Contributions
Abstract: EP1725
Type: ePoster
Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments
Introduction: Alemtuzumab is an anti-CD52 monoclonal antibody widely used for the treatment of relapsing-remitting multiple sclerosis (RRMS) with high disease activity despite previous disease-modifying therapies.1 The most common infusion-associated reaction (IAR) is cytokine-release syndrome. Incidence of cardiac-related IARs is 12.5% (tachycardia, bradycardia, palpitations), of which only 0.5% are serious cardiac-related IARs such as atrial fibrillation, sinus bradycardia, sinus tachycardia, hypotension or hypertension.2
We report a serious cardiac-related adverse event occurring during alemtuzumab-infusion in a RRMS patient.
Case report: A female 24-year-old RRMS patient, with an unremarkable personal history, started treatment with alemtuzumab due to ongoing disease activity during treatment with natalizumab. On the third day of treatment, shortly after premedication with steroids, antihistamine drugs, paracetamol and lansoprazole, the patient developed severe asymptomatic sinus bradycardia, which was treated with intravenous atropine. Infusion of alemtuzumab was resumed but on the following morning she complained of oppressive chest-pain lasting 20 minutes associated with dyspnoea. Blood tests showed high levels of troponin I, creatine kinase MB, and D-Dimer. Alemtuzumab treatment was discontinued. Continuous cardiac monitoring showed mild bradycardia in the absence of cardiac arrhythmias. Electrocardiography revealed a prolonged QTc interval. Echocardiography and cardiac magnetic resonance imaging did not detect alterations of left ventricular function nor the presence of regional wall-motion abnormalities. Computed tomography angiography and doppler ultrasonography of lower limbs did not reveal signs of acute pulmonary embolism/deep venous thrombosis. Within the subsequent week, myocardial cytolysis enzymes and D-dimer spontaneously returned within normal ranges and QTc interval normalized.
Conclusion: To our knowledge, this is the first report on a possible association between alemtuzumab treatment and acute coronary syndrome in absence of cardiovascular risk factors. We speculate that the augmentation of endothelial and myocyte membrane permeability and vasodilation induced by alemtuzumab-related cytokine- release syndrome might determine supply/demand ischemia of myocardic muscle defining type 2 myocardial ischemia.3
Disclosure:
Valentina Camera: nothing to disclose
Diana Ferraro: nothing to disclose
Francesca Vitetta: nothing to disclose
Mauro Zennaro: nothing to disclose
Anna Maria Simone: nothing to disclose
Paolo Frigio Nichelli: nothing to disclose
Patrizia Sola: nothing to disclose
Abstract: EP1725
Type: ePoster
Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments
Introduction: Alemtuzumab is an anti-CD52 monoclonal antibody widely used for the treatment of relapsing-remitting multiple sclerosis (RRMS) with high disease activity despite previous disease-modifying therapies.1 The most common infusion-associated reaction (IAR) is cytokine-release syndrome. Incidence of cardiac-related IARs is 12.5% (tachycardia, bradycardia, palpitations), of which only 0.5% are serious cardiac-related IARs such as atrial fibrillation, sinus bradycardia, sinus tachycardia, hypotension or hypertension.2
We report a serious cardiac-related adverse event occurring during alemtuzumab-infusion in a RRMS patient.
Case report: A female 24-year-old RRMS patient, with an unremarkable personal history, started treatment with alemtuzumab due to ongoing disease activity during treatment with natalizumab. On the third day of treatment, shortly after premedication with steroids, antihistamine drugs, paracetamol and lansoprazole, the patient developed severe asymptomatic sinus bradycardia, which was treated with intravenous atropine. Infusion of alemtuzumab was resumed but on the following morning she complained of oppressive chest-pain lasting 20 minutes associated with dyspnoea. Blood tests showed high levels of troponin I, creatine kinase MB, and D-Dimer. Alemtuzumab treatment was discontinued. Continuous cardiac monitoring showed mild bradycardia in the absence of cardiac arrhythmias. Electrocardiography revealed a prolonged QTc interval. Echocardiography and cardiac magnetic resonance imaging did not detect alterations of left ventricular function nor the presence of regional wall-motion abnormalities. Computed tomography angiography and doppler ultrasonography of lower limbs did not reveal signs of acute pulmonary embolism/deep venous thrombosis. Within the subsequent week, myocardial cytolysis enzymes and D-dimer spontaneously returned within normal ranges and QTc interval normalized.
Conclusion: To our knowledge, this is the first report on a possible association between alemtuzumab treatment and acute coronary syndrome in absence of cardiovascular risk factors. We speculate that the augmentation of endothelial and myocyte membrane permeability and vasodilation induced by alemtuzumab-related cytokine- release syndrome might determine supply/demand ischemia of myocardic muscle defining type 2 myocardial ischemia.3
Disclosure:
Valentina Camera: nothing to disclose
Diana Ferraro: nothing to disclose
Francesca Vitetta: nothing to disclose
Mauro Zennaro: nothing to disclose
Anna Maria Simone: nothing to disclose
Paolo Frigio Nichelli: nothing to disclose
Patrizia Sola: nothing to disclose