Dengue myocarditis presenting with mitral valve involvement


We admitted a case of dengue fever who was positive for dengue serotype 2 in the Department of Medicine, King George’s Medical University (K.G.M.U.), Lucknow, Uttar Pradesh, India. The patient had developed erythematous rashes with thrombocytopenia and bleeding manifestation in the form of microscopic hematuria. While he was recovering from the illness, he developed a sudden onset of breathlessness. On examination, his chest was full of crepitation bilaterally and his x-ray was suggestive of pulmonary edema. His troponin T (Trop T) and prohormone brain natriuretic peptide (proBNP) levels were elevated. Two-dimensional echo showed global left ventricular (LV) hypokinesia with mitral regurgitation (MR) and tricuspid regurgitation (TR). A diagnosis of myocarditis was made and the patient was managed in an intensive care unit (ICU) setting. The patient recovered from the illness and after a follow-up period of 6 weeks, showed no residual cardiac abnormality.

Keywords: Dengue fever, mitral regurgitation (MR), myocarditis

How to cite this article:
Mishra A, Singh VK. Dengue myocarditis presenting with mitral valve involvement. Ann Trop Med Public Health 2015;8:135-7
How to cite this URL:
Mishra A, Singh VK. Dengue myocarditis presenting with mitral valve involvement. Ann Trop Med Public Health [serial online] 2015 [cited 2021 Apr 14];8:135-7. Available from:

Dengue fever is a febrile illness caused by a virus of the genus Flavivirus called dengue virus, which has four serotypes (1, 2, 3, and 4). Mosquitoes of the genus Aedes are responsible for the transmission of this virus among human beings.

Dengue infections are responsible for a variety of complications like dengue hemorrhagic fever (DHF), dengue shock syndrome (DSS), liver failure, disseminated intravascular coagulation, encephalopathy, myocarditis, acute renal failure, and hemolytic uremic syndrome. [1]

Myocarditis is a rare complication of dengue virus infection. [2],[3] Global hypokinesia with low ejection fraction, and ST segment and T wave changes in the electrocardiogram (ECG) had been found in myocarditis associated with dengue fever. [4]

Case Report

A 27-year-old male patient presented in the Emergency Department with complaints of high-grade fever without chills, malaise, and headache for the past 5 days. No history of bleeding from any site of his body was noted. He did not have any systemic disease.

On arrival, his oral temperature was 100.2°F, pulse rate 98 bpm, respiratory rate 14 breaths/min, blood pressure (BP) 124/70 mmHg, and peripheral capillary oxygen saturation (SpO 2) 99%. On general examination, purpuric spots were present over both his arms without any icterus or pallor. On systemic examination, S1 S2 was heard in his cardiovascular system but no murmur; examination of his respiratory system revealed that his chest was bilaterally clear [Figure 1]; abdominal and neurological examination did not reveal any positive finding. ECG was within the normal limit [Figure 2].

Figure 1: Normal chest X-ray at the time of admission

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Figure 2: ECG at the time of admission

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Laboratory values disclosed that his peripheral white cell count was 3.7 × 109/L (normal range: 4-11 × 109/L) with 78% polymorphonuclear cells, hemoglobin (Hb) 13.5 mg/dL (normal range: 11-16 mg/dL), hematocrit 40.3% (normal range: 37-54%), platelet count 38 × 109/L (normal range: 150-400 × 109/L), prothrombin time (PT) 13.7 s (control-12.1), international normalized ratio (INR) 1.13, serum glutamic oxaloacetic transaminase (SGOT) 37.2 U/L (normal range: 10-50 U/L), serum glutamic-pyruvic transaminase (SGPT) 31.6 U/L (normal range: 10-50 U/L), and serum albumin 3.5 g/dL (normal range: 3.5-5 g/dL). The patient was found to be positive for nonstructural protein (NS1) antigen. He was also weakly positive for immunoglobulin M (IgM) antibody for dengue. His blood culture report was negative. A reverse transcriptase-polymerase chain reaction was positive for dengue virus serotype 2. Thick and thin smear for malaria and serological test for malaria and typhoid were negative. His urine examination showed 4-6 RBCs/hpf.

