Effect of orbital atherectomy in calcified coronary artery lesions as assessed by optical coherence tomography.

OBJECTIVES: We sought to assess plaque modification and stent expansion following orbital atherectomy (OA) for calcified lesions using optical coherence tomography (OCT). BACKGROUND: The efficacy of OA for treating calcified lesions is not well studied, especially using intravascular imaging in vivo. METHODS: OCT was performed preprocedure, post-OA, and post-stent (n = 58). Calcium modification after OA was defined as a round, concave, polished calcium surface. Calcium fracture was complete discontinuity of calcium. RESULTS: Comparing pre- vs post-OA OCT (n = 29), calcium area was significantly decreased post-OA (from 3.4 mm2 [2.4-4.7] to 2.9 mm2 [1.9-3.9], P < 0.001). Poststent percent calcium fracture (calcium fracture length/calcium length) correlated with post-OA percent calcium modification (calcium modification length/calcium length) (r = 0.31, P = 0.01). Among 75 calcium fractures in 35 lesions, maximum calcium thickness at the fracture site was greater with vs without calcium modification (0.58 mm [0.50-0.66] vs 0.45 mm [0.38-0.52], P = 0.003). Final optimal stent expansion, defined as minimum stent area ≥6.1 mm2 or stent expansion ≥90% (medians of this cohort) at the maximum calcium angle site, was observed in 41 lesions. Larger post-OA lumen area (odds ratio 2.64; 95% CI 1.21-5.76; P = 0.02) and the presence of calcium fracture (odds ratio 6.77; 95% CI 1.25-36.6; P = 0.03) were independent predictors for optimal stent expansion. CONCLUSIONS: Calcium modification by OA facilitates poststent calcium fracture even in thick calcium. Greater calcium modification correlated with greater calcium fracture, in turn resulting in better stent expansion.

Noncalcified coronary atherosclerotic plaque and immune activation in HIV-infected women.

BACKGROUND: Little is known about coronary plaque in human immunodeficiency virus (HIV)-infected women. METHODS: Sixty HIV-infected and 30 non-HIV-infected women without symptoms or history of cardiovascular disease were recruited to assess coronary plaque with coronary computed tomographic angiography and immune activation. Data from 102 HIV-infected men and 41 non-HIV-infected male controls were compared. RESULTS: HIV-infected women demonstrated significantly higher percentages of segments with noncalcified plaque (mean ± SD, 74% ± 28% vs 23% ± 39% compared to female control subjects; median [interquartile range], 75% [63%-100%] vs 0% [0%-56%]; P = .007) and more segments with noncalcified plaque (mean ± SD, 0.92 ± 1.48 vs 0.40 ± 1.44; median [interquartile range], 0 [0-2] vs 0 [0-0]; P = .04). Immune activation parameters, including soluble CD163 (sCD163; P = .006), CXCL10 (P = .002), and percentages of CD14(+)CD16(+) monocytes (P = .008), were higher in HIV-infected women than in female control subjects, but no differences were seen in general inflammatory markers. Among HIV-infected women with noncalcified coronary plaque, sCD163 levels were significantly higher than in HIV-infected women without noncalcified plaque (P = .04). In multivariate modeling for sCD163 levels among male and female subjects, significant effects of HIV (P < .0001), age (P = .002), and sex (P = .0002) were seen. CONCLUSIONS: Young, asymptomatic, HIV-infected women, demonstrate increased noncalcified coronary plaque and increased immune activation, particularly monocyte activation. Independent effects of sex, HIV status, and aging on immune activation may contribute to cardiovascular disease in this population. CLINICAL TRIALS REGISTRATION: NCT00455793.

In-Stent Restenosis due to Stent Recoil After Third-Generation Drug-Eluting Stent Implantation.

A 72-year-old man with a heavily calcified coronary lesion underwent percutaneous coronary intervention (PCI) using a third-generation drug-eluting stent (DES) with thin stent struts. Two months after the PCI, in-stent restenosis due to stent recoil (SR) occurred. An intravascular ultrasound (IVUS) revealed deformed stent struts and heavily calcified coronary plaque. The SR probably occurred due to persistent vessel compression as a result of heavily calcified coronary plaque. We should consider using a DES with thick stent struts rather than a third-generation DES with thin stent struts in patients with a heavily calcified coronary lesion.

Clinical application of effective atomic number for classifying non-calcified coronary plaques by dual-energy computed tomography.

BACKGROUND AND AIMS: Coronary computed tomography (CT) angiography allows non-invasive classification of non-calcified coronary plaques (NCCPs) based on Hounsfield unit (HU) values. This methodology, however, is somewhat limited for reliable classification of NCCPs. Therefore, we evaluated the effective atomic number (EAN) for classifying NCCPs by single-source dual-energy CT with fast tube voltage switching (SSDECT). METHODS: We prospectively enrolled 18 patients undergoing both SSDECT and intravascular ultrasonography (IVUS). Monochromatic images at 70 keV and EAN images were reconstructed from SSDECT data sets. Regions of interest (ROIs) within NCCPs were placed on IVUS-matched SSDECT images, and mean HU values and EANs for soft and fibrous plaques, classified using IVUS, were compared with an unpaired t-test. RESULTS: We placed 96 ROIs in 29 soft plaques and 37 ROIs in 15 fibrous plaques in 12 coronary arteries of 11 patients. The mean HU value in soft plaques (58.2 ± 32.8 HU) was significantly lower than that in fibrous plaques (103.9 ± 48.3 HU) (p < 0.001). The mean EAN in soft plaques (8.7 ± 0.5) was also significantly lower than that in fibrous plaques (9.6 ± 0.5) (p < 0.0001). Area under the curve for EAN (0.91) was significantly higher than that for HU value (0.79) in receiver operating characteristic curve analysis (p = 0.046). With a cutoff EAN of 9.3, sensitivity was 90% and specificity, 87%; whereas with a cutoff HU value of 55.0 HU, sensitivity was 62% and specificity, 93%. CONCLUSIONS: EAN measurement by SSDECT can be clinically useful for accurately classifying soft and fibrous coronary plaques.