Coronary Plaque Stabilization Research Articles

Drug intervention as an emerging concept for secondary prevention in patients with coronary disease.

Non-culprit lesion-related coronary events are a significant concern in patients with coronary artery disease (CAD) undergoing coronary intervention. Since several studies using intra-coronary imaging modalities have reported a high prevalence of vulnerable plaques in non-culprit lesions at the initial coronary event, the immediate stabilization of these plaques by intensive pharmacological regimens may contribute to the reduction in the adverse events. Although current treatment guidelines recommend the titration of statin and other drugs to attain the treatment goal of low-density lipoprotein cholesterol (LDL-C) level in patients with CAD, the early prescription of strong LDL-C lowering drugs with more intensive regimen may further reduce the incidence of recurrent cardiovascular events. In fact, several studies with intensive regimen have demonstrated a higher percentage of patients with the attainment of LDL-C treatment goal in the early phase following discharge. In addition to many imaging studies showing plaque stabilization by LDL-C lowering drugs, several recent reports have shown the efficacy of early statin and proprotein convertase subtilisin/kexin type 9 inhibitors on the immediate stabilization of non-culprit coronary plaques. To raise awareness regarding this important concept of immediate plaque stabilization and subsequent reduction in the incidence of recurrent coronary events, the term 'Drug Intervention' has been introduced and gradually applied in the clinical field, although a clear definition is lacking. The main target of this concept is patients with acute coronary syndrome as a higher prevalence of vulnerable plaques in non-culprit lesions in addition to the worse clinical outcomes has been reported in recent imaging studies. In this article, we discuss the backgrounds and the concept of drug intervention.

No evidence of coronary plaque stabilization by allopurinol in patients with acute coronary syndrome

BackgroundAllopurinol, a xanthine inhibitor that lowers uric acid concentration, has been proven to reduce inflammation and oxidative stress in patients with cardiovascular disease. However, it is unknown whether these beneficial effects translate into favorable plaque modification in acute coronary syndromes (ACS). This study aimed to investigate whether allopurinol could improve coronary plaque stabilization using coronary computed tomography angiography (CCTA). MethodsThis was a prospective, single-center, randomized, double-blind clinical trial began in March 2019. A total of 162 ACS patients aged 18–80 years with a blood level of high-sensitivity C-reactive protein (hsCRP) ​> ​2 ​mg/L were included. The subjects were randomly assigned in a 1:1 ratio to receive either allopurinol sustained-release capsules (at a dose of 0.25 ​g once daily) or placebo for 12 months. The plaque analysis was performed at CCTA. The primary efficacy endpoint was the change in low-attenuation plaque volume (LAPV) from baseline to the 12-month follow-up. ResultsAmong 162 patients, 54 in allopurinol group and 51 in placebo group completed the study. The median follow-up duration was 14 months in both groups. Compared with placebo, allopurinol therapy did not significantly alter LAPV (−13.4 ​± ​3.7 ​% vs. −17.8 ​± ​3.6 ​%, p ​= ​0.390), intermediate attenuation plaque volume (−16.1 ​± ​3.0 ​% vs. −16.2 ​± ​2.9 ​%, p ​= ​0.992), dense calcified plaque volume (12.2 ​± ​13.7 ​% vs. 9.7 ​± ​13.0 ​%, p ​= ​0.894), total atheroma volume (−15.2 ​± ​3.2 ​% vs. −16.4 ​± ​3.1 ​%, p ​= ​0.785), remodeling index (2.0 ​± ​3.9 ​% vs. 5.4 ​± ​3.8 ​%, p ​= ​0.536) or hsCRP levels (−73.6 [−91.6–17.9] % vs. −81.2 [−95.4–47.7] %, p ​= ​0.286). ConclusionsOur findings suggest that allopurinol does not improve atherosclerotic plaque stability or inflammation in ACS.

Exosomal circSCMH1/miR-874 ratio in serum to predict carotid and coronary plaque stability.

