Thalidomide-Induced Sinus Bradycardia

Kaur, Amandeep; Yu, Susan S; Lee, Audrey J; Chiao, Teresa B

doi:10.1345/aph.1d003

Cited by 55 publications

(22 citation statements)

References 14 publications

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“…Only one investigation of THL in multiple myeloma showed bradycardia in frequencies similar to our own study (53 %) [11]. In previous reports, THL-related bradycardia has been described with a variety of other untoward events and in patients using concurrent medications including chemotherapeutic agents [10][11][12][13]. Given the reports of THL-related bradycardia in conditions other than ALS, its occurrence does not appear ALS-specific.…”

Section: Discussionsupporting

confidence: 81%

Thalidomide causes sinus bradycardia in ALS

et al. 2008

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Bradycardia was the most common adverse event of THL treatment in ALS. THL-related bradycardia does not appear to be ALS-specific. It is conceivable, however, that the unexpected frequency and severity of THL-induced bradycardia may be related to subclinical involvement of the autonomic nervous system in ALS. The cardiac toxicity discourages further clinical trials and compassionate use of THL in ALS. ClinicalTrials.gov Identifier: NCT00231140.

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Section: Discussionsupporting

confidence: 81%

Thalidomide causes sinus bradycardia in ALS

et al. 2008

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“…This could lead to over-reactivity of the parasympathetic nervous system resulting in bradycardia and exacerbate underlying conduction disturbances. In addition, it has also been proposed that thalidomide may induce hypothyroidism in some patients leading to bradycardia (158,160). Diagnosis.…”

Section: Bradycardiamentioning

confidence: 99%

Cardiovascular Complications of Cancer Therapy

Yeh

Bickford

2009

Journal of the American College of Cardiology

1,095

406

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Cancer treatment today employs a combination of chemotherapy, radiotherapy, and surgery to prolong life and provide cure. However, many of these treatments can cause cardiovascular complications such as heart failure, myocardial ischemia/infarction, hypertension, thromboembolism, and arrhythmias. In this article we review the incidence of cardiotoxicity caused by commonly used chemotherapeutic agents as well as discuss the pathogenesis, diagnosis, management, and prevention of these cardiovascular side effects. Cardiotoxicity related to anticancer treatment is important to recognize as it may have a significant impact on the overall prognosis and survival of cancer patients, and it is likely to remain a significant challenge for both cardiologists and oncologists in the future due to an increasing aging population of patients with cancer and the introduction of many new cancer therapies.

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“…Although there are currently no recognised indications for the use of thalidomide in cardiac conditions, cardiac effects associated with the use of thalidomide include significant bradycardia [7,8,9]. The mechanism for this remains unclear although interference with the autonomic nervous system has been suggested, with parasympathetic over activity caused by inhibition of TNFα in the dorsal motor neurons of the vagus nerve.…”

Section: Figmentioning

confidence: 99%

Negative Chronotropic Effects and Coronary Ischaemic Abnormalities Following Thalidomide Therapy

Ali

Hothi²,

Thompson³

et al. 2013

Cardiology

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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.

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Thalidomide-Induced Sinus Bradycardia

Cited by 55 publications

References 14 publications

Thalidomide causes sinus bradycardia in ALS

Thalidomide causes sinus bradycardia in ALS

Cardiovascular Complications of Cancer Therapy

Negative Chronotropic Effects and Coronary Ischaemic Abnormalities Following Thalidomide Therapy

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