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Coronary ectasia and repeated myocardial infarction in a young man
International Journal of Cardiology 171 (2014) e74–e75
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Coronary ectasia and repeated myocardial infarction in a young man Ahmad S. Amin a,b,⁎, Sirus Hoseyni Guyomi a,b, Eugène M. Buijs a, Paul A.R. De Milliano a a b
Department of Cardiology, Tergooiziekenhuizen, Blaricum-Hilversum, The Netherlands Heart Center, Departments of Clinical and Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
a r t i c l e
i n f o
Article history: Received 5 September 2013 Accepted 30 November 2013 Available online 7 December 2013 Keywords: Coronary ectasia Kawasaki disease Myocardial infarction
To the Editor In March 2012, a 40-year-old medical doctor from Sri Lanka was referred to our hospital for repeated typical chest pain after exertion. He had left Sri Lanka in 2010, and, after a short stay in Thailand, migrated to the Netherlands. Till 2010, he had no medical history and no risk factors for atherosclerosis. In August 2010, in Bangkok, he had experienced an acute transmural myocardial infarction of the inferior wall (Fig. 1A), for which he was treated with streptokinase. Oral therapy with aspirin, metoprolol, enalapril and simvastatin was initiated. Coronary angiography was not performed. At referral to our hospital in March 2012, physical examination, blood tests, and ECG at rest and during exercise were normal. Echocardiography showed hypokinesia of the inferior septal wall. The diagnosis stable angina pectoris was made and the drug regimen was continued. In November 2012, he was admitted to the Cardiac Care Unit of our hospital after experiencing acute typical chest pain in rest. Physical examination was normal. Baseline ECG showed slight ST segment elevation in the inferior leads (Fig. 1B). The diagnosis acute coronary syndrome was made, aspirin was continued and initial loading doses of clopidogrel and fondaparinux were given. Serial blood tests revealed elevated cardiac enzymes (highly sensitive troponine-T peak of 160 ng/L). Echocardiography showed no novel abnormalities. Coronary angiography was performed and showed up to 10 mm diameter aneu-
⁎ Corresponding author at: Department of Clinical Cardiology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. Tel.: +31 20 5663072; fax: +31 20 6976177. E-mail address: [email protected] (A.S. Amin). 0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.11.102
rysms in the proximal segments of the left anterior descending coronary artery and the circumflex coronary artery (Fig. 2B) and through the entire length of the right coronary artery (Fig. 2A), with decreased blood flow in the coronary arteries and possible signs of thrombosis in the distal segments of the right coronary artery (Fig. 2A). Dual antiplatelet therapy with aspirin (100 mg daily) and clopidogrel (75 mg daily) was continued and acenocoumarol was initiated. The patient made a full recovery without recurrence of severe symptoms of angina when seen at the last follow-up in September 2013. A control coronary angiography showed no more signs of thrombosis in the coronary arteries. Localized or diffuse aneurysmal dilatation of the coronary arteries, as in our patient, is called coronary ectasia. In general, coronary ectasia is found in patients with multiple risk factors for atherosclerosis, where they probably represent an exaggerated form of vascular remodelling due to extensive atherosclerosis [1]. Coronary ectasia may also occur in systemic inflammatory vasculitides (e.g. polyarteritis nodosa, Takayasu arteritis), connective tissue disorders (e.g. rheumatoid arthritis, systemic lupus erythematosus), hereditary syndromes (e.g. EhlersDanlos syndrome, Marfan syndrome), syphilis and congenital diseases [2]. However, in adults without risk factors for atherosclerosis and no clinical and laboratory signs of systemic, inflammatory, infectious or congenital diseases, as in our patient, coronary ectasia may be remnants of the Kawasaki disease (KD), a systemic vasculitis of unknown aetiology affecting predominantly children younger than 5 years of age [3]. The incidence of the KD is highest in Asia, but is increasing in the Western countries, mainly due to increasing immigration [4]. Most symptoms of the KD, e.g. fever, rash, bilateral conjunctivitis, erythema of the lips and the oral mucosa, and cervical lymphadenopathy, are non-specific, self-limited or well treated with early intravenous immunoglobulin therapy. However, 5% of children, or up to 25% if untreated, may develop coronary ectasia, which create a substrate for thrombus formation (by reduced and turbulent blood flow), and thereby increase the risk for ischemic cardiac events and sudden death later in life [5,6]. Obtaining a history of KD remains difficult, especially since no specific diagnostic testing is available. Both parents of our patient had died, and the patient did not recall a childhood illness resembling KD. However, ruling out other diagnosis, we speculate that the coronary ectasia in our patient are remnants of KD during his childhood. Data addressing the management of coronary ectasia are limited. Anecdotal reports suggest chronic anticoagulation and antiplatelet therapy. Furthermore, dual antiplatelet therapy (for at least one year) may be considered after an ischemic cardiac event. If drug therapy is not successful, percutaneous and/or surgical coronary vascularisation and even cardiac transplantation are reported as effective options to restore myocardial perfusion [1].
