Personal history
Patient aged 49, baker by profession.
Cardiovascular risk factors: smoker of more than 25 pack-years, obese and moderate drinker. No HBP, DM, LBP or other history of interest. No cardiological history.
No other diseases of interest or chronic treatments. Current illness Consultation in the emergency department for 10 days of progressive dyspnoea, reaching minimal effort, with orthopnoea and paroxysmal nocturnal dyspnoea. He denies precordial pain, palpitations, syncope, fever or infectious symptoms at another level.


Physical examination
BP: 128/90.
HR: 105.
SatO2: 92%.
Afebrile, PVC 15 with mild RHY. BMI of 34.
AC: arrhythmic RsCs at 110 bpm, no murmurs.
AP: bibasal crackles.
Abdomen globular, without free fluid or megaliths.
LES: oedema with fovea in the lower 1⁄2⁄2. Peripheral pulses present and symmetrical. No carotid, abdominal or femoral murmurs.

COMPLEMENTARY TESTS
Blood count, biochemistry and coagulation: normal. Myocardial damage markers: HbA1c, TSH, cholesterol normal. Blood gases on admission: hypoxaemia and hypercapnia (pO2 60, pCO2 47 and bicarbonate 26). Chest X-ray: compatible with heart failure. ECG: rapid atrial fibrillation (AF) on admission, unknown. Echocardiogram: LA moderately dilated. RA slightly dilated. LV slightly dilated and hypertrophic, with global hypocontractility and moderately depressed global systolic function. EF 35-40%. RV with impaired function due to TAPSE, mild TR, estimated PSAP of 26mmHG +PVC. MV with good opening and mild reflux. AO normofunctioning. Dilated vena cava with partial collapse. No pericardial effusion. Moderate biventricular dysfunction with slightly dilated and hypertrophic vi with LVEF 35-40%. Coronary angiography: coronary arteries without significant coronary lesions.

EVOLUTION
The patient was admitted with a diagnosis of decompensated heart failure due to unknown rapid atrial fibrillation. Dilatation and moderate biventricular dysfunction were observed. When ischaemic origin was ruled out by coronary angiography, it was attributed as possibly secondary to tachycardiomyopathy or alcohol-induced cardiomyopathy. During admission, telemetry showed a spontaneous pause of 12 seconds coinciding with sleep apnoea, leaving the patient's own rhythm with narrow QRS. The patient was questioned about sleep habits and, with a high suspicion of sleep apnoea-hypopnoea syndrome (SAOS), a consultation with Pneumology was requested. The patient was diagnosed with COPD GOLD II and severe OSAHS. An outpatient polysomnography also revealed severe associated oxygen desaturation. Prior to admission, the patient was "apparently healthy". Special emphasis is placed on the importance of hygienic dietary measures, which together with CPAP, will be the most important treatment in this case, more than any pharmacological treatment. The patient commits to a change in lifestyle and anticoagulation is started in order to programme electrical cardioversion of AF. Follow-up after 3 months: an effective electrical cardioversion is performed, with the patient going into sinus rhythm and AF therefore becoming persistent. Control echocardiogram after 3 months (in sinus rhythm, without alcohol consumption, with BMI 33.3 and CPAP treatment): non-dilated ventricle with preserved LVEF. It is therefore a reversible ventricular dysfunction. We cannot say whether the dysfunction was secondary to rapid AF, alcohol or even to severe OSAHS itself.

DIAGNOSIS
First episode of heart failure.
Atrial fibrillation. Effective electrical cardioversion.
moderate biventricular isfunction.
Tachycardiomyopathy.
Severe sleep apnoea-hypopnoea syndrome (SAOS).
COPD GOLD II type. Smoking. Obesity.
