DIAMondback Atherectomy With OCT Visualization for Calcified PAD Lesions (DIAMOCT-PAD Study).

OBJECTIVE: In this study, we aimed to describe the immediate and long-term vascular effects of OAS in patients with peripheral arterial disease (PAD) and moderate to severely calcified lesions. BACKGROUND: Debulking the calcified atherosclerotic plaque with the orbital atherectomy system (OAS) can potentially enhance vessel compliance and increase the chance of reaching a desirable angioplasty result. METHODS: A total of 7 patients were evaluated both at baseline and at 6-month follow-up. Following a diagnostic peripheral angiogram, patients with significant SFA disease had a baseline intravascular optical coherence tomography (IV-OCT) and the lesion was treated with OAS. Repeat IV-OCT was performed after atherectomy and after drug-coated balloon, if used. Patients were also evaluated with angiography and IV-OCT imaging at their 6-month follow-up. RESULTS: The majority of tissue removed was fibrous tissue. During follow-up, luminal volume increased for 4 of the 7 patients from baseline to 6-month follow-up and decreased in 3 patients. On average there was a 6% increase of luminal volume (P<.01 compared with baseline). A recent virtual histology algorithm was used for automatic classification of IV-OCT images unaided by any reader. The algorithm used convolutional neural networks to identify regions as either calcium, fibrous, or lipid plaque, and it agreed with an expert reader 82% of the time. CONCLUSION: To the best of our knowledge, the current report is the first to describe vascular effects of OAS in medial calcified lesions immediately after and at follow-up using IV-OCT in patients with severe PAD.

Coronary Stent Healing in Cancer Patients-An Optical Coherence Tomography Perspective.

Objective: This study assessed stent healing patterns and cardiovascular outcomes by optical coherence tomography (OCT) in cancer patients after drug-eluting stent (DES) placement. Background: Cancer treatment, owing to its cytotoxic and antiproliferative effects, could delay stent healing and increase stent thrombosis risk, especially when dual antiplatelet therapy (DAPT) is discontinued early for oncological treatment. OCT can assess stent endothelialization and other healing parameters, which may provide clinical guidance in these challenging scenarios. Methods: This single-center retrospective study enrolled all cancer patients who underwent OCT for assessment of vascular healing patterns after prior DES placement from November 2009 to November 2018. Primary study endpoints were stent healing parameters, including stent coverage, apposition, degree of expansion, neointimal hyperplasia heterogeneity, in-stent restenosis, stent thrombosis, and overall survival (OS). Results: A total of 67 patients were included in this study. Mean time between DES placement and OCT evaluation was 154 ± 82 days. Stent healing matched published values for DES in non-cancer patients (P ≥ 0.063). At 1 year, the OS was 86% (95% confidence interval [CI]: 78-96%) with 0% incidence of acute coronary syndrome. Advanced cancers and active chemotherapies were associated with inferior OS (P = 0.024, hazard ratio [HR]: 3.50, 95% CI: 1.18-10.42 and P = 0.026, HR: 2.65, 95% CI: 1.13-6.22, respectively), while stent healing parameters were unassociated with OS. Forty-one patients (61%) had DAPT duration ≤6 months. Conclusions: Stent healing of contemporary DES appears similar in cancer and non-cancer patients. Cardiovascular risk of cancer patients after DES placement can be managed to facilitate timely cancer therapies, as the underlying malignancy and active chemotherapy ultimately determine survival.

Virtual Histology Optical Coherence Tomography Imaging of Orbital Rotational Atherectomy for Calcified Peripheral Arterial Disease.

In order to assess the vascular effects of rotational orbital atherectomy, we performed intravascular imaging with virtual histology intravascular optical coherence tomography in a 72-year-old man with critical limb ischemia of the right lower extremity.

Assessment of Vascular Patency and Inflammation with Intravascular Optical Coherence Tomography in Patients with Superficial Femoral Artery Disease Treated with Zilver PTX Stents.

