CLINICAL COMMUNICATION TO THE EDITOR
Myocardial Infarction Associated with Kawasaki Disease in Adult Man: Case Report and Review of Literature To the Editor: Kawasaki disease seems to be the most common cause of myocardial infarction in children. It draws special attention to itself because of its undisclosed etiopathogenesis and lack of definite diagnostic criteria. Although treatment schemes are established, new approaches are available because of intensive research programs and constantly updating news on the cause, pathogenesis, and previous case outcomes. Kawasaki disease is an acute systemic vasculitis and the leading cause of acquired heart disease in children in developed countries.1 It is most likely triggered by a currently unidentified antigen in genetically susceptible individuals.2,3 Without treatment, 1 in 5 children develops coronary artery aneurysms, and approximately 2.5% of cases are complicated with myocardial infarction.2,4,5 The disease most commonly affects children aged 6 months to 5 years. However, older children and even adults with Kawasaki disease have been described.6,7 We present a case report of a white man who had acute myocardial infarction 1 year after he was diagnosed with Kawasaki disease.
CASE REPORT An 18-year-old man was admitted to the intensive coronary care department with a symptomatically suspected acute myocardial infarction. Electrocardiogram showed elevation of the ST segment in anterolateral-posterobasal derivations (Figure 1). On December 28, 2011, the patient started feeling general fatigue and fever. He was diagnosed with urinary tract infection. The fever persisted, and on January 6, acute pleuropneumonia was diagnosed. Acute myocarditis, cardiopulmonary insufficiency, and hepatosplenomegaly developed. The patient was treated with cefotaxime, gentamicin, antipyretics, digoxin, and dopamine. Because of the patient’s remaining complicated condition, he was Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and played a role in writing this manuscript. Requests for reprints should be addressed to Urte Gargalskaite, Vilnius University, Faculty of Medicine, Vilnius, Lithuania. E-mail address: [email protected] 0002-9343/$ -see front matter Ó 2015 Elsevier Inc. All rights reserved.
transferred to the University hospital, where the following findings were observed: dry, strawberry tongue with coating; red, swollen throat; conjunctivitis; and peeling of the skin on the fingers of the hands. Cervical lymph nodes were not enlarged. Tachypnea and fine crepitating bilateral crackles were found during lung auscultation. Auscultation of the heart revealed tachycardia and gallop rhythm. Arterial blood pressure was 104/54 mm Hg, capillary refill time was 4 to 5 seconds, and extremities were cold. The patient’s temperature was 39.9 C. Treatment with antibiotics and aspirin was continued. Laboratory blood test results showed increased inflammation markers and thrombocytosis. On January 9, 2012, Kawasaki disease was diagnosed. Antibiotics were then discontinued, and intravenous immunoglobulin therapy plus aspirin was started. Because of the patient’s continuing fever, methylprednisolone pulse therapy was administered. After the patient’s condition improved, he was prescribed outpatient treatment with prednisolone and aspirin. During cardiac ultrasound in June 2013, dilatation of both atrial cavities was observed; the size of the left ventricle cavity had the highest normal value. During coronary artery computed tomography angiography, aneurysmatic dilatation and intraluminal thrombosis were identified. The physical loads examination showed limited functional capability. During myocardial perfusion examination, uneven perfusion in the anteroseptal area of the myocardium was identified. The patient was taking aspirin, warfarin (international normalized ratio was 2.6 three weeks before the event), carvedilol, and spironolactone. The hospital admission laboratory findings showed an elevation of troponin I (95,850 mg/L) and brain natriuretic peptide level of 150 ng/L. Echocardiogram showed decreased left ventricular inotropy and left ventricular ejection fraction (45%). Akinesis of left ventricle apical segments and hypokinesis of lateral wall apical segment were noted. The rheumatologist’s conclusion was acute myocardial infarction due to aneurysmatic lesions of coronary arteries as a complication of Kawasaki disease. Currently, there are no clinical signs of Kawasaki disease or elevation of inflammatory markers. Remission of Kawasaki disease was diagnosed. Percutaneous coronary intervention of anterior interventricular branch was performed, and an everolimuscoated stent was inserted (Figure 2).