A.S. Amin et al. / International Journal of Cardiology 171 (2014) e74–e75
e75
Fig. 1. ECG obtained in Thailand in October 2010 (A) and ECG at the time of admission to our hospital in November 2012.
References
Fig. 2. Coronary angiograms of the left coronary artery (A) and of the right coronary artery (B).
[1] Manginas A, Cokkinos DV. Coronary artery ectasias: imaging, functional assessment and clinical implications. Eur Heart J 2006;27:1026–31. [2] Antoniadis AP, Chatzizisis YS, Giannoglou GD. Pathogenetic mechanisms of coronary ectasia. Int J Cardiol 2008;130:335–43. [3] Kuo HC, Yang KD, Chang WC, Ger LP, Hsieh KS. Kawasaki disease: an update on diagnosis and treatment. Pediatr Neonatol 2012;53:4–11. [4] Uehara R, Belay ED. Epidemiology of Kawasaki disease in Asia, Europe, and the United States. J Epidemiol 2012;22:79–85. [5] Daniels LB, Gordon JB, Burns JC. Kawasaki disease: late cardiovascular sequelae. Curr Opin Cardiol 2012;27:572–7. [6] Zografos TA, Korovesis S, Giazitzoglou E, et al. Clinical and angiographic characteristics of patients with coronary artery ectasia. Int J Cardiol 2013;167:1536–41.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Coronary ectasia and repeated myocardial infarction in a young man Ahmad S. Amin a,b,⁎, Sirus Hoseyni Guyomi a,b, Eugène M. Buijs a, Paul A.R. De Milliano a a b
Department of Cardiology, Tergooiziekenhuizen, Blaricum-Hilversum, The Netherlands Heart Center, Departments of Clinical and Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
a r t i c l e
i n f o
Article history: Received 5 September 2013 Accepted 30 November 2013 Available online 7 December 2013 Keywords: Coronary ectasia Kawasaki disease Myocardial infarction
To the Editor In March 2012, a 40-year-old medical doctor from Sri Lanka was referred to our hospital for repeated typical chest pain after exertion. He had left Sri Lanka in 2010, and, after a short stay in Thailand, migrated to the Netherlands. Till 2010, he had no medical history and no risk factors for atherosclerosis. In August 2010, in Bangkok, he had experienced an acute transmural myocardial infarction of the inferior wall (Fig. 1A), for which he was treated with streptokinase. Oral therapy with aspirin, metoprolol, enalapril and simvastatin was initiated. Coronary angiography was not performed. At referral to our hospital in March 2012, physical examination, blood tests, and ECG at rest and during exercise were normal. Echocardiography showed hypokinesia of the inferior septal wall. The diagnosis stable angina pectoris was made and the drug regimen was continued. In November 2012, he was admitted to the Cardiac Care Unit of our hospital after experiencing acute typical chest pain in rest. Physical examination was normal. Baseline ECG showed slight ST segment elevation in the inferior leads (Fig. 1B). The diagnosis acute coronary syndrome was made, aspirin was continued and initial loading doses of clopidogrel and fondaparinux were given. Serial blood tests revealed elevated cardiac enzymes (highly sensitive troponine-T peak of 160 ng/L). Echocardiography showed no novel abnormalities. Coronary angiography was performed and showed up to 10 mm diameter aneu-
⁎ Corresponding author at: Department of Clinical Cardiology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. Tel.: +31 20 5663072; fax: +31 20 6976177. E-mail address: [email protected] (A.S. Amin). 0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.11.102
