. To our knowledge there have been no previous reports of coronary artery spasm associated with the use of thalidomide. The precise mechanism remains undefined, with several plausible hypothetical pathways which we discuss. We discuss various mechanisms including autonomic, autocoid and paracrine modes of action that may underlie cardiac side effects of thalidomide. We report coronary spasm in addition to bradycardia as cardiac side effects that cardiologists and oncologists need to be alert to.
journal_name
Cardiologyjournal_title
Cardiologyauthors
Ali A,Hothi SS,Thompson A,Malik Ndoi
10.1159/000348367subject
Has Abstractpub_date
2013-01-01 00:00:00pages
34-7issue
1eissn
0008-6312issn
1421-9751pii
000348367journal_volume
125pub_type
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