REVIEW For the best results, Kawasaki disease diagnosis should be determined within 10 days of the onset of illness. To date,
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The American Journal of Medicine, Vol 128, No 3, March 2015
Figure 1
Electrocardiogram of the patient: ST-segment elevation in V1-V6, V7-V9 derivations, and the QS form in V1-V3.
there are no specific diagnostic tests or pathognomonic findings. Diagnosis is based on the clinical criteria, which include fever for at least 5 days and 4 or more of the 5 major clinical features (ie, conjunctival injection, cervical lymphadenopathy, oral mucosal changes, polymorphous rash, and swelling or redness of the extremities), and exclusion of alternative diagnoses.8,9 Cardiac complications are the leading causes of morbidity and mortality in patients with Kawasaki disease.
Despite the fact that coronary disease requiring revascularization is rare, coronary artery lesions are the most common complications.4,5,8 The standard of care for Kawasaki disease is the intravenous administration of immunoglobulin plus high-dose aspirin as early as possible.8-11 Unfortunately, intravenous immunoglobulin resistance occurs in up to 20% of cases.1,10 It is alternatively cured with a second intravenous immunoglobulin pulse or additional methylprednisolone pulse therapy or alternative medications, such as tumor necrosis factor-alpha blockers or inhibitors, cytotoxic agents, and plasmapheresis.4,8
CONCLUSIONS Kawasaki disease is a serious matter for both children and adults with respect to rheumatology and cardiology. Although the etiopathogenesis of Kawasaki disease is still in the research stage, it is essential to continue studies and to clarify the disease itself and its treatment. Early and precise diagnosis with adequate multidisciplinary treatment plays a key role in preventing the poor outcomes of Kawasaki disease. Pranas Serpytis, MD, PhDa,b Zaneta Petrulioniene, MD, PhDa,b Urte Gargalskaite, MDb Aurelija Gedminaite, MDb Violeta Panaviene, MD, PhDb,c Figure 2 Giant aneurysms of the anterior interventricular branch and circumflex branch, and occlusion of seventh segment of the anterior interventricular branch.
a Vilnius University Vilnius University Hospital Santariskiu Clinics Center of Cardiology and Angiology Vilnius, Lithuania
Serpytis et al
Myocardial Infarction Associated with Kawasaki Disease b
Vilnius University Faculty of Medicine Vilnius, Lithuania c Vilnius University, Children’s Hospital Affiliate of Vilnius University Hospital Santariskiu Clinics Vilnius, Lithuania
http://dx.doi.org/10.1016/j.amjmed.2014.10.029
References 1. Eleftheriou D, Levin M, Shingadia D, et al. Management of Kawasaki disease. Arch Dis Child. 2014;99:74-83. 2. Yim D, Curtis N, Cheung M, et al. Update on Kawasaki disease: epidemiology, aetiology and pathogenesis. J Paediatr Child Health. 2013;49:704-708. 3. Rowley AH, Shulman ST. Pathogenesis and management of Kawasaki disease. Expert Rev Anti Infect Ther. 2010;8:197-203. 4. Bayers S, Shulman ST, Paller AS. Kawasaki disease part II. Complications and treatment. J Am Acad Dermatol. 2013;69:513.e1-513.e8.
e3
5. Paredes N, Mondal T, Brandão LR, Chan AK. Management of myocardial infarction in children with Kawasaki disease. Blood Coagul Fibrinolysis. 2010;21:620-631. 6. Hartopo AB, Setianto BY. Coronary artery sequel of Kawasaki disease in adulthood, a concern for internists and cardiologists. Acta Med Indones. 2013;45:69-75. 7. Inokuchi R, Kurata H, Harada M, et al. Coronary artery aneurysms after adult-onset Kawasaki disease. Circulation. 2013;127: 1636-1637. 8. Kuo H-C, Yang KD, Chang W-C, et al. Kawasaki disease: an update on diagnosis and treatment. Pediatr Neonatol. 2012;53:4-11. 9. Sivalingama SK, Parthasarathyb HK, Choong CK, et al. Severe triple vessel coronary artery disease and aneurysms in a young white man: disease progression of childhood Kawasaki disease. J Cardiovasc Med. 2009;10:170-173. 10. Bajolle F, Laux D. [Kawasaki disease: what you need to know]. Arch Pediatr. 2012;19:1264-1268. 11. Kobayashi T, Saji T, Otani T, et al. Efficacy of immunoglobulin plus prednisolone for prevention of coronary artery abnormalities in severe Kawasaki disease (RAISE study): a randomised, open-label, blindedendpoints trial. Lancet. 2012;379:1613-1620.