rysms in the proximal segments of the left anterior descending coronary artery and the circumflex coronary artery (Fig. 2B) and through the entire length of the right coronary artery (Fig. 2A), with decreased blood flow in the coronary arteries and possible signs of thrombosis in the distal segments of the right coronary artery (Fig. 2A). Dual antiplatelet therapy with aspirin (100 mg daily) and clopidogrel (75 mg daily) was continued and acenocoumarol was initiated. The patient made a full recovery without recurrence of severe symptoms of angina when seen at the last follow-up in September 2013. A control coronary angiography showed no more signs of thrombosis in the coronary arteries. Localized or diffuse aneurysmal dilatation of the coronary arteries, as in our patient, is called coronary ectasia. In general, coronary ectasia is found in patients with multiple risk factors for atherosclerosis, where they probably represent an exaggerated form of vascular remodelling due to extensive atherosclerosis [1]. Coronary ectasia may also occur in systemic inflammatory vasculitides (e.g. polyarteritis nodosa, Takayasu arteritis), connective tissue disorders (e.g. rheumatoid arthritis, systemic lupus erythematosus), hereditary syndromes (e.g. EhlersDanlos syndrome, Marfan syndrome), syphilis and congenital diseases [2]. However, in adults without risk factors for atherosclerosis and no clinical and laboratory signs of systemic, inflammatory, infectious or congenital diseases, as in our patient, coronary ectasia may be remnants of the Kawasaki disease (KD), a systemic vasculitis of unknown aetiology affecting predominantly children younger than 5 years of age [3]. The incidence of the KD is highest in Asia, but is increasing in the Western countries, mainly due to increasing immigration [4]. Most symptoms of the KD, e.g. fever, rash, bilateral conjunctivitis, erythema of the lips and the oral mucosa, and cervical lymphadenopathy, are non-specific, self-limited or well treated with early intravenous immunoglobulin therapy. However, 5% of children, or up to 25% if untreated, may develop coronary ectasia, which create a substrate for thrombus formation (by reduced and turbulent blood flow), and thereby increase the risk for ischemic cardiac events and sudden death later in life [5,6]. Obtaining a history of KD remains difficult, especially since no specific diagnostic testing is available. Both parents of our patient had died, and the patient did not recall a childhood illness resembling KD. However, ruling out other diagnosis, we speculate that the coronary ectasia in our patient are remnants of KD during his childhood. Data addressing the management of coronary ectasia are limited. Anecdotal reports suggest chronic anticoagulation and antiplatelet therapy. Furthermore, dual antiplatelet therapy (for at least one year) may be considered after an ischemic cardiac event. If drug therapy is not successful, percutaneous and/or surgical coronary vascularisation and even cardiac transplantation are reported as effective options to restore myocardial perfusion [1].
A.S. Amin et al. / International Journal of Cardiology 171 (2014) e74–e75
e75
Fig. 1. ECG obtained in Thailand in October 2010 (A) and ECG at the time of admission to our hospital in November 2012.
References
Fig. 2. Coronary angiograms of the left coronary artery (A) and of the right coronary artery (B).
[1] Manginas A, Cokkinos DV. Coronary artery ectasias: imaging, functional assessment and clinical implications. Eur Heart J 2006;27:1026–31. [2] Antoniadis AP, Chatzizisis YS, Giannoglou GD. Pathogenetic mechanisms of coronary ectasia. Int J Cardiol 2008;130:335–43. [3] Kuo HC, Yang KD, Chang WC, Ger LP, Hsieh KS. Kawasaki disease: an update on diagnosis and treatment. Pediatr Neonatol 2012;53:4–11. [4] Uehara R, Belay ED. Epidemiology of Kawasaki disease in Asia, Europe, and the United States. J Epidemiol 2012;22:79–85. [5] Daniels LB, Gordon JB, Burns JC. Kawasaki disease: late cardiovascular sequelae. Curr Opin Cardiol 2012;27:572–7. [6] Zografos TA, Korovesis S, Giazitzoglou E, et al. Clinical and angiographic characteristics of patients with coronary artery ectasia. Int J Cardiol 2013;167:1536–41.