Invasive characterization of atherosclerotic plaque in patients with peripheral arterial disease using near-infrared spectroscopy intravascular ultrasound.

OBJECTIVES: We describe the characteristics of atherosclerotic plaque in patients with peripheral arterial disease (PAD) using near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) BACKGROUND: Imaging and autopsy studies have described atherosclerotic plaque in different vascular beds, including varying degrees of lipid, fibrosis, and calcification. Recently, NIRS has been validated as an accurate method for detecting lipid-core plaque (LCP) in the coronary circulation. Invasive evaluation of plaque composition using NIRS-IVUS has not been reported in different peripheral arterial circulations. METHODS: We performed invasive angiography and NIRS-IVUS in consecutive PAD patients prior to percutaneous revascularization. Imaging evaluation included parameters from angiography, IVUS, and NIRS. NIRS-IVUS findings were compared among different vascular beds with regard to the presence and extent of calcification and LCP. RESULTS: One hundred and forty-nine lesions in 126 PAD patients were enrolled, including the internal carotid (n = 10), subclavian/axillary (n = 9), renal (n = 14), iliac (n = 35), femoropopliteal (n = 69), and infrapopliteal (n = 12) arteries. Plaque morphology was calcified in 132 lesions (89%) and fibrous in 17 lesions (11%). Calcification varied from 100% of renal artery stenoses to 55% of subclavian/axillary artery stenoses. LCP was present in 48 lesions (32%) and prevalence varied from 60% in carotid artery stenoses to 0% in renal artery stenoses (P < 0.005). LCP was only observed in fibrocalcific plaque, and was longitudinally and circumferentially surrounded by a more extensive degree of calcium. CONCLUSIONS: NIRS-IVUS in stable PAD patients demonstrates a high frequency of calcific plaque and statistically significant differences in the frequency of LCP in different arterial beds. LCP, when present in the peripheral circulation, is always associated with calcified plaque. The strong co-localization of calcified plaque and LCP in severe PAD lesions may provide plaque-stabilizing effects; further studies are needed. © 2017 Wiley Periodicals, Inc.

Invasive evaluation of plaque morphology of symptomatic superficial femoral artery stenoses using combined near-infrared spectroscopy and intravascular ultrasound.

The purpose of this study is to characterize the plaque morphology of severe stenoses in the superficial femoral artery (SFA) employing combined near-infrared spectroscopy and intravascular ultrasound (NIRS-IVUS). Atherosclerosis is the most common cause of symptomatic peripheral arterial disease. Plaque composition of SFA stenoses has been characterized as primarily fibrous or fibrocalcific by non-invasive and autopsy studies. NIRS has been validated to detect lipid-core plaque (LCP) in the coronary circulation. We imaged severe SFA stenoses with NIRS-IVUS prior to revascularization in 31 patients (46 stenoses) with Rutherford claudication ⩾ class 3. Angiographic parameters included lesion location and stenosis severity. IVUS parameters included plaque burden and presence of calcium. NIRS images were analyzed for LCP and maximum lipid-core burden index in a 4-mm length of artery (maxLCBI4mm). By angiography, 38 (82.6%) lesions were calcified and 9 (19.6%) were chronic total occlusions. Baseline stenosis severity and lesion length were 86.0 ± 11.0% and 36.5 ± 46.5 mm, respectively. NIRS-IVUS identified calcium in 45 (97.8%) lesions and LCP in 17 (37.0%) lesions. MaxLCBI4mm was 433 ± 244. All lesions with LCP also contained calcium; there were no non-calcified lesions with LCP. In conclusion, this is the first study of combined NIRS-IVUS in patients with PAD. NIRS-IVUS demonstrates that nearly all patients with symptomatic severe SFA disease have fibrocalcific plaque, and one-third of such lesions contain LCP. These findings contrast with those in patients with acute coronary syndromes, and may have implications regarding the pathophysiology of atherosclerosis in different vascular beds.