HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
No known drug allergies.
Cardiovascular risk factors (CVRF): diabetes mellitus 2 (DM2). No known hypertension or dyslipidaemia.
Toxic habits: ex-smoker (previously smoked 1.5 packs/day from the age of 12 to 46 years). No current drinker, previously a weekend drinker of 5-6 beers and 4-5 drinks.
No previous cardiological history.
Surgical interventions: conisation in 2010.
Previous home treatment: metformin 850 mg/12 hours.

Current illness
50-year-old woman, ex-smoker, with no previous cardiological history, who for the last 4 months, in relation to exertion, has had episodes of non-radiating central thoracic oppression associated with dyspnoea, without accompanying vegetative cortex and relieved by rest. These episodes were initially triggered by heavy exertion, and the level of exertion at which they appear has progressively decreased, with these changes being more pronounced in the last two weeks. They now appear with small efforts (walking more quickly or climbing stairs). Curiously, she does daily bicycle exercise of about 30 minutes without the onset of symptoms. Given that the baseline electrocardiogram showed complete left bundle branch block (LBBB), exercise testing was ruled out and the patient was admitted to cardiology to complete the study.

He denied orthopnoea or episodes of paroxysmal nocturnal dyspnoea (PND). There was no increase in peripheral oedema or reduction in diuresis. She reported weight gain in recent months. No syncope/presyncope.

Physical examination
Good general condition, well hydrated and perfused, conscious and cooperative at all times. Clinically and haemodynamically stable on admission to the cardiology ward. Afebrile. Blood pressure 136/81 mmHg. Cardiac auscultation: rhythmic tones at a good frequency. No murmurs were heard. Respiratory auscultation: good vesicular murmur without pathological noises. Abdomen: soft, depressible, without visceromegaly or other noteworthy findings. Lower limbs: no oedema or signs of deep vein thrombosis. The rest of the examination was unremarkable.

