Chronic stent recoil in severely calcified coronary artery lesions. A serial optical coherence tomography study.

Chronic second-generation drug-eluting stent recoil in severely calcified coronary lesions has not been studied. We aimed to evaluate chronic stent recoil by optical coherence tomography (OCT) in severely calcified lesions treated with thin strut stents after rotational atherectomy. In 28 lesions (26 patients with 23% on hemodialysis) treated with everolimus-eluting stents after rotational atherectomy, baseline and 8-month follow-up OCT were compared. Stent recoil was defined as >10% decrease in stent area from baseline to follow-up. Overall, there was no change in minimal stent area (6.0 mm2 [5.0, 8.1] to 6.0 mm2 [4.8, 8.6], p = 0.51) from baseline to follow-up, although neointimal hyperplasia measured 16.3 ± 15.8%. Thirty-six percent of lesions showed stent recoil associated with 6 non-nodular calcifications, 1 calcified nodule, and 3 stent deformations. The overall mean calcium angle with attenuation decreased (54° [29-76] to 31° [19-48], p < 0.0001), and calcium without attenuation increased (28° [21-67] to 64° [34-93], p < 0.0001), but primarily at the location of stent recoil. Furthermore, in the stent recoil segments in 10 recoil lesions, the stent circumference decreased primarily at non-calcium segments rather than at calcium with or without attenuation. One lesion with stent recoil and 2 lesions without stent recoil required repeat revascularization. Thin strut stents can chronically recoil in severely calcified lesions, but this rarely causes restenosis.

Effect of cutting balloon after rotational atherectomy in severely calcified coronary artery lesions as assessed by optical coherence tomography.

OBJECTIVES: Using optical coherence tomography (OCT), we evaluated the effect of a cutting balloon (CB) compared with a conventional balloon after rotational atherectomy (RA) and before stenting in severely calcified coronary lesions. BACKGROUND: A CB is designed to create discrete incisions to facilitate fracture of severely calcified plaque. METHODS: OCT was performed preintervention (if possible), post-RA, and poststent implantation. RA modification of calcium was defined as a polished, concave, round-shaped surface. Calcium fracture was defined as a break in the calcium plate. The effects of calcium modification and stent expansion between CB (n = 18) versus conventional balloon (n = 23) following RA were compared. RESULTS: Median patient age was 72 years with 24% on hemodialysis. The amount of calcium and the length of RA modification were comparable between the CB and conventional balloon groups. Final poststent OCT showed that the number and thickness of calcium fracture were greater after CB versus conventional balloon, resulting better stent expansion (78.9% [IQR: 72.4-88.1] vs. 66.7% [IQR: 55.0-76.7], p < 0.01). In the multivariable model, after adjusting for the amount of calcium, CB use was an independent predictor of the presence of calcium fracture (odds ratio 30.0; 95% confidence interval 2.7-994.1, p = 0.004) and an independent predictor for greater stent expansion (regression coefficient 7.4; 95% confidence interval 0.5-14.3, p = 0.04). CONCLUSION: In severely calcified lesions calcium fracture was more often associated with RA followed by CB compared with RA followed by conventional balloon predilation before stenting. CB use was also a determinant of greater stent expansion.

Association of Epicardial Adipose Tissue Volume and Total Coronary Plaque Burden in Patients with Coronary Artery Disease.

The relationship between epicardial adipose tissue volume (EATV) and plaque vulnerability in non-culprit coronary lesions is not clearly understood.Fifty-four consecutive patients/158 lesions with suspected coronary artery disease underwent computed tomography (CT) and 40 MHz intravascular ultrasound imaging (iMap-IVUS) in cardiac catheterization. Cross-sectional CT slices were semiautomatically traced from base to apex of the heart. Using a 3D workstation, EATV was measured as the sum of fat areas (-190 to -30 Hounsfield units [HU]). All coronary vessels were imaged using iMap-IVUS before stenting to analyze coronary plaques as fibrotic, lipidic, necrotic, or calcified tissue.Mean EATV was 73.7 ± 24.6 (range: 30.2 to 131.8) mL. Patients were divided into two groups by mean EATV (group H: n = 27, EATV ≥ 73.7 mL; group L: n = 27, EATV < 73.7 mL). Total luminal volume, total vessel volume, and total plaque volume were significantly larger in group H. Fibrotic plaque and lipidic plaque volumes were also significantly larger in group H. There was a significant negative correlation between EATV and fibrous tissue (r = -0.31, P = 0.02) and a significant positive correlation between EATV and necrotic tissue (r = 0.37, P = 0.007). EATV was related to plaque with vulnerability in the right coronary artery (RCA) (r = 0.57, P = 0.04) and the left anterior descending artery (LAD) (r = 0.53, P = 0.02). In conclusion, increased EATV was associated with the total coronary plaque burden and composition, particularly in the RCA and LAD.

