Ultrasonography, Interventional/methods

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Editorial

Legumain – Another Piece in the Complex Puzzle of Atherosclerotic Plaque Formation and Vulnerability

The atherosclerotic plaque formation process in the arterial walls is a very complex process. Plaque development occurs due to an interplay between endothelial cells, smooth muscle cells, and immune cells. There is an increase in endothelial permeability and activation of signaling molecules, including inflammatory mediators and cell adhesion molecules. Moreover, circulating lipoproteins (particularly low-density lipoproteins – LDL) can cross the endothelial layer and be deposited in the intimal space, where they undergo oxidative changes (oxLDL), increasing the local inflammatory response. Furthermore, monocytes mature into macrophages, being recruited via attractant chemokines, and while they attempt to clear oxLDL via phagocytosis, they are converted into foam cells and ultimately undergo necrosis. In addition, vascular smooth muscle cells (VSMCs) proliferate and migrate from the media to the intima, leading to intimal hyperplasia, and these cells organize and deposit extracellular matrix, forming a fibrous cap. Erosion or rupture of the fibrous cap will lead to thrombotic occlusion or distal embolism, resulting in ischemia.

In this process, matrix metalloproteinases (MMPs) play an important role. MMPs are a family of zinc-dependent endoproteases that are secreted by endothelial cells, VSMCs, fibroblasts, osteoblasts, macrophages, neutrophils, and lymphocytes. During stable atherosclerotic plaque development, MMP-2 cleaves the endogenous nitric oxide synthase, causing endothelial dysfunction and facilitating infiltration of LDL into the intima. Then, MMP-2 expressed by activated platelets promotes monocyte transmigration into the intima . MMP-2 also facilitates oxLDL-induced VSMCs migration to the intima, forming the fibrous cap. Therefore, it can induce migration and proliferation of VSMCs, enhancing plaque stability. However, MMP-2 levels are higher in unstable than in stable atherosclerotic plaque, indicating that MMP-2 plays a role in plaque vulnerability and propensity to rupture. They participate in the degradation of the extracellular matrix (ECM), which will cause thinning of the plaque fibrous cap, becoming more prone to rupture.

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Original Article

Percutaneous Coronary Intervention in Unprotected Left Main Coronary Artery Lesions

Douglas dos Santos Grion et al. Debora Carvalho Grion Igor Veiga Silverio Leonardo Shingu de Oliveira … Isabela Faria Larini Anna Victória Martins Juliana Moreira Marianne Machado Lissa Shizue Tateiwa Niekawa Adriana dos Santos Grion Cintia Magalhães Carvalho Grion

Abstract

Background

The advent of drug-eluting stents allowed the percutaneous coronary intervention to present safe results in lesions in the left main coronary artery.

Objectives

To analyze the results of the percutaneous treatment of unprotected left main coronary artery lesion with the use of intravascular ultrasound.

Methods

Study of consecutive case series carried out from January 2010 to December 2018. Clinical data were collected from patients as well as prognostic scores and data on coronary lesion. Low-grade residual lesion (less than 50%) on angiography and minimum luminal area greater than 6 mm²on intravascular ultrasound were considered successful. The adopted significance level was 5%.

Results

107 cases were analyzed. The multivessel lesion was predominant, with most (39.25%) of the lesions being found in three vessels in addition to the left main coronary artery. The SYNTAX score had a mean of 46.80 (SD: 22.95), and 70 (65.42%) patients had a SYNTAX score above 32 points. Angiographic success of percutaneous intervention was considered in 106 (99.06%) patients. The overall rate of major cardiac and cerebrovascular events in the hospital outcome was 6.54%, being similar in patients with SYNTAX score ≤ 32 (8.10%) and ≥ 33 (5.71%; p = 0.68).

Conclusions

Percutaneous intervention in cases of unprotected left main coronary artery lesion was safely performed and presented excellent results. Considerable angiographic success of treatment guided by intravascular ultrasound was achieved. The rate of major cardiac and cerebrovascular events was similar between patients at low and high risks.