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Myocardial infarction, symptomatic third degree atrioventricular block and pulmonary embolism caused by thalidomide: a case report

BACKGROUND: Thalidomide has been reported to cause numerous thromboembolic events. Deep vein thrombosis and pulmonary embolism are more common. It can also cause bradycardia and even total atrioventricular block. Rarely, it causes coronary artery spasm and even myocardial infarction. But almost simu...

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Detalles Bibliográficos
Autores principales: Zhang, Shengyu, Yang, Jing, Jin, Xiaofeng, Zhang, Shuyang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4683955/
https://www.ncbi.nlm.nih.gov/pubmed/26681197
http://dx.doi.org/10.1186/s12872-015-0164-4
Descripción
Sumario:BACKGROUND: Thalidomide has been reported to cause numerous thromboembolic events. Deep vein thrombosis and pulmonary embolism are more common. It can also cause bradycardia and even total atrioventricular block. Rarely, it causes coronary artery spasm and even myocardial infarction. But almost simultaneous onset of myocardial infarction, third degree atrioventricular block and pulmonary embolism in one patient has not been reported so far. CASE PRESENTATION: A 53-year old man presented because of chest pain, nausea and then syncope for several minutes. Previous medical history included neurodermitis for which thalidomide was given and hypercholesterolemia with simvastatin taking. The patient didn’t exhibit any other established risk factors for coronary artery disease. Electrocardiography showed sinus rhythm with third degree atrioventricular block and complete right bundle branch block, and precordial leads ST segment elevation. The diagnosis of acute coronary syndrome was suspected, but further coronary angiography demonstrated no flow-limiting lesions in coronary arteries, and temporary pacemaker was implanted. After admission, low SpO(2) and elevated D-dimer level was mentioned. Further computed tomography pulmonary angiography revealed pulmonary embolism. Thalidomide was thought to be the cause of hypercoagulability and coronary spasm, so it was ceased immediately. Therapeutic low molecule weight heparin was initiated and then switched to warfarin with appropriate INR, and nifedipine was described for coronary spasm. The patient’s symptoms completely relived and SpO(2) recovered, and atrioventricular block had disappeared during hospitalization with pacemaker removed. CONCLUSION: This is the very first case in which myocardial infarction, third degree atrioventricular block and pulmonary embolism almost simultaneously developed. We should be ware that anti-thrombotic prophylaxis, which needs further investigation for optimal drug and dosage, may be beneficial in thalidomide therapy. And it is also important to monitor patients taking thalidomide for signs and symptoms of bradycardia or higher degree atrioventricular block.