Serial 3-Vessel Optical Coherence Tomography and Intravascular Ultrasound Analysis of Changing Morphologies Associated With Lesion Progression in Patients With Stable Angina Pectoris.

BACKGROUND: Optical coherence tomographic (OCT) morphologies associated with lesion progression are not well studied. The aim of this study was to determine the morphological change for untreated lesion progression using both OCT and intravascular ultrasound (IVUS). METHODS AND RESULTS: We used baseline and 8-month follow-up 3-vessel OCT and IVUS to assess 127 nonculprit lesions (IVUS plaque burden ≥40%) in 45 patients with stable angina after target lesion treatment. Lesion progression was defined as an IVUS lumen area decrease >0.5 mm2. A layered pattern was identified as a superficial layer that had a different optical intensity and a clear demarcation from underlying plaque. Lesion progression was observed in 19% (24/127) lesions, and its pattern was characterized into 3 types: type I, new superficial layered pattern at follow-up that was not present at baseline (n=9); type II, a layered pattern at baseline whose layer thickness increased at follow-up (n=7); or type III, no layered pattern at baseline or follow-up (n=8). The increase of IVUS plaque+media area was largest in type I and least in type III (1.9 mm2 [1.6-2.1], 1.1 mm2 [0.9-1.4], and 0.3 mm2 [-0.2 to 0.8], respectively; P=0.002). Type III, but not types I or II, showed negative remodeling during follow-up (IVUS vessel area; from 14.3 mm2 [11.4-17.2] to 13.5 mm2 [10.4-16.7]; P=0.02). OCT lipidic plaque was associated with lesion progression (odds ratio, 13.6; 95% confidence interval, 3.7-50.6; P<0.001). CONCLUSIONS: Lesion progression was categorized to distinct OCT morphologies that were related to changes in plaque mass or vessel remodeling.

Association between increased epicardial adipose tissue volume and coronary plaque composition.

To assess the relationship between epicardial adipose tissue volume (EATV) and plaque vulnerability in significant coronary stenosis using a 40-MHz intravascular ultrasound (IVUS) imaging system (iMap-IVUS), we analyzed 130 consecutive patients with coronary stenosis who underwent dual-source computed tomography (CT) and cardiac catheterization. Culprit lesions were imaged by iMap-IVUS before stenting. The iMAP-IVUS system classified coronary plaque components as fibrous, lipid, necrotic, or calcified tissue, based on the radiofrequency spectrum. Epicardial adipose tissue was measured as the tissue ranging from -190 to -30 Hounsfield units. EATV, calculated as the sum of the fat areas on short-axis images, was 85.0 ± 34.0 cm(3). There was a positive correlation between EATV and the percentage of necrotic plaque tissue (R (2) = 0.34, P < 0.01), while there was a negative correlation between EATV and the percentage of fibrous tissue (R (2) = 0.24, P < 0.01). Multivariate analysis revealed that an increased low-density lipoprotein cholesterol level (ß = 0.15, P = 0.03) and EATV (ß = 0.14, P = 0.02) were independently associated with the percentage of necrotic plaque tissue. An increase in EATV was associated with the development of coronary atherosclerosis and, potentially, with the most dangerous type of plaque.

Repeat drug-eluting stent implantation for in-stent restenosis: first- or second-generation stent.

OBJECTIVE: To investigate the efficacy and safety of a second-generation drug-eluting stent (DES) for in-stent restenosis (ISR) after first-generation DES implantation. BACKGROUND: The everolimus-eluting stent is a second-generation DES that is very effective for de novo coronary lesions. METHODS: The subjects were 145 consecutive patients who underwent re-stenting, including 93 given a first-generation DES and 52 given a second-generation DES. The two groups were followed up for 37.8 ± 16.7 months and 13.8 ± 2.1 months, respectively. The primary endpoint was in-stent late luminal loss at 8-month angiographic follow-up. RESULTS: Baseline clinical and angiographic parameters were similar in the 2 groups. Follow-up angiography showed that late luminal loss (0.26 ± 0.31 mm vs 0.58 ± 0.67 mm; P=.01), the binary restenosis rate (2.6% vs 16.7%; P=.03), and the target lesion revascularization (TLR) rate (1.9% vs 11.8%; log-rank = 0.04) were smaller in the second-generation group than in the first-generation group. There was no definite stent thrombosis in either group. During follow-up, there were no significant between-group differences of major adverse cardiac events without TLR, myocardial infarction, death, and death + myocardial infarction. Multivariate analysis demonstrated that using a first-generation DES was the only independent predictor of TLR after 1 year (odds ratio, 2.78; 95% confidence interval, 1.22-5.43; P=.03). CONCLUSION: When ISR occurs after DES implantation, treatment with a second-generation DES reduces late luminal loss, binary restenosis, and TLR after 1 year compared with a first-generation DES.