To investigate the correlation between lg (circSCMH1/miR-874) and acute coronary syndrome (ACS), acute myocardial infarction (AMI), and carotid plaque stability. 701 patients were divided into stable coronary artery disease (SCAD), ACS, and control groups. Furthermore, 225 patients who underwent carotid ultrasound were selected from the above 701 patients and were divided into low-risk plaque, medium-to-high risk plaque, and control (without carotid plaques) groups. We collected their baseline characteristics and measured the contents of exosomal circSCMH1 and miR-874 in peripheral blood. Then lg(circSCMH1/miR-874) was calculated and statistical analysis was performed. The lg (circSCMH1/miR-874) values of ACS, SCAD, and the control group decreased successively (P < 0.05). Compared with the low-risk plaque and control groups, the lg (circSCMH1/miR-874) value of medium-high risk plaque group decreased (P < 0.05). Multivariate logistic regression analysis showed that with the decrease of lg (circSCMH1/miR-874), the risk of ACS, AMI, and medium-high risk plaques increased. ROC curve analysis demonstrated that lg (circSCMH1/miR-874) has a higher diagnostic value for ACS, AMI and medium-high risk plaques than previously used predictive ratios. Lg (circSCMH1/miR-874) is closely associated with coronary and carotid plaque stability.

Coronary artery calcification and plaque stability： an optical coherence tomography study

BackgroundCoronary artery calcification (CAC), a surrogate of atherosclerosis, is related to stent underexpansion and adverse cardiac events. However, the effect of CAC on plaque stability is still controversial and the morphological significance of CAC has yet to be elucidated. MethodsA retrospective series of 419 patients with acute coronary syndrome (ACS) who underwent optical coherence tomography (OCT) were enrolled. Patients were classified into three groups based on the calcification size in culprit plaques and the features of the culprit and non-culprit plaques among these groups were compared. Logistic regression was used to analyze independent risk factors for culprit plaque rupture and the nonlinear relationship between calcification parameters and culprit plaque rupture. Furthermore, we compared the detailed calcification parameters of different kinds of plaques. ResultsA total of 419 culprit plaques and 364 non-culprit plaques were identified. The incidence of calcification was 53.9 % in culprit plaques and 50.3 % in non-culprit plaques. Compared with culprit plaques without calcification, plaque rupture, macrophages and cholesterol crystals were more frequently observed in the spotty calcification group, and the lipid length was longer; the incidence of macrophages and cholesterol crystals was higher in the macrocalcification group. Calcification tended to be smaller in ruptured plaques than in non-ruptured plaques. Moreover, the arc and length of calcification were greater in culprit plaques than in non-culprit plaques. ConclusionsVulnerable features were more frequently observed in culprit plaques with spotty calcification, whereas the presence of macrocalcification calcifications did not significantly increase plaque vulnerability. Calcification tends to be larger in culprit plaques than in non-culprit plaques.

Association between Eicosapentaenoic Acid to Arachidonic Acid Ratio and Characteristics of Plaque Rupture.

Eicosapentaenoic acid (EPA) has shown beneficial effects on coronary plaque stabilization. Based on our previous study, we speculated that EPA might be associated with the development of healed plaques and might limit thrombus size. This study aimed to elucidate the association between EPA and arachidonic acid (AA) ratios and various plaque characteristics in patients with plaque rupture. A total of 95 patients with acute coronary syndrome (ACS) caused by plaque rupture who did not take lipid-lowering drugs and underwent percutaneous coronary intervention using optical coherence tomography (OCT) were included. Clinical characteristics, lipid profiles, and OCT findings were compared between patients with lower and higher EPA/AA ratios (0.41) according to the levels in the Japanese general population. In the high EPA/AA (n=29, 30.5%) and low EPA/AA (n=66, 69.5 %) groups, the high EPA/AA group was significantly older (76.1 vs. 66.1 years, P＜0.01) and had lower peak creatine kinase (556 vs. 1651 U/L, P=0.03) than those with low EPA/AA. Similarly, patients with high EPA/AA had higher prevalence of layered and calcified plaque (75.9 vs. 39.4 %, P＜0.01; 79.3 vs. 50.0 %, P＜0.01, respectively) than low EPA/AA group. Multivariate logistic regression analysis demonstrated that a high EPA/AA ratio was an independent factor in determining the development of layered and calcified plaques. A high EPA/AA ratio may be associated with the development of layered and calcified plaques in patients with plaque rupture.

