Bradycardia during therapy for multiple myeloma with thalidomide

Fahdi, Ibrahim E.; Gaddam, Venkat; Saucedo, Jorge; Kishan, C. V.; Vyas, Keyur; Deneke, Matthew G.; Razek, Hani A.; Thorn, Brett T.; Bissett, Joe K.; Anaisse, Elias; Barlogie, Bart; Mehta, Jawahar L.

doi:10.1016/j.amjcard.2003.12.061

Cited by 87 publications

(57 citation statements)

References 15 publications

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“…Interestingly, despite treatment with ␤-blockers in most patients, thalidomide reduced HR, and such an effect has also previously been reported in multiple myeloma patients receiving this medication. 25 Because selective HR reduction improves contractility and reduces ischemia, 26 this reduction in HR might contribute to the beneficial effect of thalidomide on LV function, possibly involving enhanced diastolic perfusion time and decreased myocardial oxygen demand.…”

Section: Discussionmentioning

confidence: 99%

Effect of Thalidomide on Cardiac Remodeling in Chronic Heart Failure

Gullestad¹,

Ueland²,

Fjeld³

et al. 2005

Circulation

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Background-Inflammation and matrix degradation may play a pathogenic role in chronic heart failure (CHF), and therefore, we examined whether thalidomide, a drug with potential immunomodulating and matrix-stabilizing properties, could improve left ventricular (LV) function in patients with CHF secondary to idiopathic dilated cardiomyopathy (IDCM) or coronary artery disease (CAD). Methods and Results-Fifty-six patients with CHF and an LV ejection fraction (LVEF) Ͻ40% who were already on optimal conventional cardiovascular treatment were randomized to thalidomide (25 mg QD increasing to 200 mg QD) or placebo and followed up for 12 weeks. Our main findings were as follows: (1) During thalidomide treatment but not during placebo, there was a marked increase in LVEF (Ϸ7 EF units) along with a significant decrease in LV end-diastolic volume and heart rate. (2) This improvement in LVEF was accompanied by a decrease in matrix metalloproteinase-2 without any changes in its endogenous tissue inhibitor, suggesting a matrix-stabilizing net effect.(3) Thalidomide also induced a decrease in total neutrophil count and an increase in plasma levels of tumor necrosis factor-␣, suggesting both proinflammatory and antiinflammatory effects. (4) The effect of thalidomide on LVEF was more marked in IDCM than in CAD, possibly partly reflecting that the former group was able to tolerate a higher thalidomide dosage. Conclusions-Although our results must be confirmed in larger studies that also examine the effects on morbidity and mortality, our findings suggest a role for thalidomide in the management of CHF in addition to traditional cardiovascular medications. (Circulation. 2005;112:3408-3414.)

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Section: Discussionmentioning

confidence: 99%

Effect of Thalidomide on Cardiac Remodeling in Chronic Heart Failure

Gullestad¹,

Ueland²,

Fjeld³

et al. 2005

Circulation

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“…Post-marketing data reported a 0.12% rate of thalidomide-induced bradycardia, but recent reports demonstrate that thalidomide-induced bradycardia may be more frequent, up to 5%-53% [2]. Except for one case with complete atrioventricular block, all reported cases are sinusal bradycardia [3,4]. There is no case of second-degree atrioventricular block associated with thalidomide in the literature.…”

Section: Discussionmentioning

confidence: 79%

“…Emch and his colleagues reported that TNF-α inhibits activity of the dorsal motor nucleus of the vagus nerve that supplies visceral parasympathetic fibres to the heart [7]. By this means, thalidomide could lead to overactivity of the parasympathetic system, resulting in bradycardia or block because of the reduced TNF-α levels [3]. Due to its anti-angiogenic, immunomodulating, and anti-inflammatory effects, thalidomide is increasingly used in the treatment of hematological diseases, autoimmune diseases, and cancer.…”

Section: Discussionmentioning

confidence: 99%

Symptomatic Second-Degree Atrioventricular Block Due to Thalidomide

Kaya¹

2016

Ann Clin Anal Med

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Anahtar KelimelerAtriyoventriküler Blok; Senkop; Talidomid; Multiple Myelom Abstract Due to its anti-inflammatory, anti-angiogenic, and immunomodulatory effects, thalidomide is increasingly used in the treatment of various diseases. Previous studies have demonstrated that thalidomide may cause sinusal bradycardia. Thalidomide-associated complete atrioventricular block has been reported in only a single case, but there is no case of second-degree atrioventricular block associated with thalidomide in the literature. Here, we present the case of a 50-year-old patient who had been using thalidomide for multiple myeloma. The patient was admitted to the emergency service with syncope, and had second-degree (2:1) atrioventricular block. The patient was using thalidomide (100 mg/day) for the previous 5 months and had not had any abnormal findings in previous electrocardiographies. His heart rate on presentation was variable, from 45 to 75 bpm. He was treated with a temporary pacemaker because of hypotension and syncope. Five days after the completion of the thalidomide treatment, the patient's heart rate was 80 bpm. The following day, the pacemaker was removed and a Holter ECG did not show any abnormalities. Patients undergoing thalidomide treatment should be followed up for cardiac and electrocardiographic parameters.

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“…The symptoms are related to possible damage to the autonomic nerves that control heart rate, blood pressure, and digestion, among other functions. Additional investigation is warranted to clarify the possible association of autonomic neuropathy with bortezomib (Orlowski et al, 2002;Shah et al, 2004) and thalidomide (Fahdi et al, 2004;Singhal & Mehta, 2001). Symptoms such as bradycardia or irregular heartbeat while on thalidomide or hypotension while on bortezomib therapy may indicate autonomic chemotherapy-induced peripheral neuropathy.…”

Section: Issue Statementmentioning

confidence: 99%

Peripheral Neuropathy Associated With Novel Therapies in Patients With Multiple Myeloma: Consensus Statement of the IMF Nurse Leadership Board

Tariman

Love²,

McCullagh³

et al. 2008

Clinical Journal of Oncology Nursing

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The novel therapies thalidomide and bortezomib can cause peripheral neuropathy, a challenging adverse event that can affect quality of life and compromise optimal treatment for patients with multiple myeloma. At baseline, patients should be evaluated for signs and symptoms of peripheral neuropathy with a neurotoxicity assessment tool and educated about the symptoms and the importance of reporting them. Signs, symptoms, and the ability to perform activities of daily living should be evaluated regularly so that appropriate interventions can be employed if necessary. Specific management strategies for peripheral neuropathy are based on the grade of severity and on signs and symptoms; strategies include dose and schedule modifications, pharmacologic interventions, nonpharmacologic approaches, and patient education.

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Bradycardia during therapy for multiple myeloma with thalidomide

Cited by 87 publications

References 15 publications

Effect of Thalidomide on Cardiac Remodeling in Chronic Heart Failure

Effect of Thalidomide on Cardiac Remodeling in Chronic Heart Failure

Symptomatic Second-Degree Atrioventricular Block Due to Thalidomide

Peripheral Neuropathy Associated With Novel Therapies in Patients With Multiple Myeloma: Consensus Statement of the IMF Nurse Leadership Board

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