HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
The case is a 37-year-old woman, with no known drug allergies, a former smoker for 20 years, who in 2016 presented with central retinal vein obstruction, complicated by vitreous haemorrhage that eventually required vitrectomy. In addition, she has a probable antiphospholipid syndrome, for which she is being treated with hydroxychloroquine 200 mg/24 h and acetylsalicylic acid 100 mg/24 h. The patient was being followed up by a private cardiologist due to the accidental finding of a murmur during an examination at work. The echocardiogram (TTE) showed moderate aortic insufficiency (AIo) with mild stenosis, normal mitral valve, non-dilated left ventricle (LV) with preserved LV ejection fraction (LVEF), and no evidence of pulmonary hypertension (PH). Pregnant at 20 weeks, she was referred from obstetrics for cardiology follow-up during pregnancy. Monthly follow-ups were started to rule out the appearance of cardiac decompensation. Special attention was paid to the appearance of congestive symptoms or signs: the patient only reported dyspnoea on moderate exertion. Serial analyses were performed, including NT-proBNP, which was normal, and TTE, which showed a non-dilated LV with normal LVEF, severe mitral (MR) and aortic insufficiency, with no evidence of pulmonary hypertension. The patient had presented proteinuria since early gestation. At around week 30, she started with arterial hypertension (AHT), with blood pressure around 140/72 mmHg, plateletopenia and incipient oedema.

Present illness
In week 34 she was referred to the obstetrics emergency department for high blood pressure of 168/84 mmHg: complementary tests showed proteinuria and plateletopenia, so it was decided to admit her for pulmonary maturation and observation on suspicion of possible pre-eclampsia versus alterations secondary to antiphospholipid syndrome.

Initially, vaginal delivery was attempted (because it was associated with less blood loss and less risk of infection and venous thromboembolism), but due to the risk of loss of foetal well-being, caesarean section was finally indicated. The patient had remained stable from a cardiological point of view during admission, but 12 hours after the caesarean section, cardiology was notified due to desaturation up to 77%. The patient only reported having started, while at rest, with a feeling of warmth and dizziness, without loss of consciousness, clear dyspnoea, orthopnoea or chest pain. Physical examination She was conscious and oriented, well perfused, blood pressure (BP) 160/90 mmHg, heart rate (HR) 75 bpm and oxygen saturation (SO2) 91-92% with oxygen therapy with nasal goggles (NG) at 2 l/min, eupneic at rest and tolerating decubitus. Cardiac auscultation: rhythmic with diastolic and systolic murmur. Pulmonary auscultation in the anterior plane: preserved vesicular murmur. Slight oedema with pretibial fovea similar to that of that morning.

COMPLEMENTARY TESTS
Laboratory tests: hypoxaemia with hypocapnia, with normal pH and lactic acid, mild renal failure with ions in range, NT-proBNP of 1466 ng/dl, and leukocytes with left deviation and CRP of 75 mg/l. Electrocardiogram (ECG): sinus rhythm at 80 bpm, with a normal PR and a narrow QRS without repolarisation alterations. Echocardioscopy: non-dilated and non-hypertrophic LV with preserved LVEF, without alterations in segmental contractility. Aortic root not dilated. Trivalve aortic valve, with thickened leaflets, especially at the level of the free edge, which generates a central coaptation deficit, resulting in severe AoI and mild stenosis. Mitral valve with diffusely thickened leaflets, with involvement of the subvalvular apparatus that restricts the movement of the posterior leaflet generating moderate-severe MR, directed towards the lateral wall of the left atrium and with a Coanda effect. Right ventricle normal in size and function. Tricuspid valve of normal appearance, without tricuspid insufficiency. No evidence of pulmonary hypertension. No pericardial effusion.

CLINICAL EVOLUTION
After a joint assessment with gynaecology and resuscitation, it was decided to transfer the patient for a computed tomography (CT) scan, which showed extensive bilateral alveolar consolidations and septal thickening affecting both lungs, suggestive of bilateral pneumonia. Mild bilateral pleural effusion. In addition, a small repletion defect was identified in a segmental branch of the left lower lobe, compatible with pulmonary thromboembolism, without overload of the right heart chambers. During the CT scan, the patient presented intense dyspnoea without desaturation, which improved with sitting and increased oxygen therapy. In view of the findings of the complementary tests, it was decided to admit her to resuscitation for treatment of the suspected bilateral pneumonia, in addition to diuretic treatment to force a negative water balance.
During her stay, she had a very good clinical evolution, with very abundant diuresis, resolution of dyspnoea, and improvement in SO2 that allowed her to de-escalate from oxygen therapy with high-flow glasses (HFG) to NG, and later withdrawal of the same, so that the picture was more likely to be one of acute heart failure (HF). The patient was discharged to the obstetrics ward after 48 hours in resuscitation, where she presented a good clinical evolution with resolution of the congestive semiology, and was finally discharged. Since her discharge, the patient has continued to undergo cardiological check-ups, initially more closely, which have been spaced out to be performed every three months. Her blood pressure remains practically normal, and the clinical signs of heart failure have completely resolved: she has no dyspnoea, orthopnoea or oedema, which has allowed complete suspension of the diuretic without the need to reintroduce it. The last echocardiogram showed severe aortic insufficiency with moderate-severe mitral insufficiency and preserved biventricular function. The decompensation that occurred during the puerperium was interpreted in the context of the haemodynamic changes that occur during pregnancy, so for the time being a wait-and-see attitude is maintained with close clinical and echocardiographic monitoring.

DIAGNOSIS
Preeclampsia (gestational hypertension + severity criteria - thrombopenia).
Acute pulmonary oedema, favoured by severe mitral and aortic insufficiency, with preserved LVEF.
Antiphospholipid syndrome (carrier of lupus anticoagulant and B2-glycoprotein, with thrombotic episodes).