Effect of Intensive Lipid-Lowering Therapy on Coronary Plaque Stabilization Derived from Optical Coherence Tomography: a Meta-analysis and Meta-regression.

The definitive impacts of intensive lipid-lowering therapy (LLT) on plaque stabilization and the relationship between the key markers during LLT and plaque stability remain unquestioned. Thus, these meta-analysis and meta-regression intend to holistically evaluate the influence exerted by rigorous LLT on the minimum fibrous cap thickness (FCT) and maximum lipid arc as discerned through optical coherence tomography (OCT). This study further scrutinizes the correlation of this impact with variations in high-sensitivity C-reactive protein (hs-CRP), low-density lipoprotein cholesterol (LDL-C), or additional parameters within patients diagnosed with coronary artery disease (CAD). Comprehensive searches were conducted on platforms including PubMed, Embase, and the Cochrane Library for randomized controlled trials (RCTs) published until June 1, 2023. The search was language agnostic and targeted RCTs elaborating on the correlation between high-intensity statin therapy or statins used concomitantly with other lipid-lowering medications and the minimum FCT and maximum lipid arc as assessed by OCT. The meta-analyses were executed employing a standard mean difference (SMD) algorithm with random-effects on continuous variables. These methodologies align with the Preferred Reporting Items for Systematic and Meta-analysis (PRISMA) guidelines. A spectrum of 12 RCTs engaging 972 patients were identified and mobilized for these analyses. Meta-analysis outcomes depicted a conspicuous correlation between intensive LLT and an enhanced minimum FCT (12 studies with 972 participants; SMD, 0.87; 95% CI, 0.54 to 1.21; P < 0.01), reduced maximum lipid arc (9 studies with 564 participants; SMD, -0.43; 95% CI, -0.58 to -0.29; P < 0.01). Meta-regression analysis has determined an association of elevated minimum FCT with decreased LDL-C (β, -0.0157; 95% CI, -0.0292 to -0.0023; P = 0.025), total cholesterol (TC) (β, -0.0154; 95% CI, -0.0303 to -0.0005; P = 0.044), and apolipoprotein B (ApoB) (β, -0.0209; 95% CI, -0.0361 to -0.0057; P = 0.022). However, no significant association was discerned relative to variations in hs-CRP/CRP (β, -0.1518; 95% CI, -1.3766 to -1.0730; P = 0.772), triglyceride (TG) (β, -0.0030; 95% CI, -0.0258 to -0.0318; P = 0.822), and high-density lipoprotein cholesterol (HDL-C) (β, 0.0313; 95% CI, -0.0965 to 0.1590; P = 0.608). Subsequent subgroup meta-analysis demonstrated that high-intensity statin therapy (5 studies with 204 participants; SMD, 1.03; 95% CI, 0.67 to 1.39; P < 0.01), as well as a combinative approach including PCSK9 antibodies and statins (3 studies with 522 participants; SMD, 1.17; 95% CI, 0.62 to 1.73; P < 0.01) contributed to an increase in minimum FCT. Parallelly, high-intensity statin therapy (4 studies with 183 participants; SMD, -0.42; 95% CI, -0.65 to -0.19; P < 0.01) or the combined application of PCSK9 antibodies and statins (2 studies with 222 participants; SMD, -0.98; 95% CI, -1.26 to -0.70; P < 0.01) was evidenced to decrease the maximum lipid arc. Intensive LLT, mainly high-intensity statin therapy and combined PCSK9 antibody with statin, has a beneficial effect on coronary plaque stabilization derived from OCT in patients with CAD. Coronary plaque stabilization is primarily due to lipid-lowering effect, not anti-inflammatory effect. Moreover, the lipid-lowering effect has nothing to do with the changes in HDL-C and TG, but is mainly related to the reduction of LDL-C, TC, and ApoB.

