Case of Dengue Myocarditis presenting as ST segment elevation MI
Dengue is the most common arthropod-borne viral (arboviral) illness in humans. Globally, 2.5-3 billion individuals live in approximately 112 countries that experience dengue transmission. Annually, approximately 50-100 million individuals are infected. The incidence has increased manifold in India due to unplanned urbanization and migration of population to urban areas. Although initially reported from urban locales, dengue is now being reported from urban and rural backgrounds alike.¹ Clinically, a non-specific afebrile illness, a mild-form dengue hemorrhagic fever (DHF), and dengue shock syndrome (DSS) are commonly encountered in dengue epidemics. Of note, a variety of cardiac complications have been reported in dengue-affected patients, which include atrioventricular conduction disorders, supraventricular arrhythmia, and myocarditis.
Courtesy Journal of Association of Physicians of India
A 50 years old female presented to the emergency department of our hospital with a history of left-sided chest pain, epigastric pain and vomiting of 4 hours duration. Her pulse rate was 56/min, regular and BP was 70/40 mm Hg. Electrocardiogram done in casualty showed ST segment elevation in leads II, III and aVF (Figure 1). She was thrombolysed with alteplase and admitted to cardiac care unit. She was started on dopamine infusion to maintain her cardiac output and blood pressure. She was also prescribed antiplatelets and other supportive drugs. Her blood urea nitrogen and serum creatinine on admission were documented to be 34 mg/dl and 0.8 mg/dl, serum aspartate transaminase (AST) 339 U/L, serum alanine aminotransferase (ALT) 774 U/L. Her platelet count was 2,14,000/cumm. Troponin T was positive, creatinine kinase (MB fraction) was 42 µg/L (1.0-.6.0 µg/L). Over the next 3 days her urine output dropped to 200 ml in 24 hours, she had azotemia (Serum creatinine 5.6 mg/dl). She was given hemodialysis after nephrologist’s advise. Echocardiography showed global hypokinesia and an ejection fraction of 52%. Her platelet count had dropped to 81,000/cumm when she came out of cardiology unit to the general ward.
A detailed and meticulous history elicited in the ward revealed that the patient had a history of fever, headache, body ache and joint pains for 4 days prior to presentation to the hospital. She also divulged a history of itching over palmar and plantar aspects of souls. She denied any significant past history. She persistently complained of distension of abdomen. Clinical examination revealed a maculopapular erythematous rash over the face and the trunk. She also had facial puffiness, bilateral pedal edema, and ascites. Her chest radiographs revealed minimal pleural fluid bilaterally. Ultrasound abdomen had revealed moderate free fluid in peritoneal cavity, peri-cholecystic fluid, peri-hepatic fluid and gall bladder wall edema. Her IgM for dengue was sent and it was reported as positive.
History of fever, headache, bodyache, joint pains, erythematous rash over body, itching, thrombocytopenia, polyserositis, gall bladder wall edema and positive dengue serology clinched the diagnosis in favour of dengue infection. She had dengue induced myocarditis masquerading as acute inferior wall myocardial infarction and acute kidney failure. She was managed on lines of dengue, over the next 4 days, her urine output progressively improved and azotemia settle.
Dengue myocarditis should be kept in mind in a patient, presenting with acute chest pain and electrocardiographic features suggestive of acute myocardial infarction, who has had the history and clinical features suggestive of dengue virus infection. Timely diagnosis can prevent unnecessary cardiac intervention and results in a more favourable outcome.