Anadolu Kardiyol Derg 2014; 14: 658-62
Acute myocardial infarction induced by axitinib
Letters to the Editor
References 1.
To the Editor, Axitinib is a novel tyrosine kinase inhibitor which is a second-line option for the treatment of metastatic renal cell carcinoma with progression after previous therapy (1, 2). We present the first reported case of acute myocardial infarction in a patient receiving axitinib. In July 2010, a 40-year-old male with no history of smoking, hypertension, diabetes or hypercholesterolemia, and no family history of coronary artery disease, underwent right nephrectomy due to renal cell carcinoma. Chest computed tomography, at the time of diagnosis, revealed the presence of multiple nodules in both lung areas, the largest of which was in the right middle lobe measuring 1.2 cm. Pathologic examination of a transbronchial lung biopsy showed metastatic clear-cell type renal cell carcinoma. Abdominal magnetic resonance imaging detected no metastatic lesion. Normal bone scan was observed in technetium-99m methylene diphosphonate scintigraphy. Whole-body fluorodeoxyglucose positron emission tomography imaging exhibited increased uptake in proven metastatic pulmonary lesions while the rest of the body showed physiological distribution. Transthoracic echocardiography documented normal left ventricular systolic and diastolic function, and normal valvular structures. Adjuvant systemic therapy was initiated to treat residual metastatic disease. After the failure of three consecutive chemotherapeutic agents (interpheron-alpha for 3 months, everolimus for 2 years, sunitinib for 1 year, consecutively), treatment with oral axitinib was started at Ordu State Hospital, in November 2013. One week after beginning axitinib, he developed chest pain with sudden onset. The electrocardiogram (ECG), which was recorded during chest pain, demonstrated ST segment elevation in leads II, III, aVF and V3 to V6, reciprocal ST depressions in lead I, aVL, and third-degree atrioventricular block. On physical examination, there were no abnormal findings. The patient was diagnosed with acute myocardial infarction of inferolateral wall, and transthoracic echocardiography showed mildly hypokinetic myocardium (involving the right coronary artery territory), with an estimated left ventricular ejection fraction of 55%. After pretreatment with clopidogrel (600 mg of oral loading dose), aspirin (300 mg, oral) and heparin (10000 U, intravenous), he was immediately transferred to the catheter laboratory for a primary percutanous coronary intervention. Coronary angiography revealed that the right coronary artery (RCA) was totally occluded by a thrombus in the proximal segment, while the left main, the left anterior descending and the circumflex artery showed no significant stenosis. After successful wire crossing in the RCA, the totally occluded lesion was pre-dilated with a 2.5 x 15 mm balloon at 10 atms. Subsequently, 3.0 x 20 mm bare-metal stent was implanted at 15 atms and thrombolysis in myocardial infarction (TIMI) 3 flow was achieved. The patient’s symptoms were relieved, and ST elevations on ECG regressed. A week after the procedure, he was discharged from the hospital in a stable condition, with the prescription of clopidogrel 75 mg, aspirin 300 mg, metoprolol 25 mg and atorvastatin 10 mg (all once a day). Axitinib was discontinued immediately after the diagnosis of myocardial infarction and the patient was referred to oncology department of our hospital following discharge, for the arrangement of his chemotherapy drugs. Emre Gürel, Zeki Yüksel Günaydın1, Müge Karaoğlanoğlu*, Tuncay Kırış Departments of Cardiology and *Oncology, Ordu State Hospital; Ordu-Turkey 1Department of Cardiology, Ordu University Hospital; Ordu-Turkey
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2.