Low-density lipoprotein cholesterol reduction is associated with computed tomography angiography signs of regression and stabilization of coronary plaque: from the TARGET trial

Background and purpose: The effectiveness of low-density lipoprotein cholesterol (LDL-C) lowering therapy in patients with higher baseline LDL-C levels has been extensively studied in Western populations. However, it remains uncertain whether the standard low-to-moderate lipid-lowering therapy practiced in Chinese individuals can lead to coronary plaque regression. Our objective is to explore the connections between plaque regression/stabilization, baseline LDL-C levels, and the extent of LDL-C reduction. Methods: This study constitutes a post hoc analysis derived from the TARGET trial, which initially recruited patients diagnosed with stable coronary artery disease (CAD) exhibiting an intermediate stenosis range of 30% to 90% as detected through coronary computed tomographic angiography (CCTA). Eligible participants for this analysis had undergone both baseline CCTA and a minimum 1-year follow-up. Patients were categorized into four groups based on their LDL-C levels and the degree of LDL-C reduction during the follow-up period. The assessment of coronary plaque regression within each group was conducted through the analysis of CCTA images, examining parameters such as total plaque (TP), percent atheroma volume (PAV), non-calcified plaque (NCP), low-attenuation plaque (LAP), and calcified plaque (CP). Results: Among the participants analyzed, totaling 287 individuals with an average age of 59.7 ± 7.1 years, comprising 69.7% men, the median duration between the initial and subsequent scans stood at 21 months (Q1–Q3, 15–29 months). Among these, 76 patients (26.5%) had been receiving statin therapy consistently before the baseline scan (defined as continued statin treatment), while 179 patients (62.3%) had commenced statin therapy after the baseline scan but before the follow-up scan (classified as new statin therapy). Notably, plaque regression was observed in 79 patients (28%), notably more frequent in those with higher baseline LDL-C levels and individuals who achieved a &gt;25% reduction in LDL-C (P &lt; 0.001). The median annual progression of TP was 1.9 (interquartile range [IQR] = −3.6 to 11.8), while for NCP, it was 1.5 (IQR = −4.6 to 11.0). In a multivariate logistic regression analysis, plaque regression demonstrated independent associations with LDL-C reduction exceeding 25% (odds ratio [OR] = 2.103, 95% confidence interval [95% CI] = 1.408–3.836) and baseline LDL-C levels (OR = 1.024, 95% CI = 1.004–1.044). Conclusions: Modest LDL-C reduction was associated with computed tomography angiography (CTA) evidence of coronary plaque regression and stabilization. The plaque regression is particularly marked in patients with a high baseline LDL-C level and LDL-C reduction of &gt;25%.

First-in-Human Drug-Eluting Balloon Treatment of Vulnerable Lipid-Rich Plaques: Rationale and Design of the DEBuT-LRP Study.

Patients with non-obstructive lipid-rich plaques (LRPs) on combined intravascular ultrasound (IVUS) and near-infrared spectroscopy (NIRS) are at high risk for future events. Local pre-emptive percutaneous treatment of LRPs with a paclitaxel-eluting drug-coated balloon (PE-DCB) may be a novel therapeutic strategy to prevent future adverse coronary events without leaving behind permanent coronary implants. In this pilot study, we aim to investigate the safety and feasibility of pre-emptive treatment with a PE-DCB of non-culprit non-obstructive LRPs by evaluating the change in maximum lipid core burden in a 4 mm segment (maxLCBImm4) after 9 months of follow up. Therefore, patients with non-ST-segment elevation acute coronary syndrome underwent 3-vessel IVUS-NIRS after treatment of the culprit lesion to identify additional non-obstructive non-culprit LRPs, which were subsequently treated with PE-DCB sized 1:1 to the lumen. We enrolled 45 patients of whom 20 patients (44%) with a non-culprit LRP were treated with PE-DCB. After 9 months, repeat coronary angiography with IVUS-NIRS will be performed. The primary endpoint at 9 months is the change in maxLCBImm4 in PE-DCB-treated LRPs. Secondary endpoints include clinical adverse events and IVUS-derived parameters such as plaque burden and luminal area. Clinical follow-up will continue until 1 year after enrollment. In conclusion, this first-in-human study will investigate the safety and feasibility of targeted pre-emptive PE-DCB treatment of LRPs to promote stabilization of vulnerable coronary plaque at risk for developing future adverse events.

