A 63-year-old female initially presented to our hospital with repeated retrosternal crushing pain. She reported a 5-year history of hypertension which was well controlled; she denied any history of diabetes, smoking, drinking of alcohol, allergies and familial genetic diseases. On admission, her ECG showed abnormal Q waves in leads III and avF (Figure 1). The laboratory examination showed: an elevated hypersensitive cardiac troponin I of 1.80 µg/L, total cholesterol of 5.66 mmol/L, low density lipoprotein of 3.54 mmol/L, hypersensitive C-reactive protein of 4.9 mg/L, and erythrocyte sedimentation rate of 32 mm/h. Coronary computed tomography angiography (CCTA) demonstrated occlusion in the proximal left anterior descending (LAD) artery with severe PCFS, moderate stenosis in the proximal left circumflex (LCX) artery with PCFS, and no lesion in the right coronary artery (RCA) (Figures 2(a)-(d)). The LAD was then treated with a drug-eluting stent, and her symptoms resolved. However, 2 months later, the patient was admitted to our hospital with a recurrence of retrosternal paina

gain. CCTA indicated LAD stent patency and normal RCA, and in the LCX, rapidly increased PCFS with progression of stenosis to subocclusion (Figure 2(e)). Subsequent intravascular ultrasound showed fatty dominant plaques in the LCX. The LCX was also then treated with a drug-eluting stent, and intravascular ultrasound indicated good stent placement (Figure 2(f)). Unfortunately, 4 months later, catheterization angiography showed that in the LAD there had been rapid progression to in-stent occlusion as well as severe restenosis in the LCX (Figure 2(g)), On several occasions, coronary artery bypass grafting was suggested to the patient, but she refused, and following this, the patient was admitted to hospital 9 times, once every 2 - 6 months, due to repeated and rapid in-stent restenosis or occlusion. Moreover, CCTA during her 4th hospital admission (14 months after the initial hospital admission) showed new and severe PCFS with severe stenosis in the proximal RCA (Figures 2(h)-(i)). The patient underwent re-implantation stent, balloon angioplasty including drug-coated balloon, and reinforcement drug treatment including PCSK9, but the outcomes were not good.

A 55-year-old female initially presented to our hospital with intermittent precordial crushing pain. She reported a 4-year history of hypertension which was well controlled; she denied any history of diabetes, hyperlipidemia, smoking, drinking alcohol, allergies and familial genetic diseases. On admission, ECG indicated ST segment depression and giant T wave inversion (Figure 3). The laboratory examination showed elevated creatine kinase of 220 IU/L, hypersensitive cardiac troponin I of 3.095 µg/L, CK-MB of 17.7 mg/L, hypersensitive C-reactive protein of 17.7 mg/L, and erythrocyte sedimentation rate of 27 mm/h. CCTA showed occlusion in the proximal LAD and LCX with severe PCFS, moderate stenosis in left main coronary artery (LMA) with PCFS, and mild stenosis in the mid RCA (Figures 4(a)-(c)). The LMA, LAD and LCX arteries were treated with drug-eluting stents, and her symptoms resolved. However, 3 months later, she was admitted to our hospital with precordial painagain, and subsequent catheterization angiography showed rapid progression to in-stent occlusion in the LMA, LAD and LCX (Figure 4(d)). Therefore, coronary artery bypass grafting was then performed for the LAD, diagonal branch and LCX. One year later, follow-up CCTA indicated all three grafts were intact, and there was new mild PCFS and stenosis in the proximal RCA (Figure 4(e)). Four years later, both CCTA and catheterization angiography during her 3rd hospital admission indicated all three grafts were still intact, while the PCFS in the RCA had significantly increased with the severe progression of the stenosis. The RCA was then treated with a drug-eluting stent (Figures 4(f)-(h)).