COMPLEMENTARY TESTS
Electrocardiogram (ECG): sinus rhythm at 78 bpm. PR 160 ms. Normal axis. Wide QRS (120 ms) with LBBB image. Secondary repolarisation alterations.
Chest X-ray: cardiothoracic index not increased in size. No images of pulmonary condensation. Free costophrenic sinuses.
Analysis: Glucose 143 mg/dl. Creatinine 0.84 mg/dl. Urea 41 mg/dl. Sodium 148 mEq/l. Potassium 4.8 mEq/l. Lipid profile: total cholesterol 148 mg/dl, HDL cholesterol 62 mg/dl, LDL cholesterol 68 mg/dl, triglycerides 90 mg/dl. Normal liver profile. Normal thyroid hormones. Glycated haemoglobin: 7.3%. No mobilisation of myocardial damage markers: peak ultrasensitive cTnT 9 ng/dl. Haemogram with 4,990 leucocytes (normal formula), Hb 13.2 g/dl and 203,000 platelets. Coagulation normal.
Echocardiography: moderately dilated left atrium (LA) (42 mm AP diameter; Vol 42 ml/m2). Normal mitral valve morphology, with fibrocalcification of the posterior annulus and 2) restriction of the posterior leaflet mobility, with central insufficiency grade II (ORE 0.15 c.m.)
Dilated left ventricle (DTD 61 mm; DTS 48 mm; VTD 197 ml; VTD index 98 ml/m2; VTS 120 ml), normal myocardial thickness (septum 6 mm; pp 7 mm). LVEF 40% calculated by Simpson Biplane, with akinesia of the basal and middle segments of the septum and inferior face, as well as hypokinesia of the anterior face, with better contractility of the apical segments and lateral-inferior face. GLS -15% with more diminished values in the septal and inferior segments. Mitral filling E/A 1.3: E 108.7 cm/s; A 84 cm/s; e' sept 5.15 cm/s; e' lat 8.7 cm/s. E/e' 15 . Trivalve aortic valve, with preserved opening and closing, without insufficiency. Annulus 20 mm. Sinuses of Valsalva 32 mm. Right ventricle (RV) of normal dimensions (RVDVD 29 mm), with preserved systolic function. TAPSE 26 mm. S' 12.6 cm/s. Trivial IT that does not allow estimation of pulmonary gradient. Pulmonary flow with acceleration time of 110 ms. Inferior vena cava (IVC) not dilated, with adequate inspiratory collapse. No pericardial effusion. Conclusions: 1) dilated cardiomyopathy with moderate dysfunction and the described contractility alterations. 2) Diastolic dysfunction (dilated LA, E/e' >14; e' <10). 3) Functional mitral regurgitation (MR) grade II. 4) RV with preserved systolic function.
Coronary angiography: right radial access. Angiographically normal coronary arteries. Right dominance.
Cardiac magnetic resonance imaging (MRI): normal relationships and anatomical arrangement of the central cardiovascular structures. No interatrial septal defects or anatomical alterations in cardiac valves. Normal systemic and pulmonary venous drainage. Systolic area AD 20 cm2; left atrium 21.6 cm2 (4C plane estimate). Right ventricle neither dilated nor hypertrophic, without alterations in segmental contractility, with preserved systolic function (EF 66 %). Dilated left ventricle (dTD 61 mm; VTD 126.2 ml/m), without alterations in segmental thickness (images 4-5). No alterations in segmental thickening were observed. Dyssynchronous movement of the septum with respect to the non-septal wall of the LV, attributable to HH bundle branch block, to be correlated with ECG findings. Moderately depressed systolic function (EF 40%).Jet of central mitral insufficiency. Estimated regurgitant fraction between 13.6% (by calculation from ventricular volumes) and 17.8% (by calculation from LVlat and aorta). In the black myocardial sequences, a subtle linear intramyocardial enhancement is recognisable in the basal and middle septum, as well as in some areas of free wall, especially in the lateral and lower middle basal wall. Assessment in several sequences is very limited by respiratory motion. Conclusions: non-ischaemic left dilated cardiomyopathy, associated with moderate systolic dysfunction (LVEF 40%). Dyssynchronous movement of the septum. Non-coronary late enhancement pattern, as described above. Compatible with sequelae of myocarditis. Mitral insufficiency (RF 13.6%-17.8%).

CLINICAL EVOLUTION
On admission, after echocardiography detected findings of dilated cardiomyopathy with the segmental alterations described, the next step in the diagnostic algorithm was coronary angiography, which ruled out the presence of coronary artery disease. In view of this, cardiac MRI was requested for the aetiological study of the ventricular dysfunction, the result of which suggested a non-ischaemic origin of the condition (with a pattern of enhancement compatible with the sequelae of myocarditis).
The response during admission to depletive treatment was adequate, and treatment with beta-blockers, angiotensin-converting enzyme inhibitors (ACE inhibitors) and mineralocorticoid receptor antagonists (MRAs) was initiated, with good tolerance and consequent disappearance of the symptoms that led to admission.
On discharge from hospital, treatment was prescribed with enalapril 5 mg/12 hours, spironolactone 25 mg/24 hours and bisoprolol 2.5 mg/12 hours. As for anti-diabetic treatment, the patient was under treatment with metformin 850 mg/12 hours and, despite this, she had a glycosylated haemoglobin of 7.3%, above the target recommended by the guidelines in patients such as the one we present (7%). In this regard, dapagliflozin was added based on the results of cardiovascular efficacy obtained with this drug in recent studies on patients with heart failure. In addition, in order to improve adherence to treatment, both hypoglycaemic drugs were prescribed in a single presentation: metformin 850 mg/dapagliflozin 5 mg every 12 hours.
After discharge, the patient remains asymptomatic 11 months later and has not had any new hospital readmissions to date. In addition, the last blood test showed an objective decrease in HbA1c to 6.5%, below the recommended target level.

DIAGNOSIS
Idiopathic dilated cardiomyopathy with moderate dysfunction (EF 40%) probably in the context of old myocarditis.
Coronary arteries without angiographically significant lesions.
DM2 without optimal control (Hb1Ac 7.3%).
