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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]

Air pollution is emerging as an important risk factor for acute coronary syndrome (ACS). In this study, we investigated the association between short-term air pollution exposure and mechanisms of coronary plaque instability evaluated by optical coherence tomography (OCT) imaging in ACS patients. Patients with ACS undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT. Based on each case's home address, the mean daily exposures to several pollutants, including particulate matter 2.5 (PM 2.5), on the same day of ACS and in the immediate days (up to 6 days) prior to the index ACS, were collected. 139 ACS patients were included [69 (49.6%) had PR and 70 (50.4%) IFC]. Patients with PR, compared to those with IFC, had higher PM 2.5 exposure levels on the same day of ACS, without differences in the immediate 6 days before index ACS. At multivariate analysis, PM 2.5 exposure on the same day of ACS was the only independent predictor of PR [OR = 1.912 per SD (8.6 μg/m3), CI95 % (1.087–3.364), p = 0.025]. Patients with PR presented a steady increase in PM 2.5 daily exposure levels in the days preceding the occurrence of ACS, with a peak the day of ACS (p for trend = 0.042) This study demonstrates for the first time that a higher short-term PM2.5 exposure, on the same day of ACS, is associated with an increased risk of PR as a pathobiological mechanism of coronary plaque instability. [Display omitted] • Air pollution is emerging as an important risk factor for acute coronary syndrome (ACS). • Acute PM 2.5 exposure, especially on the same day of ACS, is associated with an increased risk of plaque rupture as mechanism of coronary plaque instability. • Mitigation strategies are crucial to reduce the burden of ischemic heart disease, especially in patients with a higher risk of cardiovascular events. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) is the leading cause of disability and death in both women and men; considerable differences in clinical presentation, natural history and prognosis are reported between sexes. Different pathophysiological mechanisms play a major role, including sex-related and gender-related features or a combination of both. Reports from intracoronary imaging studies pointed towards morphological plaque features, which seemed to differ between men and women, albeit results reported so far were not conclusive. The purpose of this review is to shed light on differences in the pathophysiology underlying CAD in women vs men including the description of coronary plaque phenotype and mechanisms of plaque instability, as assessed by intracoronary imaging. We will also discuss potential clinical implications with the aim to move towards a sex and gender-based personalized approach in CAD patients. [Display omitted] • Women develop CAD later, as compared to men, and experience worse prognosis. • Sex- and gender-related features are implicated in differences in CAD between sexes. • Intracoronary imaging pointed out differences in plaque phenotype and mechanisms of plaque instability between sexes. • Biological and psychosocial characteristics lead to an accelerated atherosclerosis in women with aging. • A broader and targeted therapeutic approach is required in women with CAD. [ABSTRACT FROM AUTHOR]