Statins, Targets and Chronic Kidney Disease

Abstract

Submit Manuscript | http://medcraveonline.com A 66 year-old man, with hypertension, non-insulin dependent diabetes mellitus, a prior myocardial infarction (MI) in 1990, and family history for hypertension and nephropathy, was admitted to hospital with non-ST elevation MI (NSTEMI). He had been on hemodialysis (once-a-week) for 3 weeks due to end-stage membranous glomerulonephritis previously treated with Rituximab. Therapy at admission included ASA, bisoprolol, amlodipine, doxazosin, oral antidiabetics and medications for kidney failure. Ejection fraction (EF) was 50%. Coronary angiography showed a severe and diffuse calcific three-vessel disease (Figure 1), with eccentric critical stenosis of mid-distal left main (LM), proximal circumflex (Cx), proximal and mid left anterior descending (LAD), with involvement of the first diagonal branch (D1), which was occluded at its mid portion. The distal LAD was calcific and diffusely diseased, peri-apically occluded (thus preventing an effective surgical revascularization) and refilled by ipsilateral collaterals. The obtuse marginal branch was diffusely and severely diseased; a secondary marginal branch was occluded. The right coronary artery was hypoplasic and occluded at its proximal segment, refilled by weak contralateral collaterals. The culprit lesion was located on the dominant proximal Cx, and it was treated by a 3.5/18 mm drug-eluting stent (DES) implantation in the same session. After 3 days revascularization was completed with IVUS-guided percutaneous coronary intervention (PCI) on LM (4/28 mm DES) and LAD (3.5/38 mm DES), with kissing balloons at the LAD-D1 and the LM-LAD-Cx bifurcations. Blood tests showed that LDL-Cholesterol (LDL-C) was 125 mg/dL on admission; Troponin I peak reached 0.54 ng/ mL. Therapy during hospitalization and at discharge included bisoprolol, ASA, ticagrelor bid and rosuvastatin 5 mg daily. The patient remained asymptomatic. Elective angiographic follow-up performed after 7 months showed patency of all implanted DES (Figure 2); the value of LDL-C 102 was mg/dL and rosuvastatin 5 mg was changed into atorvastatin 20 mg daily. Three months later the patient was switched to hemodialysis twice-a-week. After a few days, he was re-admitted to our department due to NSTEMI + atrial fibrillation (AF). Coronary angiography showed patency of all stents, but progression of disease at the mid portion of the Cx, which was treated by implantation of two DES (Figure 3). Despite LDL-C value was 43.4 mg/dL, atorvastatin 20 mg was replaced by rosuvastatin 10 mg. One month later the patients was admitted again due to angina during paroxysmal AF; Troponin I was slightly elevated (2.01 ng/mL); LDL-C was 35.4 mg/dL. The patient experienced a severe exfoliative dermatitis as a possible late reaction to contrast mean or to a non definite drug; no coronary angiography was performed. Rosuvastatin 10 mg was confirmed. A new hospitalization occurred after three months due to pulmonary edema related to fluids overload. The patient was switched to hemodialysis three times a week with benefit. The value of LDL-C was 40.8 mg/dL, nevertheless rosuvastatin 10 mg was changed with atorvastatin 20 mg. No further event occurred, and after 8 months from the last hospitalization, the patient is asymptomatic for angina and dyspnea and in good clinical status. The last value of LDL-C is 38 mg/dL and he has maintained the same therapy, including atorvastatin 20 mg daily.