Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis.

BACKGROUND: Atherosclerosis is a progressive disease that results from endothelial dysfunction, inflammatory arterial wall disorder and the formation of the atheromatous plaque. This results in carotid artery stenosis and is responsible for atherothrombotic stroke and ischemic injury. Low-grade plaque inflammation determines biological stability and lesion progression. METHODS: Sixty-seven cases with active perilesional inflammatory cell infiltrate were selected from a larger cohort of patients undergoing carotid endarterectomy. CD68+, iNOS2+ and Arg1+ macrophages and CD31+ endothelial cells were quantified around the atheroma lipid core using digital morphometry, and expression levels were correlated with determinants of instability: ulceration, thrombosis, plaque hemorrhage, calcification patterns and neovessel formation. RESULTS: Patients with intraplaque hemorrhage had greater CD68+ macrophage infiltration (p = 0.003). In 12 cases where iNOS2 predominated over Arg1 positivity, the occurrence of atherothrombotic events was significantly more frequent (p = 0.046). CD31 expression, representing neovessel formation, correlated positively with atherothrombosis (p = 0.020). CONCLUSIONS: Intraplaque hemorrhage is often described against the background of an intense inflammatory cell infiltrate. Atherothrombosis is associated with the presence of neovessels and pro-inflammatory macrophages expressing iNOS2. Modulating macrophage polarization may be a successful therapeutic approach to prevent plaque destabilization.

A single-center prospective study on the efficiency of negative pressure wound therapy versus conventional wound therapy in the postoperative management of devitalized and infected wounds.

INTRODUCTION: In this study, we aim to present the benefits of using negative pressure wound therapy, particularly with respect to the speed up of recovery time of devitalized and infected post-operative wounds, cost-effectiveness of local healing, pain relief during treatment, and returning to work and resuming normal daily activities at an earlier time. MATERIALS AND METHODS: This was a prospective study performed in General Surgery Clinic, between 2016-2018. The study comprised 67 patients divided into two groups: A (29 patients who underwent negative pressure wound therapy) and B (38 patients who underwent conventional wound therapy). RESULTS: The average age of patients included in group A was 64.2 ± 12.3 years and in group B, 63.2 ± 9.7 years (p=0.440). The wounds were located on the foot, thigh, abdomen, and other areas, and the average length of stay in hospital was 33 ± 18 days for group A versus 17 ± 14 days for group B (p=0.042) but with an average local healing time of 12 ± 5 days in group A versus 44 ± 17 days in group B (p<0.001). The average cost of hospitalization was higher in group A: 17,868 ± 9,560 RON (3,834 ± 2,051 euros) compared to group B: 6,025 ± 4,137 RON (1,292 ± 887 euros) (p=0.443) but the average cost of local healing was lower in group A: 5,437 ± 2,238 RON (1,166 ± 480 euro) compared to group B: 6,840 ± 3,520 RON (1,467 ± 755 euro) (p=0.005). CONCLUSIONS: The treatment of devitalized and infected post-operative wounds by using negative pressure wound therapy reduces local and complete healing time by approximately 30%, local healing costs by 26%, and allows better pain management during treatment with minimal complications. KEY WORDS: Negative pressure wound Therapy, Conventional wound therapy, Local healing, average cost.

Inflammation, Microcalcification, and Increased Expression of Osteopontin Are Histological Hallmarks of Plaque Vulnerability in Patients with Advanced Carotid Artery Stenosis.

BACKGROUND: severe carotid artery stenosis is a major cause of ischemic stroke and consequent neurological deficits. The most important steps of atherosclerotic plaque development, leading to carotid stenosis, are well-known; however, their exact timeline and intricate causal relationships need to be more characterized. METHODS: in a cohort of 119 patients, who underwent carotid endarterectomy, we studied the histological correlations between arterial calcification patterns and localization, the presence of the inflammatory infiltrate and osteopontin expression, with ulceration, thrombosis, and intra-plaque hemorrhage, as direct signs of vulnerability. RESULTS: in patients with an inflammatory infiltrate, aphasia was more prevalent, and microcalcification, superficial calcification, and high-grade osteopontin expression were characteristic. Higher osteopontin expression was also correlated with the presence of a lipid core. Inflammation and microcalcification were significantly associated with plaque ulceration in logistic regression models; furthermore, ulceration and the inflammatory infiltrate were significant determinants of atherothrombosis. CONCLUSION: our results bring histological evidence for the critically important role of microcalcification and inflammatory cell invasion in the formation and destabilization of advanced carotid plaques. In addition, as a calcification organizer, high-grade osteopontin expression is associated with ulceration, the presence of a large lipid core, and may also have an intrinsic role in plaque progression.