Myocardial Infarction Associated with Kawasaki Disease in Adult Man: Case Report and Review of Literature To the Editor: Kawasaki disease seems to be the most common cause of myocardial infarction in children. It draws special attention to itself because of its undisclosed etiopathogenesis and lack of definite diagnostic criteria. Although treatment schemes are established, new approaches are available because of intensive research programs and constantly updating news on the cause, pathogenesis, and previous case outcomes. Kawasaki disease is an acute systemic vasculitis and the leading cause of acquired heart disease in children in developed countries.1 It is most likely triggered by a currently unidentified antigen in genetically susceptible individuals.2,3 Without treatment, 1 in 5 children develops coronary artery aneurysms, and approximately 2.5% of cases are complicated with myocardial infarction.2,4,5 The disease most commonly affects children aged 6 months to 5 years. However, older children and even adults with Kawasaki disease have been described.6,7 We present a case report of a white man who had acute myocardial infarction 1 year after he was diagnosed with Kawasaki disease.
CASE REPORT An 18-year-old man was admitted to the intensive coronary care department with a symptomatically suspected acute myocardial infarction. Electrocardiogram showed elevation of the ST segment in anterolateral-posterobasal derivations (Figure 1). On December 28, 2011, the patient started feeling general fatigue and fever. He was diagnosed with urinary tract infection. The fever persisted, and on January 6, acute pleuropneumonia was diagnosed. Acute myocarditis, cardiopulmonary insufficiency, and hepatosplenomegaly developed. The patient was treated with cefotaxime, gentamicin, antipyretics, digoxin, and dopamine. Because of the patient’s remaining complicated condition, he was Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and played a role in writing this manuscript. Requests for reprints should be addressed to Urte Gargalskaite, Vilnius University, Faculty of Medicine, Vilnius, Lithuania. E-mail address: [email protected] 0002-9343/$ -see front matter Ó 2015 Elsevier Inc. All rights reserved.
transferred to the University hospital, where the following findings were observed: dry, strawberry tongue with coating; red, swollen throat; conjunctivitis; and peeling of the skin on the fingers of the hands. Cervical lymph nodes were not enlarged. Tachypnea and fine crepitating bilateral crackles were found during lung auscultation. Auscultation of the heart revealed tachycardia and gallop rhythm. Arterial blood pressure was 104/54 mm Hg, capillary refill time was 4 to 5 seconds, and extremities were cold. The patient’s temperature was 39.9 C. Treatment with antibiotics and aspirin was continued. Laboratory blood test results showed increased inflammation markers and thrombocytosis. On January 9, 2012, Kawasaki disease was diagnosed. Antibiotics were then discontinued, and intravenous immunoglobulin therapy plus aspirin was started. Because of the patient’s continuing fever, methylprednisolone pulse therapy was administered. After the patient’s condition improved, he was prescribed outpatient treatment with prednisolone and aspirin. During cardiac ultrasound in June 2013, dilatation of both atrial cavities was observed; the size of the left ventricle cavity had the highest normal value. During coronary artery computed tomography angiography, aneurysmatic dilatation and intraluminal thrombosis were identified. The physical loads examination showed limited functional capability. During myocardial perfusion examination, uneven perfusion in the anteroseptal area of the myocardium was identified. The patient was taking aspirin, warfarin (international normalized ratio was 2.6 three weeks before the event), carvedilol, and spironolactone. The hospital admission laboratory findings showed an elevation of troponin I (95,850 mg/L) and brain natriuretic peptide level of 150 ng/L. Echocardiogram showed decreased left ventricular inotropy and left ventricular ejection fraction (45%). Akinesis of left ventricle apical segments and hypokinesis of lateral wall apical segment were noted. The rheumatologist’s conclusion was acute myocardial infarction due to aneurysmatic lesions of coronary arteries as a complication of Kawasaki disease. Currently, there are no clinical signs of Kawasaki disease or elevation of inflammatory markers. Remission of Kawasaki disease was diagnosed. Percutaneous coronary intervention of anterior interventricular branch was performed, and an everolimuscoated stent was inserted (Figure 2).
