Background
Cardiovascular risk factors (CVRF): arterial hypertension (HT) with target organ damage, type 2 diabetes mellitus (DM) with macro and microvascular involvement, LBP, active smoker (estimated IPA: 135).
Stage II chronic kidney disease of probably mixed aetiology (hypertensive and diabetic), with estimated glomerular filtration rate around 60 ml/min and proteinuria in non-nephrotic range (1.1 g/24 hours).
Chronic ischaemic heart disease with severe three-vessel disease surgically revascularised in 2016 (AMI-DA and VSI-OM grafts, the latter chronically occluded), with mild LV systolic dysfunction.
Paroxysmal atrial fibrillation (AF) anticoagulated with acenocoumarol.
Ischaemic stroke in the right posterior cerebral artery (PCA) territory of probable cardioembolic aetiology.
Moderate sleep apnoea-hypopnoea syndrome (SAHS).
Chronic grade IIA ischaemia in the right lower limb.


Home treatment:
Atorvastatin 80 mg 0-0-1, acetylsalicylic acid (ASA) 100 mg 0-1-0, bisoprolol 5 mg 1-0-1, acenocoumarol according to INR controls, ivabradine 5 mg 1-0-1, amlodipine 5 mg 1-0-0, candesartan 4 mg 1-0-1, spironolactone 25 mg 1-0-0, metformin 850 mg 1-0-0, furosemide 40 mg 2-0.5-0, omeprazole 20 mg 1-0-0.

Present illness
The patient is a 60-year-old man with the aforementioned history, including multiple CVRF and established vascular disease, with chronic ischaemic heart disease, surgically revascularised and with mild residual LV systolic dysfunction, who is admitted to the neurology department for ischaemic stroke of atherothrombotic aetiology in the left middle cerebral artery (MCA), with mechanical thrombectomy and destent implantation at the level of the left carotid artery. During admission, the patient presented an episode of decompensation of heart failure and was transferred to the cardiology department for monitoring, study and intensive diuretic treatment.

Physical examination
On assessment by cardiology:
General condition is fair. Conscious, oriented in all 3 spheres and cooperative. Normal colour, normohydrated and normoperfused. Afebrile to the touch. Tachypneic at rest, with intolerance to decubitus.
Blood pressure (BP): 160/70 mm Hg. Heart rate (HR): 73 bpm. SpO2: 91% with low-flow oxygen therapy (nasal cannulas).
Cardiac auscultation: rhythmic heart sounds. No murmurs, extratonos or pericardial friction rub.
Pulmonary auscultation: generalised hypoventilation in both lung fields. Lower extremities: pedial pulses present and symmetrical. Edema with bilateral fovea up to the knees.

COMPLEMENTARY TESTS
Electrocardiogram (ECG) on admission: sinus rhythm, PR 160 ms, narrow QRS, without repolarisation alterations suggestive of acute ischaemia.
Chest X-ray: AP projection. Bilateral pleural effusion (minimal left, more evident on the right). Congestive hilarity and vascular redistribution.

Laboratory tests on admission:
Biochemistry: glucose 186 mg/dl, creatinine 0.98 mg/dl, sodium 140 mEq/l, total protein 7.5 g/dl, potassium 4.59 mEq/l, albumin 4.0 g/dl, chlorine 102 mEq/l, ALT (GPT) 21 U/l, AST (GOT) 25 U/l, gamma-GT 34 U/l, alkaline phosphatase 125 U/l, LDH 384 U/l, bilirubin 0.8 mg/dl, C-reactive protein 3.02 mg/dl.
Haemogram: red cells 4.56 xmill/μl, haemoglobin 14.9 g/dl, haematocrit 45.6%, MCH 32.8 pg, MCV 100.2 fl, MCHC 32.7 g/dl, RDW 14.5%, platelets 277 x1000/μl, MPV 8.8 fl, leucocytes 8.4 x1000/μl, neutrophils 6.8 x1000/μl, neutrophils % 81.2%, lymphocytes 0.8 x1000/μl, lymphocytes % 9.9%, monocytes 0.7 x1000/μl, monocytes % 7.9%, eosinophils 0.0 x1000/μl, eosinophils % 0.5%, basophils 0.0 x1000/μl, basophils % 0.5%.
Coagulation: prothrombin time 16.3 sec, prothrombin activity 61%, INR (lab) 1.41, TTPa 36 sec, fibrinogen (derivative) 597 mg/dl. NT-proBNP: 10053 pg/ml.
Blood tests with cardiovascular risk factors: Hb glycated (DCCT) 7.2 (%Hbtotal) %, TSH 4.49 μlU/ml, free T4 1.17 ng/dl, cholesterol 108 mg/dl, triglycerides 102 mg/dl, LDL (Friedewald estimation) 67 mg/dl, HDL 21 mg/dl.
Blood tests at discharge: glucose 153 mg/dl, creatinine 1.69 mg/dl, sodium 134 mEq/l, potassium 5.1mEq/l, chlorine 98 mEq/l, calcium 9.2 mg/dl, NT-proBNP 2640 pg/ml.
Transthoracic echocardiogram: left ventricle not dilated, with normal wall thickness. Moderately depressed systolic function with alterations in segmental contractility. Non-dilated right ventricle with normal systolic function. Slightly dilated left atrium. Moderate-severe pulmonary hypertension.
Coronary angiography: severe lesion in the proximal segment of the anterior descending artery (ADA), which is revascularised with drug-eluting stent. Mammary anastomosis permeable and without lesions. Non-dominant circumflex, giving a first OM occluded from the origin, with distal filling by homocoronary circulation. Saphenous graft and right coronary artery not probed as they were previously occluded.

CLINICAL EVOLUTION
The patient had a good clinical and analytical evolution (initial NT-proBNP of 10053 pg/ml and final of 2640 pg/ml) after starting combined diuretic treatment (furosemide, chlorthalidone and 3-day cycle of acetazolamide given the tendency to metabolic alkalosis). A transthoracic echocardiogram was performed which showed deterioration of ventricular function compared to the previous study; in addition, the patient reported episodes of typical chest pain both at home and during admission, so coronary angiography was performed, revealing severe stenosis in the proximal segment of the LAD, which was revascularised by implanting a drug-eluting stent. She was maintained on triple antithrombotic therapy with ASA, clopidogrel and dabigatran 110 mg during hospitalisation, and ASA was withdrawn on discharge. Given the analytical finding of poor chronic metabolic control of his type 2 DM (Hb glycaemia 7.2%), it was decided to introduce an iSGLT2 (empagliflozin) for secondary prevention of cardiovascular events despite acute renal failure of probably mixed origin (pre-renal and contrast nephropathy), with a glomerular filtration rate (GFR) at discharge calculated according to the CKD-EPI formula of 43 ml/min/m .

DIAGNOSIS
Congestive heart failure in anasarca. Moderate left ventricular dysfunction.
Type 2 diabetes mellitus with poor chronic metabolic control (HbA1c 7.2%) and macro and microvascular involvement.
Three-vessel coronary artery disease: severe stenosis of the proximal anterior descending artery, revascularised percutaneously by means of a drug-eluting dsetent implant.
Ischaemic stroke secondary to left carotid artery occlusion, revascularised by stent. Initial NIHSS of 9. NIHSS at discharge of 2.