A chest x-ray-postanterior (CXR-PA) view showed clear lung fields with normal cardiac silhouette. Platelet count was monitored every day since the day of admission. On the second day, his platelet count reduced to 33,000/μL. Considering the microscopic hematuria and purpuric spots, four units of platelet were transfused. Rising trends in his platelet count were observed from day 3 onward. On the morning of day 4, he developed a sudden onset of breathlessness. There was no history of chest pain or cough with expectoration. On examination, his BP was 130/80 mmHg, pulse rate 110 bpm, respiratory rate 24 breaths/min; on examination of his cardiovascular system, S1 S2 was heard and examination of his respiratory system revealed bilateral crepitations throughout his chest. Chest X-ray showed congestion over bilateral lung fields, suggestive of pulmonary edema [Figure 3]. Troponin T (Trop T) value was 0.34 (range: 0-0.014) and prohormone brain natriuretic peptide (proBNP) value was 13863 (range: 0-125). Two-dimensional echo showed global left ventricular (LV) hypokinesia, left ventricular ejection fraction (LVEF) to be 44%, and moderate mitral regurgitation (MR) with mild tricuspid regurgitation (TR), suggestive of myocarditis. ECG showed T wave inversion in V1, V2, and V3 and equivocal T wave in V4, V5, and V6 [Figure 4].

Figure 3: Chest X-ray on day 5

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Figure 4: ECG on day 5

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The patient was kept in a propped-up position and was given intravenous (IV) furosemide 20 mg with an interval of 8 h, with restriction of fluids and physical activity. Low-flow nasal oxygen was given with strict SpO2 monitoring. On the morning of day 5, the patient was feeling better and was not dyspneic. On auscultation of his chest, crepitations were present only at the base of his lungs.

On continuing the same treatment for the next 5 days, the patient improved fully. His chest was bilaterally clear [Figure 5]. Trop T (value: 0.18, range: 0-0.014), and proBNP (value: 816, range: 0-125) values were also improved. ST segment and T wave changes reverted to normal [Figure 6].

Figure 5: Chest X-ray on the day of discharge

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Figure 6: ECG on the day of discharge

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He was discharged on day 12, with his platelet count value being 2.5 lakhs/μL. He was regularly followed up and remained stable without any systemic abnormality clinically. Two-dimensional echo review after 6 weeks revealed LVEF to be 62% without any regional wall motion abnormalities (RWMA)/MR/TR.


Dengue had been found to be associated with acute myocarditis and many studies in the literature are available revealing the same. [2],[3],[5],[6],[7]

In these studies, the clinical features, in general, of myocarditis revealed high fever, tachycardia, tachypnea, and dyspnea due to acutely developing pulmonary edema. Clinical examination of our patient revealed bilateral crepitations in his chest fields. Investigations showed changes in the ST segment and T wave in ECG, increased Trop T, and increased proBNP; x-ray of his chest showed bilateral congestion, suggesting pulmonary edema. Two-dimensional echo revealed global hypokinesia. [4] Reports of valvular leak have been very sparse and uncommon. A study conducted by Satarasinghe et al. reported tricuspid valvular leak in their studied patient. [7]

In our case, the patient showed most features of myocarditis associated with dengue fever, and he got back to normal in duration of 6 weeks. However, an interesting finding observed was the clinically appreciable murmur of MR and TR, which had been confirmed by two-dimensional echo evaluation as well. In our case, the event of pulmonary edema had been acute and severe, with SpO2 falling to 76%. The response to prompt management had been rewarding. It took our patient almost 5 days to improve from the clinical state of pulmonary edema. It appears that occurrence of more structural alterations/damages in cardiac tissue and subsequent hemodynamic circulatory instability in patients of myocarditis can lead to acutely occurring serious complications of markedly severe LV failure. This being a life-threatening state, requires a keen watch and handy emergency management in patients of dengue-observed developing myocarditis.

Shepherd SM, Hinfey PB, Shoff WH, Bronze MS. Dengue: Overview-eMedicine Infectious Diseases Dengue/ Dengue Fever eMedicine. Available from: [Last accessed on 2014 Mar 14].
Kabra SK, Juneja R, Madhulika, Jain Y, Singhal T, Dar L, et al. Myocardial dysfunction in children with dengue haemorrhagic fever. Natl Med J India 1998;11:59-61.
Promphan W, Sopontammarak S, Pruekprasert P, Kajornwattanakul W, Kongpattanayothin A. Dengue myocarditis. Southeast Asian J Trop Med Public Health 2004;35:611-3.
Wali JP, Biswas A, Chandra S, Malhotra A, Aggarwal P, Handa R, et al. Cardiac involvement in Dengue Haemorrhagic Fever. Int J Cardiol 1998;64:31-6.
Lee IK, Lee WH, Liu JW, Yang KD. Acute myocarditis in dengue hemorrhagic fever: A case report and review of cardiac complications in dengue-affected patients. Int J Infect Dis 2010;14:e919-22.
Lee CH, Teo C, Low AF. Fulminant dengue myocarditis masquerading as acute myocardial infarction. Int J Cardiol 2009;136:e69-71.
Satarasinghe RL, Arultnithy K, Amerasena NL, Bulugahapitiya U, Sahayam DV. Asymptomatic myocardial involvement in acute dengue virus infection in a cohort of adult Sri Lankans admitted to a tertiary referral centre. Br J Cardiol 2007;14:171-3.

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.162393


[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]

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