HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
78-year-old male with the following history:
Cardiovascular risk factors (CVRF): arterial hypertension (AHT), type 2 diabetes mellitus (DM2), dyslipidaemia.
Cardiological history: heart failure with preserved LVEF. Hypertensive heart disease under cardiology follow-up (last NT-proBNP 2127 pg/ml in the previous month).
Other history: biliary colic secondary to cholelithiasis.
Usual treatment: nebivolol 2.5 mg each day; eplerenone 25 mg each day; furosemide 40 mg each day; dapagliflozin/metformin 5/1000 mg each 12 hours; fenofibrate 160 mg each day; simvastatin 20 mg each day; amlodipine/valsartan/hydrochlorothiazide 10/160/12.5 mg each day; acetylsalicylic acid 100 mg each day; omeprazole 20 mg each day; gabapentin 300 mg every 8 hours; clorazepate 5 mg each day.

Present illness
A 78-year-old male presented to the emergency department with progressive dyspnoea in the last month until minimal effort (NYHA III/IV with previous NYHA I-II/IV), associated with oedematisation of the lower limbs (MMII), without orthopnoea, paroxysmal nocturnal dyspnoea or oliguria. In addition, he reported
episodes of self-limited chest pain during the last few months, related to exertion, for which he had previously consulted the emergency department, with no electrocardiographic changes or mobilisation of markers of myocardial damage.

Physical examination
On arrival at the hospital, the patient was in fair general condition, tachypnoea, blood pressure (BP) 190/99 mmHg, heart rate (HR) 80 bpm and SpO2 88%, so supplementary O2, diuretics, intravenous nitroglycerin and bronchodilators were started, obtaining the following constants: BP 170/85 mmHg; HR 70 bpm; SatO2 94% (FiO2 0.26).
Cardiac auscultation: regular heart sounds, no audible murmurs.
Pulmonary auscultation: bilateral midbasal crackles and hypophonesis in the right base.
Tibiomalleolar oedema in MMII.

COMPLEMENTARY TESTS
Tests performed in the emergency department:
Electrocardiogram (ECG): sinus rhythm at 63 bpm. PR 200 ms, 0o axis, narrow QRS, ST segment sub-rectification in V4-V6, II and aVF.
Chest X-ray: increased cardiothoracic index. Bilateral cottony infiltrates. Right pleural effusion. No condensation was seen.

Laboratory tests:
Blood count: haemoglobin 11 g/dl. Haematocrit 32.5%. MCV 86.4 fl. Leukocytes, leukocyte formula and platelets without alterations.
Coagulation: no alterations.
Biochemistry: glucose 145 mg/dl, urea 77 mg/dl, creatinine 1.89 mg/dl. Ions in range, liver function without alterations. Calcium 8.9 mg/dl. Protein 6.7 g/dl. CRP 1.1 mg/dl.
Biomarkers of myocardial damage: hsTnI 22 ng/l --> 30 ng/l.
Tests performed during admission:
Heart failure markers: NT-proBNP maximum 3258.0 pg/ml. CA 125 17 IU/ml.
Echocardiography: left ventricle with moderate concentric hypertrophy of septal predominance, with normal diameters, increased volumes and preserved global systolic function. Normal aortic root and valve. Pseudonormal transmitral filling, with data suggestive of increased end-diastolic pressures (grade II diastolic dysfunction). Normal right ventricle. Inferior vena cava plethora. Mild tricuspid insufficiency that allows estimation of pulmonary artery systolic pressure at 50 mmHg (moderate pulmonary hypertension).
Examination in sinus rhythm.
Coronary angiography via the left radial artery: mild-moderate stenosis in the proximomedial LAD and proximal segment of the 1st diagonal. It was decided to perform a functional assessment of both lesions with a pressure guide, obtaining negative results both at rest (iFR) and with i.v. regadenoson (FFR). Given chest pain and HF with preserved LVEF, an acetylcholine test was performed. After the second dose (20 mcg), electrocardiographic changes were observed (ST segment elevation and mild negativisation of T waves in V1-V3 and III), diffuse vasospasm of the entire left coronary tree, associated with central thoracic oppression. Signs and symptoms resolved with intracoronary nitroglycerin.

Conclusion: functionally non-significant moderate stenosis in LAD and diagonal. Positive epicardial acetylcholine test.

CLINICAL EVOLUTION
During his stay in the cardiology ward, depletive treatment was administered and, given the results of the coronary angiography, beta-blocker treatment (nebivolol) was suspended and a non-dihydropyridine calcium antagonist (diltiazem) was added. The patient showed clinical and haemodynamic improvement, with resolution of peripheral oedema and dyspnoea, tolerating ambulation without new episodes of chest pain or other complications. Following improvement in renal function, discharge home was decided.
During outpatient follow-up, the patient remained asymptomatic without dyspnoea or chest pain, with NYHA functional class I.

DIAGNOSIS
Acute hypertensive pulmonary oedema in a patient with heart failure and preserved systolic function.
Endothelial dysfunction with epicardial coronary vasospasm.
Grade II diastolic dysfunction.