Motzer RJ, Escudier B, Tomczak P, Hutson TE, Michaelson MD, Negrier S, et al. Axitinib versus sorafenib as second-line treatment for advanced renal cell carcinoma: overall survival analysis and updated results from a randomised phase 3 trial. Lancet Oncol 2013; 14: 552-62. [CrossRef] Rini BI, Escudier B, Tomczak P, Kaprin A, Szczylik C, Hutson TE, et al. Comparative effectiveness of axitinib versus sorafenib in advanced renal cell carcinoma (AXIS): a randomised phase 3 trial. Lancet 2011; 378: 1931-9. [CrossRef]
Address for Correspondence: Dr. Emre Gürel, Bahçelievler Mah. 293. Sok. Gürsoy-Varol Sitesi B-blok, No: 4/13, Ordu-Türkiye
Phone: +90 533 423 21 51 Fax: +90 452 234 32 32 E-mail:
[email protected] Available Online Date: 22.08.2014 ©Copyright 2014 by Turkish Society of Cardiology - Available online at www.anakarder.com DOI:10.5152/akd.2014.5713
Peripartum cardiomyopathy associated with triplet pregnancy To the Editor, A 22-year-old puerpera after c/section for a triplet at thirty sixth week of gestation was admitted to obstetric clinic in our institution. Pregnancy record for his triplet did not show any problem. After an elective cesarean section under epidural anesthesia, three healthy babies were born. Before pregnancy there was no documented cardiac disease. Progressive dyspnea and orthopnea began within two hours following birth. Arterial blood pressure was 100/60 mm Hg and heart rate was 110/ min. On auscultation S3 heart sound was heard. Arterial blood gas analysis revealed, O2 saturation: 87%, PaO2: 85 mm Hg, PaCO2: 40 mm Hg, pH: 7.30. Lung examination showed bilateral crepitan crackles reaching to upper middle zone. Consequently the patient was transferred to the coronary intensive care unit with the diagnosis of an acute pulmonary edema. Intravenous nitroglycerin, furosemide and continuous positive airway pressure (CPAP) therapy decreased the shortness of breath. On transthoracic echocardiography, left ventricular ejection fraction (LVEF) was 23% and left ventricular diastolic diameter (LVDD) was 61 mm. We considered peripartum cardiomyopathy (PPCMP) as an ethiology of acute pulmonary edema. 25 mg of metoprolol, 25 mg of sprinolactone, 40 mg of furosemide and 2.5 mg of ramipril, all with oral use, were added to the daily treatment of the patient after positive response to the acute treatment. Patient followed up 2 weeks in our intensive care unit and orthopnea gradually decreased. LVEF was measured 25% at the time of discharge. 1 month after discharge, LVEF was 30% with NYHA class 1 functional status. 2 months later the LVEF was advanced to the 45% while LVDD regressed to 55 mm. However, sixth month control echocardiography demonstrated LVEF of 60% and LVDD of 49 mm and that the patient was symptom free. Twelfth month control was also showed normal left ventricular systolic function. Classical risk factors of PPCMP include race (African origin), advanced maternal age, twin pregnancy, preeclampsia, hypertension, infections and long-standing tocolytic therapy (1, 2). Although twin pregnancy is a known risk factor, PPCMP associated with triplet pregnancy has not been described previously in the literature. The pathogenesis of
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Letters to the Editor
peripartum cardiomyopathy is controversial and still not fully understood (2). The most important assumption focuses on the increased fluid load in pregnancy. Increased blood volume and cardiac output and decreased systemic vascular resistance may result in a reduction of LVEF, in response to this augmented load (3). However, several hypotheses have also been postulated such as myocarditis, viral infection, inflammatory cytokines, selenium deficiency and abnormal autoimmune activity of maternal antibodies. These autoantibodies may cross react with the myocardium and can cause cardiomyopathy (4, 5). Triplet pregnancy and peripartum cardiomyopathy are uncommon separately, thus, the association of these two entities seems to be interesting. Zeki Yüksel Günaydın, Yusuf Emre Gürel1, Güney Erdoğan1, Ahmet Kaya Department of Cardiology, Ordu University; Ordu-Turkey 1Department of Cardiology, Ordu State Hospital; Ordu-Turkey
References 1.
Okeke T, Ezenyeaku C, Ikeako L. Peripartum cardiomyopathy. Ann Med Health Sci Res 2013; 3: 313-9. [CrossRef] 2. Givertz MM. Cardiology patient page: Peripartum cardiomyopathy. Circulation 2013; 127: 622-6. [CrossRef] 3. Task Force on the Management of Cardiovascular Diseases During Pregnancy of the European Society of Cardiology. Expert consensus document on management of cardiovascular diseases during pregnancy. Eur Heart J 2003; 24: 761-81. [CrossRef] 4. Ansari AA, Fett JD, Carraway RE, Mayne AE, Onlamoon N, Sundstrom JB. Autoimmune mechanisms as the basis for human peripartum cardiomyopathy. Clin Rev Allergy Immunol 2002; 23: 301-24. [CrossRef] 5. Bhattacharyya A, Basra SS, Sen P, Kar B. Peripartum cardiomyopathy: a review. Tex Heart Inst J 2012; 39: 8-16.