Effect of PCSK9 antibodies on coronary plaque regression and stabilization derived from intravascular imaging in patients with coronary artery disease: A meta-analysis

BackgroundDespite extensive evidence demonstrating the beneficial effects of the additional PCSK9 antibodies with high-density statins treatment on cardiovascular clinical outcomes, the potent causes underlying these effects remain elusive. This meta-analysis aimed at exploring the underlying causes to assess the effect of PCSK9 antibodies on the regression and stabilization of coronary plaque derived from intravascular imaging in statin-treated patients with coronary artery disease (CAD). MethodsPubMed, Embase, and Cochrane Library were searched from inception to February 1, 2023, for randomized controlled trials (RCTs), nonrandomized studies without language restrictions if they described the association between PCSK9 antibodies with coronary plaque regression and stabilization evaluated by intravascular imaging in statin-treated patients with CAD. Meta-analyses were performed for mean difference (MD) and odds ratio (OR) using a random-effects model. This study followed the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) reporting guideline. ResultsA total of 9 studies (7 RCTs and 2 non-RCTs) with 2290 CAD patients were identified and included. Among statin-treated CAD patients, the addition use of PCSK9 antibodies was associated with IVUS-derived percent atheroma volume (PAV) (4 studies with 1875 participants; MD, −1.26; 95% CI, −1.51 to −1.00; P < 0.01), total atheroma volume (TAV) (4 studies with 1875 participants; MD, −7.23; 95% CI, −11.28 to −3.18; P < 0.01), incidence of PAV regression (4 studies with 1875 participants; OR, 2.24; 95% CI, 1.81 to 2.77; P < 0.01) and incidence of TAV regression (3 studies with 1256 participants; OR, 1.66; 95% CI, 1.33 to 2.09; P < 0.01) in Caucasians instead of Asians from multiple countries; OCT-derived minimum fibrous cap thickness (FCT) (6 studies with 841 participants; MD, 25.16; 95% CI, 14.06 to 36.27; P < 0.01), incidence of thin-capped fibroatheroma (TCFA) regression (2 studies with 222 participants; OR, 2.56; 95% CI, 1.42 to 4.61; P < 0.01) and maximum lipid arc (4 studies with 280 participants; MD, −14.96; 95% CI, −22.10 to −7.83; P < 0.01) in Asians and Caucasians without races restrictions. ConclusionsPCSK9 antibodies resulted in significantly greater coronary plaque regression and stabilization in statin-treated CAD patients, mostly Caucasians from multiple countries. Further studies are needed to assess the effect for Asian patients.

High dietary inflammatory index is associated with decreased plaque stability in patients with coronary heart disease

Coronary plaque stability is a key pathological mechanism of coronary heart disease (CHD). Inflammation is recognized as a key factor of coronary plaque stability. The dietary inflammatory index (DII) is calculated from 21 dietary nutrients to predict the inflammation potential of an individual's diet. We hypothesized that high DII may be associated with decreased coronary plaque stability in CHD patients; therefore, this study aimed to evaluate the association between DII and plaque stability in patients with CHD. This cross-sectional study included 314 patients with CHD. DII was calculated based on food frequency questionnaires. Plaque stability was measured with optical coherence tomography. The DII ranged from –1.41 to 3.04. After adjusting for confounding factors, higher DII scores were associated with unstable plaque characteristics including thin-capped fibroatheroma (odds ratio [OR], 3.60; 95% confidence interval [CI], 1.78–7.29), macrophage infiltration (OR, 2.16; 95% CI, 1.01–4.61), and plaque rupture (OR, 3.55; 95% CI, 1.73–7.29). Mediation analyses revealed that DII was important mediator of the relationship between plaque stability and food intake including soybeans and nuts, fish and shrimp, eggs (P < .05). The present study confirmed that higher DII is significantly associated with decreased plaque stability in CHD patients, suggesting an important protective role of anti-inflammatory diets in the pathogenesis of CHD.