PURPOSE: Zilver PTX nitinol self-expanding drug-eluting stent with paclitaxel coating is effective for treatment of superficial femoral artery (SFA) disease. However, as with any stent, it induces a measure of vascular inflammatory response. The current clinical trial (NCT02734836) aimed to assess vascular patency, remodeling, and inflammatory markers with intravascular optical coherence tomography (OCT) in patients with SFA disease treated with Zilver PTX stents. METHODS: Serial OCT examinations were performed in 13 patients at baseline and 12-month follow-up. Variables evaluated included neointimal area, luminal narrowing, thrombus area, stent expansion as well as measures of inflammation including, peri-strut low-intensity area (PLIA), macrophage arc, neovascularization, stent strut apposition and coverage. RESULTS: Percentage of malapposed struts decreased from 10.3 ±â€¯7.9% post-intervention to 1.1 ±â€¯2.2% at 12-month follow-up, but one patient showed late-acquired stent malapposition (LASM). The percent of uncovered struts at follow-up was 3.0 ±â€¯4.5%. Average expansion of stent cross-sectional area from baseline to follow-up was 35 ±â€¯19%. The average neointimal area was 7.8 ±â€¯3.8 mm2. Maximal luminal narrowing was 61.1 ±â€¯25.0%, and average luminal narrowing was 35.4 ±â€¯18.2%. Average peri-strut low-intensity area (PLIA) per strut was 0.017 ±â€¯0.018 mm2. Average number of neovessels per mm of stent was 0.138 ±â€¯0.181. Average macrophage angle per frame at follow-up was 7 ±â€¯11°. Average thrombus area at follow-up was 0.0093 ±â€¯0.0184 mm2. CONCLUSION: At 12-month follow-up, OCT analysis of Zilver PTX stent shows outward remodeling and minimal neointimal growth, but evidence of inflammation including PLIA, neovessels, thrombus and macrophages. SUMMARY: Thirteen patients with PAD had paclitaxel-coated stents implanted in their SFAs and were then imaged with OCT at baseline and 12-month follow-up. OCT proxy metrics of inflammation were quantified.

Impact of ticagrelor and aspirin versus clopidogrel and aspirin in symptomatic patients with peripheral arterial disease: Thrombus burden assessed by optical coherence tomography.

PURPOSE: To compare OCT identified white thrombus decline, neointimal hyperplasia and clinical outcomes of patients treated with ticagrelor plus aspirin with those patients treated with clopidogrel plus aspirin after peripheral interventions. BACKGROUND: Ticagrelor is a potent platelet inhibitor. In patients with coronary artery disease, ticagrelor and aspirin demonstrated reduced rates of stent thrombosis, compared to aspirin and clopidogrel. The clinical importance of potent antiplatelet inhibition after peripheral endovascular interventions is unknown. METHODS: We enrolled 18 patients with superficial femoral artery disease and the presence of OCT-detected clot post-stent placement. Patients were randomized to 75 mg clopidogrel once daily for 1 month vs. 90 mg ticagrelor twice daily for 6 months, both in addition to 81 mg aspirin for 6 months. Clot volumes, ankle-brachial index (ABI), 6-minute walk test, and Rutherford classification were measured at baseline and 6-month follow-up. Neointimal hyperplasia and neovascularization were calculated at 6-month follow-up. RESULTS: N = 11 patients were enrolled in the clopidogrel group and N = 7 in the ticagrelor group. There was a significantly greater decrease in white thrombus in the ticagrelor group (median volume/stent length (0.067 vs 0.014 mm3/mm, p = 0.05)). No differences were found in % neointima (0.412 vs 0.536 mm3/mm, p = 0.44) and neovascularization (28 vs 44, p = 0.16). ABI and Rutherford classification were improved significantly after 6 months in the clopidogrel group, with no difference between groups at 6 months in ABI or Rutherford. CONCLUSION: In symptomatic patients with PAD, ticagrelor showed significant improvement relative to clopidogrel with respect to white thrombus burden decline.

Lipid-lowering therapy stabilizes the complexity of non-culprit plaques in human coronary artery: a quantitative assessment using OCT bright spot algorithm.

To quantitatively evaluate the change of plaque complexity with cholesterol lowering therapy. A total of 44 non-culprit plaques from 30 patients who had serial image acquisition at baseline, 6-months, and 12-months by both optical coherence tomography (OCT) and intravascular ultrasound (IVUS) were included. Patients were treated with atorvastatin 60 mg (AT60, n = 16) or 20 mg (AT20, n = 14). We applied an OCT bright spot algorithm, which identifies a variety of plaque components including macrophages. The density of bright spot was measured within the superficial 250 µm of the vessel wall. Significant reduction of bright spot density was observed from baseline to 12-months [-0.49% (-0.95, -0.20), p < 0.001], particularly during the second 6 months [first 6 months: -0.01% (-0.57, 0.60), p = 0.939; second 6 months: -0.49% (-0.98, 0.14), p < 0.001]. Although there was no significant difference at 12 months in the reduction of bright spot density between plaques with acute coronary syndrome (ACS, n = 33) and those with stable angina (n = 11) [-0.49% (-0.93, -0.19) vs. -0.39% (-1.01, -0.21), p = 0.748], a significant reduction of bright spot density during the first 6 months was observed only in plaques with ACS. There was no significant difference in the change of bright spot density between the AT60 group (n = 22) and AT20 group (n = 22) [-0.61% (-0.93, -0.34) vs. -0.41% (-0.98, -0.19), p = 0.483]. Coronary plaque complexity evaluated by a quantitative OCT algorithm significantly decreased with 12 month atorvastatin therapy irrespective of the dose and initial clinical presentation.

Diagnosis of Thin-Capped Fibroatheromas in Intravascular Optical Coherence Tomography Images: Effects of Light Scattering.