Anadolu Kardiyol Derg 2014; 14: 658-62
segment III, which was interpreted as focal omental infarction. He was fully investigated regarding the etiology of omental infarction including detailed hypercoagulable work up, however no abnormality was found. The possibility of PFO was considered and transcranial Doppler ultrasound (TCD) bubbles test was done and demonstrated strongly positive embolic signals during the Valsalva phase, suggesting severe right to left shunting Transesophageal echocardiography (TEE) revealed a positive saline contrast study demonstrating right to left shunting at the atrial level. Large PFO was considered as the cause of omental infarction. Given his occupation, percutaneous closure of PFO with Starflex absorbable device was inserted successfully. To our knowledge this is the first case to report omental infarction due to a paradoxical embolism. Omental infarction may occur due to torsion caused by adhesions, cysts and tumors, hernias; thrombosis caused by hypercoagulopathy and vascular abnormalities and congestion caused by right-sided heart failure (1, 2). As in our patient prololonged airplane travel appears to increase the risk of venous thromboembolism (VTE) ; this association has been called “economy class syndrome” (3). A variant “economy class stroke syndrome” has been described in a case in whom ischemic stroke occurred during or immediately after a long flight presumably due to paradoxical embolism (4). Our case presented with abdominal pain secondary to omental infarction during a long flight due to a paradoxical embolism that may be another variant of “economy class syndrome”. As a peripheral embolism during or immediately after a long flight is suggestive of paradoxical embolism through the PFO. Moving about every hour or two, alcohol avoidance and using below-knee stockings may reduce thromboembolic complications during prolonged travel (4). Fatih Yaşar, Özcan Özdemir*, Mahmut Kebapcı**, Ömer Göktekin1, Enver İhtiyar, Necmi Ata*** Departments of General Surgery, *Neurology, **Radiology, ***Cardiology, Faculty of Medicine, Eskisehir Osmangazi University; Eskişehir-Turkey 1Department of Cardiology, Faculty of Medicine, Bezmialem Vakıf University; İstanbul-Turkey
Address for Correspondence: Dr. Zeki Yüksel Günaydın, Ordu Üniversitesi Tıp Fakültesi, Kardiyoloji Anabilim Dalı, 52100 Ordu-Türkiye
Phone: +90 452 223 52 52 Fax: +90 452 223 50 78 E-mail:
[email protected] Available Online Date: 22.08.2014 ©Copyright 2014 by Turkish Society of Cardiology - Available online at www.anakarder.com DOI:10.5152/akd.2014.5668
Omental infarction due to a patent foramen ovale after a long flight: a variant of economy class syndrome To the Editor, We describes a patient with omental infarction secondary to paradoxical embolism via patent foramen ovale (PFO) during a long flight that may be described as a variant of “economy class syndrome”. A-31-years old gentleman who is a flight attendant in Turkish Airlines presented with a sudden onset severe right upper quadrant abdominal pain during his flight from Japan-Osaka to İstanbul. After 2 days he was seen in emergency department with abdominal tenderness to palpation with guarding in the upper right quadrant. An abdominal tomographic scan revealed mesenteric fibro fatty adjacent to the liver
References 1.
Puylaert JB. Right-sided segmental infarction of the omentum: clinical, US, and CT findings. Radiology 1992; 185: 169-72. [CrossRef] 2. Park TU, Oh JH, Chang IT, Lee SJ, Kim SE, Kim CW, et al. Omental infarction: Case series and review of the literature. J Emerg Med 2012; 42: 149-54. [CrossRef] 3. Cruickshank JM, Gorlin R, Jennett B. Air travel and thrombotic episodes: the economy class syndrome. Lancet 1988; 2: 497-8. [CrossRef] 4. Isayev Y, Chan RK, Pullicino PM. “Economy class” stroke syndrome? Neurology 2002; 58: 960-1. [CrossRef] Address for Correspondence: Dr. Özcan Özdemir, Eskişehir Osmangazi Üniversitesi Tıp Fakültesi, Nöroloji Anabilim Dalı, Meşelik, Eskişehir-Türkiye
Phone: +90 222 239 29 79-3650 Fax: +90 222 230 96 96 E-mail:
[email protected] Available Online Date: 22.08.2014 ©Copyright 2014 by Turkish Society of Cardiology - Available online at www.anakarder.com DOI:10.5152/akd.2014.5620
