Iliac vein compression (LIVC) is a prevalent finding in the general population, but a smaller number of patients are symptomatic. ILVC should be considered in symptomatic patients with unexplained unilateral lower leg swelling. Patients typically complain of one or more of the following symptoms: lower leg pain, heaviness, venous claudication, swelling, hyperpigmentation and ulceration. ILVC can be thrombotic, combined with acute or chronic DVT, or non-thrombotic. ILVC is best diagnosed with intravascular ultrasound (IVUS), but computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have emerged as valid screening tests. Venography underestimates the severity of ILVC but may provide insights into the anatomy and the presence of collaterals. Based on current available evidence, endovascular therapy with stenting remains the main treatment strategy for ILVC. Dedicated nitinol venous stents are currently under review by the Food and Drug Administration for potential approval in the United States. These stents have been released outside the US. There is no consensus to the optimal anticoagulation regimen post-ILVC stenting. Oral anticoagulants, however, remain a preferred therapy in patients with history of thrombotic ILVC.

Angiography remains a widely utilized imaging modality during vascular procedures. Angiography, however, has its limitations by underestimating the true vessel size, plaque morphology, presence of calcium and thrombus, plaque vulnerability, true lesion length, stent expansion and apposition, residual narrowing post intervention and the presence or absence of dissections. Intravascular ultrasound (IVUS) has emerged as an important adjunctive modality to angiography. IVUS offers precise imaging of the vessel size, plaque morphology and the presence of dissections and guides interventional procedures including stent sizing, assessing residual narrowing and stent apposition and expansion. IVUS-guided treatment has shown to yield superior outcomes when compared to angiography-only guided therapy. The cost-effectiveness of the routine use of IVUS during vascular procedures needs to be further studied.

Purpose: To investigate if imaging with intravascular ultrasound (IVUS) yields a more accurate estimate of vessel diameter and the presence of dissections after intervention when treating the infrapopliteal arteries. Materials and Methods: A prospective, single-center study enrolled 20 consecutive patients (mean age 74.1±12.4 years; 12 women) with infrapopliteal disease who were treated with PTA (n=10) or orbital atherectomy (OA) followed by PTA (n=10). The majority of patients were hypertensive and half were diabetic. The overall lesion length was 7.3±6.3 cm, and the diameter stenosis was 80.3%±22.1%. The baseline characteristics did not differ between the groups. Vessel diameters were measured using IVUS from the internal elastic lamina (IEL) to the IEL. IVUS was performed at baseline, post PTA or OA, and post OA+PTA. Quantitative vascular angiography (QVA) and IVUS were analyzed by a core laboratory. Dissections on cine images were categorized based on the National Heart Lung and Blood Institute (NHLBI) classification, while the arc and depth were used to characterize dissections on IVUS images. Results: Mean vessel diameter by QVA was 2.9±0.6 vs 4.0±1.0 mm by IVUS according to the core laboratory (mean difference 1.1±0.9, p<0.001). On angiography, there were 7 dissections after PTA (6 C, 1 D), 1 dissection after OA (1 B), and 2 dissections after OA+PTA (1 A, 1 B; p=0.028 vs post PTA). IVUS uncovered 3.8 times more dissections than seen on angiography. There were 23 dissections after PTA (18 intima, 3 media, 2 adventitia), 12 dissections after OA (8 intima, 1 media, 3 adventitia), and 11 dissections following OA+PTA (7 intima, 1 media, 3 adventitia; p=0.425 vs PTA). Bailout stenting (all due to angiographic dissections ≥C) was necessary in 6 of the PTA cohort and none of the OA+PTA group. Conclusion: In addition to underestimating the infrapopliteal vessel diameter by ~25%, angiography underappreciated the presence and severity of post-intervention dissections vs IVUS, particularly in the OA+PTA group.

Introduction Inflammation is a substantial mediator of atherosclerosis. Colchicine has anti-inflammatory effects and has been investigated in many randomized controlled trials (RCTs) in patients with coronary artery disease (CAD). Methods We searched PubMed/MEDLINE, Cochrane library, and Embase databases (inception through 28 February 2020) for RCTs evaluating colchicine in CAD patients. The outcomes of interest were major adverse cardiovascular events (MACE), myocardial infarction (MI), all-cause mortality, cardiovascular mortality, and stroke. Estimates were pooled using inverse-variance random-effects model. We reported effect sizes as risk difference (RD) with 95% confidence interval (CI). Results A total of six RCTs with 6154 patients were included. The mean age ± SD for the patients in the colchicine group was 61.6 ± 10.8 and control group was 61.5 ± 10.7 years. At the median follow-up of 3.5 months, use of colchicine in patients with CAD was not associated with statistically significant reduction of MACE (RD −0.032; 95% CI −0.083 to 0.018; P = 0.15; I2 = 75%; low level of evidence), MI (RD −0.011; 95% CI −0.030 to 0.007; P = 0.16; I2 = 11.3%; low level of evidence), all-cause mortality (RD −0.001; 95% CI −0.009 to 0.006; P = 0.65; I2 = 0%; low level of evidence), cardiovascular mortality (RD −0.003; 95% CI −0.010 to 0.004; P = 0.34; I2 = 0%; low level of evidence), and stroke (RD −0.001, 95% CI −0.005 to 0.004; P = 0.69; I2 = 0%; very low level of evidence). Conclusion This meta-analysis suggests that colchicine was not associated with a significant decrease in cardiovascular endpoints and mortality in patients with CAD.

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