Research letter
Midventricular Takotsubo cardiomyopathy after oxaliplatin infusion: an unreported side effect Stefano Coli, Filippo Pigazzani and Nicola Gaibazzi J Cardiovasc Med 2015, 16:646–649 Parma University Hospital, Parma, Italy Correspondence to Filippo Pigazzani, Parma University Hospital, Via Gramsci, 14, 43124 Parma, Italy E-mail: [email protected] Received 10 December 2013 Revised 20 July 2014 Accepted 25 July 2014
Letter to the editor Oxaliplatin is used as adjuvant chemotherapy in patients with advanced colorectal cancer, in combination with fluorouracil or capecitabine [a fluorouracil oral (p.o.) prodrug].1 Acute cardiotoxicity during treatment with fluorouracil and capecitabine is well recognized and coronary artery vasospasm is thought to be the main underlying mechanism,2 but these drugs have also been recently associated with Takotsubo cardiomyopathy (TTC).3,4 Cardiotoxicity is instead a rare side effect of oxaliplatin and has been linked to coronary artery spasm,5,6 but never to TTC. TTC is a syndrome characterized by transient regional left ventricular systolic dysfunction extending beyond a single coronary vascular bed, partially mimicking myocardial infarction, with chest pain and/or dyspnoea and ischemic ECG changes, in the absence of obstructive coronary artery disease7 (although the presence of ‘innocent’ coronary stenosis in elderly patients should not be a definitive exclusion criterion).8,9 The onset of TTC is generally preceded by a stressful emotional or physical event,10 but drugs are increasingly acknowledged as possible triggers.11 The proposed pathogenetic mechanisms include a cathecolaminergic hyperstimulation with either a direct myocardial damage or an acute microcirculatory dysfunction.12 We describe a case of TTC triggered by oxaliplatin infusion, which appears to be the first report in medical literature to the best of our knowledge.
previous smoker, had no history of prior heart disease and had a normal baseline ECG. At the end of the third session of oxaliplatin infusion, the patient reported perioral dysesthesia (described as a ‘strange feeling on the skin of face around the mouth’) without any cutaneous rash, immediately followed by chest pain, jugular constriction, dyspnoea and hypotension. ECG showed mild transient ST elevation in D1-aVL and then diffuse negative T waves with QT prolongation (Fig. 1). Even though there were no clear signs of anaphylaxis (absence of cutaneous rash, wheezes, stridor), the caring oncologist suspected an allergic reaction and administered methylpredsnisolone 40 mg i.v. and adrenaline 0.5 mg intramuscularly (i.m.). Given the persistence of chest pain with ECG changes, the patient was urgently transferred to the coronary care unit and a coronary angiogram was readily performed, showing normal coronary arteries except for a less than 50% stenosis in the mid of the right coronary artery (Fig. 2). Left ventriculogram revealed akinesia of all mid segments with sparing of basal and apical ones (Fig. 3). Cardiac ultrasound confirmed the peculiar distribution of regional akinesia13 involving only midventricular segments. A moderate increase of cardiac biomarkers was observed: peak CK-MB 13.6 ng/ml (normal range
Midventricular Takotsubo cardiomyopathy after oxaliplatin infusion: an unreported side effect Stefano Coli, Filippo Pigazzani and Nicola Gaibazzi J Cardiovasc Med 2015, 16:646–649 Parma University Hospital, Parma, Italy Correspondence to Filippo Pigazzani, Parma University Hospital, Via Gramsci, 14, 43124 Parma, Italy E-mail: [email protected] Received 10 December 2013 Revised 20 July 2014 Accepted 25 July 2014
Letter to the editor Oxaliplatin is used as adjuvant chemotherapy in patients with advanced colorectal cancer, in combination with fluorouracil or capecitabine [a fluorouracil oral (p.o.) prodrug].1 Acute cardiotoxicity during treatment with fluorouracil and capecitabine is well recognized and coronary artery vasospasm is thought to be the main underlying mechanism,2 but these drugs have also been recently associated with Takotsubo cardiomyopathy (TTC).3,4 Cardiotoxicity is instead a rare side effect of oxaliplatin and has been linked to coronary artery spasm,5,6 but never to TTC. TTC is a syndrome characterized by transient regional left ventricular systolic dysfunction extending beyond a single coronary vascular bed, partially mimicking myocardial infarction, with chest pain and/or dyspnoea and ischemic ECG changes, in the absence of obstructive coronary artery disease7 (although the presence of ‘innocent’ coronary stenosis in elderly patients should not be a definitive exclusion criterion).8,9 The onset of TTC is generally preceded by a stressful emotional or physical event,10 but drugs are increasingly acknowledged as possible triggers.11 The proposed pathogenetic mechanisms include a cathecolaminergic hyperstimulation with either a direct myocardial damage or an acute microcirculatory dysfunction.12 We describe a case of TTC triggered by oxaliplatin infusion, which appears to be the first report in medical literature to the best of our knowledge.
previous smoker, had no history of prior heart disease and had a normal baseline ECG. At the end of the third session of oxaliplatin infusion, the patient reported perioral dysesthesia (described as a ‘strange feeling on the skin of face around the mouth’) without any cutaneous rash, immediately followed by chest pain, jugular constriction, dyspnoea and hypotension. ECG showed mild transient ST elevation in D1-aVL and then diffuse negative T waves with QT prolongation (Fig. 1). Even though there were no clear signs of anaphylaxis (absence of cutaneous rash, wheezes, stridor), the caring oncologist suspected an allergic reaction and administered methylpredsnisolone 40 mg i.v. and adrenaline 0.5 mg intramuscularly (i.m.). Given the persistence of chest pain with ECG changes, the patient was urgently transferred to the coronary care unit and a coronary angiogram was readily performed, showing normal coronary arteries except for a less than 50% stenosis in the mid of the right coronary artery (Fig. 2). Left ventriculogram revealed akinesia of all mid segments with sparing of basal and apical ones (Fig. 3). Cardiac ultrasound confirmed the peculiar distribution of regional akinesia13 involving only midventricular segments. A moderate increase of cardiac biomarkers was observed: peak CK-MB 13.6 ng/ml (normal range