BACKGROUND: Intravascular optical coherence tomography (IVOCT) images are recorded by detecting light backscattered within coronary arteries. We hypothesize that non-thin-capped fibroatheroma (TCFA) causes may scatter light to create the false appearance of IVOCT TCFA. METHODS AND RESULTS: Ten human cadaver hearts were imaged with IVOCT (n=14 coronary arteries). IVOCT and histological TCFA images were coregistered and compared. Of 21 IVOCT TCFAs (fibrous cap <65 µm, lipid arc >1 quadrant), only 8 were true histological TCFA. Foam cell infiltration was responsible for 70% of false IVOCT TCFA and caused both thick-capped fibroatheromas to appear as TCFA, and the appearance of TCFAs when no lipid core was present. Other false IVOCT TCFA causes included smooth muscle cell-rich fibrous tissue (12%) and loose connective tissue (9%). If the lipid arc >1 quadrant (obtuse) criterion was disregarded, 45 IVOCT TCFAs were identified, and sensitivity of IVOCT TCFA detection increased from 63% to 87%, and specificity remained high at 92%. CONCLUSIONS: We demonstrate that IVOCT can exhibit 87% (95% CI, 75%-93%) sensitivity and 92% specificity (95% CI, 86%-96%) to detect all lipid arcs (both obtuse and acute, <1 quadrant) TCFA, and we also propose new mechanisms involving light scattering that explain why other plaque components can masquerade as TCFA and cause low positive predictive value of IVOCT for TCFA detection (47% for obtuse lipid arcs). Disregarding the lipid arc >1 quadrant requirement enhances the ability of IVOCT to detect TCFA.

Macrophages and intravascular OCT bright spots: a quantitative study.

OBJECTIVES: This study hypothesized that bright spots in intravascular optical coherence tomography (IVOCT) images may originate by colocalization of plaque materials of differing indexes of refraction. To quantitatively identify bright spots, we developed an algorithm that accounts for factors including tissue depth, distance from light source, and signal-to-noise ratio. We used this algorithm to perform a bright spot analysis of IVOCT images and compared these results with histological examination of matching tissue sections. BACKGROUND: Bright spots are thought to represent macrophages in IVOCT images, and studies of alternative etiologies have not been reported. METHODS: Fresh human coronary arteries (n = 14 from 10 hearts) were imaged with IVOCT in a mock catheterization laboratory and then processed for histological analysis. The quantitative bright spot algorithm was applied to all images. RESULTS: Results are reported for 1,599 IVOCT images co-registered with histology. Macrophages alone were responsible for only 23% of the bright spot-positive regions, although they were present in 57% of bright spot-positive regions (as determined by histology). Additional etiologies for bright spots included cellular fibrous tissue (8%), interfaces between calcium and fibrous tissue (10%), calcium and lipids (5%), and fibrous cap and lipid pool (3%). Additionally, we showed that large pools of macrophages in CD68(+) histology sections corresponded to dark regions in comparative IVOCT images; this is due to the fact that a pool of lipid-rich macrophages will have the same index of refraction as a pool of lipid and thus will not cause bright spots. CONCLUSIONS: Bright spots in IVOCT images were correlated with a variety of plaque components that cause sharp changes in the index of refraction. Algorithms that incorporate these correlations may be developed to improve the identification of some types of vulnerable plaque and allow standardization of IVOCT image interpretation.

Clinical utility of quantitative bright spots analysis in patients with acute coronary syndrome: an optical coherence tomography study.

To investigate the clinical significance of bright spots in coronary plaque detected by optical coherence tomography (OCT) in patients with coronary artery disease. We identified 112 patients [acute coronary syndromes (ACS): n = 50, stable angina pectoris (SAP): n = 62] who underwent OCT imaging of the culprit lesion. A novel OCT algorithm was applied to detect bright spots representing the juxtaposition of a variety of plaque components including macrophages. The density of bright spots within the most superficial 250 µm of the vessel wall was measured at the site of culprit lesion. Bright spot density in the culprit lesion was significantly higher in patients presenting with ACS compared to those presenting with SAP (0.51 ± 0.43% vs. 0.37 ± 0.26%, P = 0.04), particularly in the subgroup with ruptured culprit plaque (0.59 ± 0.52%). Thin-cap fibroatheroma (TCFA) was associated with a trend towards a higher density of bright spots compared to non-TCFA plaques (0.57 ± 0.50% vs. 0.41 ± 0.31%, P = 0.08). Similar results were also obtained within 1000 µm depth. Positive linear correlation was demonstrated between bright spot density and hsCRP level (r = 0.45, P = 0.002). Using a novel algorithm, we demonstrated a significantly higher density of bright spots in the culprit lesions of patients presenting with ACS, particularly in case of plaque rupture, compared to those presenting with SAP. The density of bright spots also correlates with inflammatory status. These results suggest that the quantitative assessment of bright spot density may be useful in evaluating plaque vulnerability.