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Jinchun Liu,1 Zhijun Yu,2,3 Guohua Wang2 1Department of Medicine, Henan Vocational College of Nursing, Anyang, Henan Province, 455000, People’s Republic of China; 2Department of Neurophysiology and Neuropharmacology, Institute of Special Environmental Medicine and Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu, 226019, People’s Republic of China; 3Department of Thoracic Surgery, Nantong Second People’s Hospital, Nantong, Jiangsu, 226001, People’s Republic of ChinaCorrespondence: Guohua Wang, Email wgh036@hotmail.comAbstract: Coronary artery fistulae (CAF) are a rare anomaly characterized by abnormal connections between a coronary artery and a cardiac chamber or a great vessel, with most patients remaining asymptomatic. Despite being predisposed to severe complications like heart failure, patients with CAF infrequently experience severe stenosis in the coronary artery. This study delineates a case involving a 46-year-old male presenting with a fistula bridging the right coronary artery (RCA) and right atrium (RA), manifesting a pronounced 99% stenosis at the right extremity of the coronary artery proximal to the fistula. Concurrently, the individual exhibits six conventional risk factors: age over 40, male gender, hypertension, diabetes, smoking, and hypertriglyceridemia. Following pharmaceutical intervention, the patient was discharged and subjected to extended follow-up. This case highlights the dual processes of “accelerating damage” and “retarding renewal” in the progression of atherosclerosis. Factors such as shear stress, smoking, and hypertension are posited to expedite endothelial cell damage, while aging and diabetes may impede the renewal and repair of these cells. Together with the concept of secondary atherosclerotic plaque healing, this case prompts the introduction of a “Double Endothelial Healings” hypothesis, proposing a potential pathogenetic mechanism for coronary artery atherosclerosis.Keywords: coronary artery fistulae, atherosclerosis, pathogenesis, plaque healing, endothelial injury

Atherosclerotic cardiovascular disease is the leading cause of morbidity and mortality worldwide. Several cardiovascular risk factors are implicated in atherosclerotic plaque promotion and progression and are responsible for the clinical manifestations of coronary artery disease (CAD), ranging from chronic to acute coronary syndromes and sudden coronary death. The advent of intravascular imaging (IVI), including intravascular ultrasound, optical coherence tomography and near-infrared diffuse reflectance spectroscopy has significantly improved the comprehension of CAD pathophysiology and has strengthened the prognostic relevance of coronary plaque morphology assessment. Indeed, several atherosclerotic plaque phenotype and mechanisms of plaque destabilization have been recognized with different natural history and prognosis. Finally, IVI demonstrated benefits of secondary prevention therapies, such as lipid-lowering and anti-inflammatory agents. The purpose of this review is to shed light on the principles and properties of available IVI modalities along with their prognostic significance. [ABSTRACT FROM AUTHOR]

Keywords: Air pollution; Plaque healing; Acute coronary syndromes; Thrombosis; Inflammation EN Air pollution Plaque healing Acute coronary syndromes Thrombosis Inflammation 2403 2405 3 07/11/23 20230707 NES 230707 Introduction Plaque healing plays a key role in coronary atherosclerosis[1] and represents "the second hit" required to cause an acute coronary syndrome (ACS) after plaque destabilization, this latter being the "first hit".[[1], [3]] Moreover, an impaired plaque healing has been found in patients with recurrent ACS, suggesting its importance in preventing repeated symptomatic coronary thrombosis.[3] Nonetheless, mechanisms modulating plaque healing are unknown. In first acute coronary syndrome patients, particulate matter 2.5 chronic exposure levels were similar between patients with and without healed plaques in the culprit lesion, while particulate matter 2.5 was higher in those with macrophage infiltration and thin-cap fibroatheroma at the culprit plaque. Among recurrent ACS patients, 6 patients (20.7%) had TCFA at the culprit lesion, and these patients had higher PM2.5 (17.9 ± 3.6 vs. 13.6 ± 3.4 I µ i g/m SP 3 sp , I P i = 0.030) and PM10 (28.8 ± 3.2 vs. 24.2 ± 3.9 I µ i g/m SP 3 sp , I P i = 0.014) exposure levels compared to those without TCFA. [Extracted from the article]

Atherosclerotic cardiovascular disease is the leading cause of morbidity and mortality worldwide. Several cardiovascular risk factors are implicated in atherosclerotic plaque promotion and progression and are responsible for the clinical manifestations of coronary artery disease (CAD), ranging from chronic to acute coronary syndromes and sudden coronary death. The advent of intravascular imaging (IVI), including intravascular ultrasound, optical coherence tomography and near-infrared diffuse reflectance spectroscopy has significantly improved the comprehension of CAD pathophysiology and has strengthened the prognostic relevance of coronary plaque morphology assessment. Indeed, several atherosclerotic plaque phenotype and mechanisms of plaque destabilization have been recognized with different natural history and prognosis. Finally, IVI demonstrated benefits of secondary prevention therapies, such as lipid-lowering and anti-inflammatory agents. The purpose of this review is to shed light on the principles and properties of available IVI modalities along with their prognostic significance.

In selected cases, when STEMI caused by mild or moderate degree lesion with a large concomitant thrombus, additional OCT-guided PCI strategy after thrombus removal allows us to defer stenting with the follow- up natural healing of the vessel wall. [ABSTRACT FROM AUTHOR]

[Display omitted] [ABSTRACT FROM AUTHOR]

Abstract In selected cases, when STEMI caused by mild or moderate degree lesion with a large concomitant thrombus, additional OCT‐guided PCI strategy after thrombus removal allows us to defer stenting with the follow‐up natural healing of the vessel wall.

Abstract: Objective: Strokes, a major cause of disability, are often caused by embolism from unstable carotid plaques. The aim of this study was to validate a biobank of human carotid endarterectomies as a platform for further exploration of pathways for plaque instability. For this purpose, we investigated the relationship between clinical parameters of plaque instability and expression of genes previously shown to be associated with either plaque instability or healing processes in the vessel wall. Methods: A database of clinical information and gene-expression microarray data from 106 carotid endarterectomies were used. Results: Expression of matrix metalloproteinase (MMP)-9 and MMP-7 was 100-fold higher in plaques than in normal artery. In general, genes associated with inflammation (such as RANKL and CD68) were overexpressed in symptomatic compared with asymptomatic plaques. Plaques obtained from patients undergoing surgery within 2 weeks after an embolic event showed up-regulation of genes involved in healing reactions in the vessel wall (including elastin and collagen). Statin treatment, as well as echodense lesions, were associated with a more stable phenotype. Conclusion: Here, we demonstrate that gene-expression profiles reflect clinical parameters. Our results suggest that microarray technology and clinical variables can be used for the future identification of central molecular pathways in plaque instability. [Copyright &y& Elsevier]