Associations of High-Density Lipoprotein Functionality with Coronary Plaque Characteristics in Diabetic Patients with Coronary Artery Disease: Integrated Backscatter Intravascular Ultrasound Analysis.

High-density lipoprotein (HDL) functionality has been reported to be associated with coronary artery disease (CAD). However, little is known about the impact of HDL functionality on coronary atherosclerosis. Thirty-eight type 2 diabetic patients with CAD who underwent percutaneous coronary intervention were examined. Coronary atheroma burden and plaque composition of the culprit lesions were assessed using conventional gray-scale and integrated backscatter intravascular ultrasound. HDL-mediated cholesterol efflux capacity (HDL-CEC) and HDL antioxidant capacity, estimated as HDL inflammatory index (HII), were examined. The associations between HDL functionality and coronary plaques were analyzed using multivariate data analysis, including principal components analysis and orthogonal partial least squares (OPLS) models. Percent atheroma volume was correlated with HDL-CEC (r = 0.34, p = 0.04) but not with HII (p = 0.65). The OPLS model demonstrated that the percentage lipid volume was significantly associated with HDL functionality [coefficient (95% confidence interval); HDL-CEC: -0.26 (-0.49, -0.04); HII: 0.34 (0.08, 2.60), respectively]. HII exhibited the highest variable importance in projection score, indicating the greatest contribution. HDL functionality was associated with coronary plaque composition, a key component of plaque vulnerability. Our findings highlight the potential importance of HDL functionality for coronary plaque stabilization.

449-P: Truncations of Apolipoproteins C-I and C-II Are Associated with Coronary Artery Calcium Progression in Multiethnic Study of Atherosclerosis (MESA)

Higher truncated-to-native proteoform ratios of apolipoproteins (apo) C-I (C-I’/C-I) and C-II (C-II’/C-II) are associated with less atherogenic lipid profiles, including lower triglycerides (TG) and higher HDL levels. Here we examined the relationships of C-I’/C-II and C-II’/C-II, and total apoC-I and apoC-II concentrations with coronary artery calcium (CAC) progression. Apo C-I and C-II proteoforms were measured by mass spectrometry immunoassay in 5,791 baseline MESA plasma samples. Total apo C-I and C-II concentrations were assayed in 3,851 samples. CAC was measured 1 to 4 times (mean 2.5) over 10 years. Repeated measures regression models were adjusted for age, gender, race/ethnicity, and follow-up time (Model 1), then for BMI, diabetes, systolic BP, use of tobacco, statins and antihypertensive medications (Model 2), and then for plasma HDL and TG (Model 3). Among 5,069 participants with at least one follow-up CAC CT scan, 2,513 had CAC progression defined as events of CAC changing from 0 to &amp;gt; 0, or ≥ 10 units/yr from CAC &amp;gt; 0 but ≤ 100, or ≥ 10%/yr from CAC &amp;gt; 100. Progression was inversely associated with C-I’/C-I (Risk Ratio per 1 SD: 0.93 [95% CI 0.87, 0.97], Model 3). In those with baseline CAC = 0 (n = 2,581), risk of CAC &amp;gt; 0 (897 events) was inversely associated with C-I’/C-I in Model 1 only (0.85 [0.79, 0.93]). In those with baseline CAC &amp;gt; 0, C-II’/C-II was positively associated with follow-up change in density score (β-estimate per 1 SD 0.02 [95% CI: 0.001, 0.03] units) in Model 3, indicating a potentially more stable plaque. Baseline-adjusted follow-up density score was also positively related to total apoC-I in Model 2 (0.02 [0.004, 0.04]). None of the CAC measures were related to total apoC-II. In conclusion, increased truncation of apo C-I and C-II is associated with reduced CAC progression and/or improved stability of coronary atherosclerotic plaque that is not explained by total concentrations of both apolipoproteins. Disclosure J.Koska: None. J.Furtado: Employee; Biogen. Y.Hu: None. D.Billheimer: Advisory Panel; AstraZeneca. M.Allison: None. M.Budoff: Research Support; Novo Nordisk, Novartis, Boehringer Ingelheim Inc., Speaker's Bureau; Boehringer Ingelheim and Eli Lilly Alliance. D.Nedelkov: None. R.Mcclelland: None. P.Reaven: Research Support; Dexcom, Inc. Funding National Heart, Lung, and Blood Institute (R01HL138969, 75N92020D00001, HHSN268201500003I, N01HC95159, 75N92020D00005, N01HC95160, 75N92020D00002, N01HC95161, 75N92020D00003, N01HC95162, 75N92020D00006, N01HC95163, 75N92020D00004, N01HC95164, 75N92020D000

