HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
We are dealing with a 70-year-old patient with no known drug allergies or toxic habits; no known diabetes mellitus but hypertensive and dyslipidaemic.
He has a family history of ischaemic heart disease.
The patient's cardiological history began in July 2012, when Holter monitoring was requested after presenting symptomatic bradycardia that required chronotropic drugs during arthroscopy. The 24-hour recording showed spells of atrial fibrillation with MVF 100 bpm (max 150) alternating with the patient's baseline rhythm which was sinus bradycardia (45 bpm).
An echocardiographic study was completed, with no abnormalities. In November 2012, a bicameral pacemaker was implanted via the subclavian artery and anticoagulation with acenocoumarol was started. Due to persistent atrial fibrillation with poor clinical control, electrical cardioversion was performed and she was discharged with amiodarone 200 mg/24 h and bisoprolol 2.5 mg/24 h, in addition to anticoagulation.
In January 2014, he was referred to the outpatient cardiology department for dyspnoea and chest tightness related to exertion of 2 months' duration. An echocardiogram was performed showing LV with moderately depressed EF. Depletive treatment was started (furosemide and eplerenone) and an analytical study and coronary angiography were requested.
Coronary angiography showed stenosis of the proximal anterior descending artery (DAp) 80%, circumflex at the level of the exit of the first obtuse marginal (Cx- OM1) 100% and proximal right coronary (CDp) 90%, and middle (CDm) 60%, opting for surgical revascularisation. The intervention was performed in September 2014, with triple coronary puncture to the middle LAD with internal mammary artery (IMA) and sequence with saphenous vein (SVF) to 1st OM and posterolateral branches. Postoperative evolution was torpid with multiple admissions for dyspnoea and cardiac decompensation. SPECT was performed and showed mild lateral ischaemia, so a new coronary angiography was requested, showing patency of all bypasses performed. The MCP was reviewed, revealing MCP dysfunction, which was corrected by modifying the programming. Since then, asymptomatic in functional class II. Treatment with amiodarone was withdrawn and replaced with dronedarone due to hypothyroidism.
He repeatedly consulted for muscle pain related to statins (simvastatin 10 mg and atorvastatin 10 mg), for which he was referred to the Lipidology unit of reference, despite which the myalgias always recurred with the reintroduction of statins. Finally, given the high cardiovascular risk, intolerance to lipid-lowering drugs and severe dyslipidaemia, treatment with IPCSK9 was started with good tolerance and LDL levels were reduced to 88 mg/dl from an initial level of 218 mg/dl.

COMPLEMENTARY TESTS
Blood tests 12-07-16 (patient's baseline): creatinine 0.98 mg/dl, urea 38.8 mg/dl, total cholesterol 289 mg/dl, HDL 44 mg/dl, LDL 218 mg/dl, TG 240 mg/dl, AST 22U/l, ALT 23 U/l, GGT 52 U/l, FA 72 U/l, sodium 143 mEq/l, potassium 4.3 mEq/l, TSH 2.27 IUI/ml, T4L 1.14 ng/dl. Hb 16.4 g/dl, Ht 50.5%, leukocytes 7.11 x 10^9/L, platelets 164x10^9/L.
Blood tests 15-11-16 (after 3 months with IPCSK9): creatinine 0.93mg/dl, urea 49.6 mg/dl, total cholesterol 201.6 mg/dl, HDL 44 mg/dl, LDL 109.6mg/dl, AST 26U/l, ALT 24 U/l, GGT 56 U/l, FA 77 U/l, sodium 143 mEq/l, potassium 4.5 mEq/l, TSH 2.47 IUI/ml, T4L 1.3 ng/dl. Hb 17 g/dl, Hto 52.6%, leukocytes 6.24 x 10^9/l, platelets 172x10^9/l.
After this analytical result, he decided to increase the dose of IPCSK9 from 75 mg to 150 mg fortnightly.
Blood tests 06-04-17 (control 6 months after starting treatment): creatinine 0.76 mg/dl, urea 53.6 mg/dl, total cholesterol 162 mg/dl, HDL 45 mg/dl, LDL 88.40 mg/dl, TG 143 mg/dl, AST 24U/l, ALT 25 U/l, GGT 44 U/l, FA 77 U/l, sodium 143 mEq/l, potassium 5.1 mEq/l, TSH 2.59 IUI/ml, T4L 1.28 ng/dl. Hb 17.3 g/dl, Ht 53.5%, leukocytes 6.11x 10^9/L, platelets 142x10^9/L.

EVOLUTION
The patient is currently in stable class of his cardiopathy. With functional class II, asymptomatic for chest pain and tolerating medication without incident.
The last echocardiogram showed recovery of the ejection fraction, which was classified as preserved in the last echocardiogram.
Due to back pain that had been present for months, an abdominal CT scan was performed, which revealed an abdominal aortic aneurysm, pending surgery for the placement of an endoprosthesis.
This is therefore a patient at very high cardiovascular risk due to ischaemic heart disease, aortic vascular disease and dyslipidaemia in whom treatment with statins was not possible due to intolerance, in whom the introduction of IPCSK9 has managed to reduce his LDL-c levels by more than 50%, and he is increasingly close to reaching the desired level for his high cardiovascular risk, which is less than 70 mg/dL.

DIAGNOSIS
Chronic ischaemic heart disease with 3-vessel disease.
History of triple aorto-coronary bypass with IMA to LAD and SFN sequence to MO1 and PD.
Transient left ventricular dysfunction (currently normal LVEF).
Abdominal aortic aneurysm pending endovascular repair.
Stable heart failure in functional class II.
Sinus dysfunction with paroxysmal AF. Carrier of normofunctioning DDD MCP at the present time.
Severe dyslipidaemia. Intolerance to statins. Treatment with IPCSK9 with good evolution.
