ABC | Volume 114, Nº4, Suplement, April 2020

Case Report Acute Decompensated Heart Failure due to Chikungunya Fever Carolina Cunto de Athayde, 1 F abio Akio Nishijuka , 1 M árcia Cavalcanti de Campos Queiroz, 1 Monica Medeiros Luna, 1 Jaime Lobo Figueiredo, 1 Nadia Matias de Albuquerque, 1 Sebastião Carlos Ribeiro de Castilho, 1 Renata R. T. Castro 1, 2 Hospital Naval Marcilio Dias – Cardiologia, 1 Rio de Janeiro, RJ - Brazil Brigham and Womens Hospital – Medicine, 2 Boston – USA Introduction Heart failure (HF) is a chronic condition with worldwide high and growing prevalence. 1-3 It is extremely important to identify the cause of decompensated HF in order to manage cases correctly, given that identification makes it possible to implement specific treatment and prevent new hospitalizations. In Brazil, the main causes are poor adherence to medical treatment (30%) and infections (23%), 1 mainly pulmonary bacterial ones. 4 For this reason, patients with HF should receive the pneumococcal vaccine. Although it is less common, decompensation may occur due to viral infections, which justifies vaccination against influenza in these patients. 3 Over the past years, diverse Brazilian cities have been affected by epidemics of arboviruses that had previously been considered rare, such as those caused by the Zika and the chikungunya viruses. 5 These epidemics have drawn the scientific community’s attention, not only due to the number of patients affected, but mainly due to the common sequelae, such as microcephaly in children of pregnant women affected by the Zika virus and the disabling, chronic arthralgia secondary to chikungunya fever. Although there are case reports of myocarditis caused by arboviruses, 6-8 little is known regarding the risks of compliactions when patients previously diagnosed with heart failure are affected. The high prevalence of HF worldwide and the high incidence of arboviruses in Brazil justify the following case report. Case Report A 71-year-old retired male patient sought emergency service due to dyspnea during light exertion, which had progressively worsened over the past two days, evolving to resting dyspnea and paroxysmal nocturnal dyspnea after an episode of unmeasured fever the previous evening. He denied coughing, chest pain, dizziness, and syncope. The patient has previously been diagnosed with hypertensive/ alcoholic cardiomyopathy, chronic non-dialytic renal failure, permanent atrial fibrillation, hyperuricemia, chronic obstructive pulmonary disease, and cholelithiasis. He suffered from alcoholism, and he was a former smoker (47 packs/year, having ceased six years before). He regularly took carvedilol (12.5 mg in the morning and 25 mg at night), hydralazine (25 mg, 3 times daily), amlodipine (5 mg daily), furosemide (40 mg, 4 times daily), digoxin (0.125 mg daily), apixaban (2.5 mg, 2 times daily), bamifylline (300 mg daily), and formoterol/ budesonide (12 mcg + 400 mcg, 2 times daily). Upon admission, the patient presented blood pressure of 110/84 mmHg, heart rate of 86 bpm, respiratory rate of 26 rpm, and jugular venous distention at 30°. Pulmonary auscultation revealed universally audible vesicular murmurs, without adventitious sounds, and cardiac auscultation revealed an irregular rhythm, with normal heart sounds and no accessory sounds. The patient had lower limb edema (2+/4+), and there was no ascites on physical examination. There was no clinical evidence of angina, new arrhythmias, or infection (Table 1). The patient and his wife denied poor adherence to medical treatment, consumption of alcohol, or excessive salt or liquid intake. It was, therefore, not possible to identify precipitating factors for the clinical picture of decompensated HF. The patient’s admission electrocardiogram showed atrial fibrillation rhythm and left bundle branch block. There were no electrocardiographic alterations suggestive of myocardial ischemia. Chest radiography showed an increase in the cardiothoracic index, with slight pulmonary congestion and no pleural effusion or pulmonary consolidation. For the purpose of screening for infection, a urinary sediment test was performed, and the results were normal. The patient was admitted, classified as hemodynamic profile B 9 , and he underwent treatment with intravenous diuretics (Figure 1). On the third day of hospitalization, the patient progressed with worsened renal function, with creatinine clearance (Cockroft-Gault) of 19ml/min (creatinine 3.0 mg/dL) and hyperkalemia (6.1 mEq/l). On account of this complication, digoxin was suspended. After five days, the patient reached hemodynamic profile A, and the physician opted to change the furosemide route of administration from intravenous to oral. The same day, the patient presented macroscopic hematuria, and anticoagulation was suspended. On the seventh day of hospitalization, the patient complained of mild arthralgia in his knees and elbows, which he associated with his position in bed. Notwithstanding use of dipyrone, the following day, the symptoms worsened to bilateral arthralgia, which was highly intense in the knees, ankles, wrists, and elbows, thus restricting the patient’s movement in bed. The patient did not present dyspnea or precordial pain, and he maintained hemodynamic profile A. Slight pain control was achieved with the regular use Mailing Addres: Carolina Athayde • Hospital Naval Marcilio Dias – Cardiologia - Rua Cesar Zama, 185. Postal Code 20725-090, Rio de Janeiro, RJ – Brazil E-mail: carol.athayde@me.com Manuscript received October 31, 2018, revised manuscript January 26, 2019, accepted March 10, 2019 Keywords Heart Failure/physiopathology; Treatment Refusai; Pneumococcal Vaccine, Arbovirus Infections; Zika Virus Infection; ChiKungunia fever. DOI: https://doi.org/10.36660/abc.20180316 19