A 59-year-old woman presented to the Emergency Department for sudden dyspnoea.

History, current illness and physical examination
A 59-year-old woman from San Juan (Argentina) attended the Emergency Department for sudden dyspnoea, with the following history: Ischaemic heart disease: silent inferior infarction of undetermined date. Previous myocardial infarction 1 year earlier, treated with fibrinolysis and subsequent cardiac catheterisation in which he had an intermediate lesion in the anterior descending and circumflex arteries and chronic occlusion of the DC, not revascularised, dilated left ventricle with depressed LVEF (40%). Cardiovascular risk factors: Arterial hypertension. Dyslipidaemia. Obesity. Ex. smoker of 10 cigarettes/day for the last 3 months. Chronic venous insufficiency of the lower limbs. Family history: Father with Chagas disease and myocardial infarction at the age of 59. Surgical interventions: cholecystectomy, tonsillectomy, appendectomy. Usual treatment: Clopidogrel/acetylsalicylic acid 75/100 mg c/24h, bisoprolol 2.5/24h, ramipril 2.5/24h, ranitidine 150mg c/24h, alprazolam 0.25 mg c/24h. The patient came to the emergency department for sudden and intense dyspnoea of less than 1 hour's duration, at rest, without chest pain. She presented 1 vomit of food coinciding with the dyspnoea. He denies fever, withdrawal of medication or other intercurrent process. He also reports exertional dyspnoea in recent months, which has been progressing until it has become light exertion and nocturnal dyspnoea for weeks. She has been sleeping with three pillows for years. On physical examination the patient was awake, alert, tachypneic, sweating, afebrile. BP 140/80 MMHG, intercostal stretch, intolerance to decubitus, no jugular engorgement, no carotid murmurs. AC: rhythmic, no murmurs. AP: preserved vesicular murmur, isolated wheezing and bibasal crackles. The rest of the physical examination was unremarkable.

Complementary tests
- Biochemistry: sodium 145 mmol/L, potassium 3.6 mmol/L CPK-MB 3.7 ng/mL, myoglobin 86* ng/mL (VN: 15-72), ultrasensitive troponin T 44.5**ng/L (VN: 0-14), urea 64, creatinine 1.30 mg/dL.
- Haemoglobin 13.1 g/dL, haematocrit 39.8%, leucocytes 9,320, platelets 244,00. Coagulation normal.
- Blood gas on arrival: Global respiratory failure with acidosis pH 7.145, pCO2 61.3 mmHg, pO2 46.6 mmHg. Bicarbonate 20.6 mmol/L, O2Sat 66.2%.
- Blood gases after treatment: pH 7,365, pCO2 32.6 mmHg, pO2 65.6 mmHg. Bicarbonate 18.2 mmol/L, O2Sat 92.9%.
- ECG: Sinus rhythm at 90 bpm. Axis 60o. Inferior Q and QS V3-V6, with negative T. Normal PR. Narrow QRS (110ms) (similar to previous recordings).
- Chest X-ray: global cardiomegaly, pulmonary vascular redistribution.
- Chest CT: Large cardiomegaly. Signs of apical vascular redistribution. Moderate bilateral pleural effusion. Bilateral basal atelectasis of lung tissue, mainly on the right. Mild signs of bilateral interstitial pattern. No signs of PTE (central/bilateral).
- Echocardiogram: Left ventricle severely dilated (Dd 6.9 cm, volume 222 cm3), with thinning of walls, akinesia of all anterior segments, only basal septum and lateral segments contracting. Estimated LVEF: 31% M-mode and 35% by Simpson. Restrictive mitral pattern (E/A 2.8; deceleration time 170 ms). Dilated left atrium (4.4 cm area 30 cm2). Dilated right chambers, with decreased TAPSE. Aorta not dilated. No significant valvular alterations. Pulmonary acceleration time shortened by 87 ms. Normal pericardium. Inferior vena cava not dilated.

Clinical evolution
The patient improved rapidly with the treatment prescribed in the emergency department (high-flow oxygen, nitroglycerine and morphine chloride). Given the suddenness of the symptoms with acute respiratory failure and elevated D-dimers, a chest CT scan was performed to rule out pulmonary thromboembolism. He was subsequently transferred to the cardiology ward where he remained clinically and haemodynamically stable, tolerating increasing doses of beta-blockers, ACE inhibitors and eplerenone and progressive reduction of furosemide. A new cardiac catheterisation was performed which showed no changes in the coronary arteries with respect to the one performed a year earlier. The patient had dilated cardiomyopathy of probable ischaemic origin with progressive deterioration until dyspnoea at rest. However, the patient came from a Chagas endemic area and had a family history of the disease, so it was decided to request serology for Trypanosoma cruzi, which was positive. DNA amplification by PCR of Trypanosoma cruzi in whole blood was also positive and the patient was diagnosed with chronic Chagas disease.
Given the severe ventricular dysfunction and poor functional class that persisted despite optimising medical treatment, an implantable cardioverter defibrillator (ICD) was implanted as primary prevention of sudden death. In our case we are left with the doubt as to whether the cardiac involvement is only due to ischaemic heart disease, as seems more likely, or whether there is also chagasic involvement due to the patient being chronically infected with Trypanosoma cruzi. We have not found any case in the literature in which both processes are described together.  


Diagnosis
- Acute heart failure: Acute pulmonary oedema.
- Dilated cardiomyopathy of probable ischaemic origin with severe ventricular dysfunction (LVEF 30-35%) vs. chagasic cardiomyopathy.
- Chronic ischaemic heart disease: inferior and anterior necrosis.
