Abstract
An increasing number of studies have reported intimal atherosclerotic changes, or neoatherosclerosis in the late phase after bare metal stent implantation, however, only a few reports have showed the presence of severe intimal calcification in a bare metal stent. We herein report a case of a 68-year-old male with severely calcified neointima occurring 9 years after the bare metal stent implantation. Pre-procedural coronary computed tomography angiography and peri-procedural intravascular ultrasound demonstrated severe calcification within the in-stent restenotic lesion. Although the pre-dilation balloon ruptured due to the calcification, the lesion was nevertheless successfully dilated with the stent. Calcified lesions often require complex techniques, and we therefore should be aware of the potential occurrence of a severely calcified neointima in coronary stents, and performing coronary computed tomography angiography in advance is a great help for performing effective coronary intervention.
1
Introduction
Coronary stents play an important role in the treatment of coronary artery disease, and a large number of stents are implanted in diseased coronary arteries all over the world. The tri-phasic luminal response after coronary stent implantation has been reported , including; the early restenotic phase (until 6 months), the intermediate-term regression phase (from 6 months to 3 years), and the late re-narrowing phase, while several factors are also considered to influence the response . Although long-term angiographic follow-up studies are limited, recent case reports have demonstrated vulnerable or ruptured plaque in a bare metal stent implanted for more than 5 years . Moreover, a few cases of severely calcified intima within a bare metal stent have also been reported , however, the pathophysiology of neointimal atherosclerotic changes, or neoatherosclerosis in bare metal stents has not yet been fully elucidated . We herein report a case of severely calcified restenosis in a bare metal stent implanted 9 years previously, and such calcification was demonstrated by computed tomography and intravascular ultrasound (IVUS).
2
Case
A 68-year-old man with dyslipidemia was referred to our hospital for transient inverted T waves in V 4–6 leads. He had been implanted 2 bare-metal stents in the proximal segments of the left anterior descending artery (LAD) for acute coronary syndrome 9 years previously ( Fig. 1 A , B). He had taken aspirin 100 mg, ticlopidine 200 mg, enalapril 7.5 mg, bisoprolol 5 mg, isosorbide dinitrate 40 mg and pravastatin 10 mg for his daily dose without experiencing any heart attacks. The ticlopidine had been discontinued after follow-up angiography 6 months after the placement, which had shown insignificant narrowing in the stents ( Fig. 1 C). On this visit, his non-high-density lipoprotein cholesterol level and low-density lipoprotein cholesterol level were 157 and 104 mg/dl, respectively, and the hemoglobin A1c level was 5.3%. Coronary computed tomography scans demonstrated in-stent restenosis with a high intensity focal site of 143 Hounsfield unit, which thus indicated neointimal calcification ( Fig. 2 ) . Left coronary angiography demonstrated a subtotal occlusion in the proximal portion of the stent in the LAD ( Fig. 3 A ). Intravascular ultrasound (IVUS) study after the dilation with a 1.5 mm balloon showed severe calcium deposition with acoustic shadow inside the stents ( Fig. 3 B, C). Additional dilation with a 3.0 mm non-compliant balloon resulted in balloon rupture due to the severe calcification, and then 2 sirolimus-eluting stents (Cypher stent, Cordis, Miami, Florida) were deployed with an overlap. Subsequently, the lesion was successfully dilated ( Fig. 3 D) and the IVUS finding showed good stent expansion in the calcified lesions ( Fig. 3 E, F).
2
Case
A 68-year-old man with dyslipidemia was referred to our hospital for transient inverted T waves in V 4–6 leads. He had been implanted 2 bare-metal stents in the proximal segments of the left anterior descending artery (LAD) for acute coronary syndrome 9 years previously ( Fig. 1 A , B). He had taken aspirin 100 mg, ticlopidine 200 mg, enalapril 7.5 mg, bisoprolol 5 mg, isosorbide dinitrate 40 mg and pravastatin 10 mg for his daily dose without experiencing any heart attacks. The ticlopidine had been discontinued after follow-up angiography 6 months after the placement, which had shown insignificant narrowing in the stents ( Fig. 1 C). On this visit, his non-high-density lipoprotein cholesterol level and low-density lipoprotein cholesterol level were 157 and 104 mg/dl, respectively, and the hemoglobin A1c level was 5.3%. Coronary computed tomography scans demonstrated in-stent restenosis with a high intensity focal site of 143 Hounsfield unit, which thus indicated neointimal calcification ( Fig. 2 ) . Left coronary angiography demonstrated a subtotal occlusion in the proximal portion of the stent in the LAD ( Fig. 3 A ). Intravascular ultrasound (IVUS) study after the dilation with a 1.5 mm balloon showed severe calcium deposition with acoustic shadow inside the stents ( Fig. 3 B, C). Additional dilation with a 3.0 mm non-compliant balloon resulted in balloon rupture due to the severe calcification, and then 2 sirolimus-eluting stents (Cypher stent, Cordis, Miami, Florida) were deployed with an overlap. Subsequently, the lesion was successfully dilated ( Fig. 3 D) and the IVUS finding showed good stent expansion in the calcified lesions ( Fig. 3 E, F).