REVIEW For the best results, Kawasaki disease diagnosis should be determined within 10 days of the onset of illness. To date,
e2
The American Journal of Medicine, Vol 128, No 3, March 2015
Figure 1
Electrocardiogram of the patient: ST-segment elevation in V1-V6, V7-V9 derivations, and the QS form in V1-V3.
there are no specific diagnostic tests or pathognomonic findings. Diagnosis is based on the clinical criteria, which include fever for at least 5 days and 4 or more of the 5 major clinical features (ie, conjunctival injection, cervical lymphadenopathy, oral mucosal changes, polymorphous rash, and swelling or redness of the extremities), and exclusion of alternative diagnoses.8,9 Cardiac complications are the leading causes of morbidity and mortality in patients with Kawasaki disease.
Despite the fact that coronary disease requiring revascularization is rare, coronary artery lesions are the most common complications.4,5,8 The standard of care for Kawasaki disease is the intravenous administration of immunoglobulin plus high-dose aspirin as early as possible.8-11 Unfortunately, intravenous immunoglobulin resistance occurs in up to 20% of cases.1,10 It is alternatively cured with a second intravenous immunoglobulin pulse or additional methylprednisolone pulse therapy or alternative medications, such as tumor necrosis factor-alpha blockers or inhibitors, cytotoxic agents, and plasmapheresis.4,8
CONCLUSIONS Kawasaki disease is a serious matter for both children and adults with respect to rheumatology and cardiology. Although the etiopathogenesis of Kawasaki disease is still in the research stage, it is essential to continue studies and to clarify the disease itself and its treatment. Early and precise diagnosis with adequate multidisciplinary treatment plays a key role in preventing the poor outcomes of Kawasaki disease. Pranas Serpytis, MD, PhDa,b Zaneta Petrulioniene, MD, PhDa,b Urte Gargalskaite, MDb Aurelija Gedminaite, MDb Violeta Panaviene, MD, PhDb,c Figure 2 Giant aneurysms of the anterior interventricular branch and circumflex branch, and occlusion of seventh segment of the anterior interventricular branch.
a Vilnius University Vilnius University Hospital Santariskiu Clinics Center of Cardiology and Angiology Vilnius, Lithuania
Serpytis et al
Myocardial Infarction Associated with Kawasaki Disease b
Vilnius University Faculty of Medicine Vilnius, Lithuania c Vilnius University, Children’s Hospital Affiliate of Vilnius University Hospital Santariskiu Clinics Vilnius, Lithuania
http://dx.doi.org/10.1016/j.amjmed.2014.10.029
References 1. Eleftheriou D, Levin M, Shingadia D, et al. Management of Kawasaki disease. Arch Dis Child. 2014;99:74-83. 2. Yim D, Curtis N, Cheung M, et al. Update on Kawasaki disease: epidemiology, aetiology and pathogenesis. J Paediatr Child Health. 2013;49:704-708. 3. Rowley AH, Shulman ST. Pathogenesis and management of Kawasaki disease. Expert Rev Anti Infect Ther. 2010;8:197-203. 4. Bayers S, Shulman ST, Paller AS. Kawasaki disease part II. Complications and treatment. J Am Acad Dermatol. 2013;69:513.e1-513.e8.
e3
5. Paredes N, Mondal T, Brandão LR, Chan AK. Management of myocardial infarction in children with Kawasaki disease. Blood Coagul Fibrinolysis. 2010;21:620-631. 6. Hartopo AB, Setianto BY. Coronary artery sequel of Kawasaki disease in adulthood, a concern for internists and cardiologists. Acta Med Indones. 2013;45:69-75. 7. Inokuchi R, Kurata H, Harada M, et al. Coronary artery aneurysms after adult-onset Kawasaki disease. Circulation. 2013;127: 1636-1637. 8. Kuo H-C, Yang KD, Chang W-C, et al. Kawasaki disease: an update on diagnosis and treatment. Pediatr Neonatol. 2012;53:4-11. 9. Sivalingama SK, Parthasarathyb HK, Choong CK, et al. Severe triple vessel coronary artery disease and aneurysms in a young white man: disease progression of childhood Kawasaki disease. J Cardiovasc Med. 2009;10:170-173. 10. Bajolle F, Laux D. [Kawasaki disease: what you need to know]. Arch Pediatr. 2012;19:1264-1268. 11. Kobayashi T, Saji T, Otani T, et al. Efficacy of immunoglobulin plus prednisolone for prevention of coronary artery abnormalities in severe Kawasaki disease (RAISE study): a randomised, open-label, blindedendpoints trial. Lancet. 2012;379:1613-1620.