Is electrical neuromodulation able to affect the extent and stability of coronary atheromatous plaques?

Is electrical neuromodulation able to affect the extent and stability of coronary atheromatous plaques?

Correlation between coronary artery plaque composition ratio and plaque stability evaluated by 124-layer CT.

Correlation between coronary artery plaque composition ratio and plaque stability evaluated by 124-layer CT.

The potential role of SARS‐CoV‐2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread

Coronavirus disease 2019 (COVID-19) is a novel pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It has been shown that SARS-CoV-2 infection-induced inflammatory and oxidative stress and associated endothelial dysfunction may lead to the development of acute coronary syndrome (ACS). Therefore, this review aimed to ascertain the link between severe SARS-CoV-2 infection and ACS. ACS is a spectrum of acute myocardial ischemia due to a sudden decrease in coronary blood flow, ranging from unstable angina to myocardial infarction (MI). Primary or type 1 MI (T1MI) is mainly caused by coronary plaque rupture and/or erosion with subsequent occlusive thrombosis. Secondary or type 2 MI (T2MI) is due to cardiac and systemic disorders without acute coronary atherothrombotic disruption. Acute SARS-CoV-2 infection is linked with the development of nonobstructive coronary disorders such as coronary vasospasm, dilated cardiomyopathy, myocardial fibrosis, and myocarditis. Furthermore, SARS-CoV-2 infection is associated with systemic inflammation that might affect coronary atherosclerotic plaque stability through augmentation of cardiac preload and afterload. Nevertheless, major coronary vessels with atherosclerotic plaques develop minor inflammation during COVID-19 since coronary arteries are not initially and primarily targeted by SARS-CoV-2 due to low expression of angiotensin-converting enzyme 2 in coronary vessels. In conclusion, SARS-CoV-2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin-angiotensin system may aggravate underlying ACS or cause new-onset T2MI. As well, arrhythmias induced by anti-COVID-19 medications could worsen underlying ACS.

1 - A spatial transcriptomic approach to understanding coronary atherosclerotic plaque stability

1 - A spatial transcriptomic approach to understanding coronary atherosclerotic plaque stability

Clinical case of medical treatment of chronic coronary syndrome at E Hospital

Coronary artery disease is a leading cause of death and disability in developing and developed countries. In Vietnam, coronary artery disease has also become one of the leading causes of death.&#x0D; Chronic coronary syndrome is a disease related to the relative stability of coronary atherosclerotic plaque, in the absence of sudden rupture or after the acute phase or after intervention/surgery. As plaque progresses, causing significant narrowing of the coronary lumen (usually stenosis greater than 70% of the lumen diameter), symptoms may be present, most notably angina/dyspnea on exertion. and help when resting. Medical treatment of chronic coronary syndrome is an important issue. Two patients diagnosed as chronic coronary syndrome in 2015 received medical treatment after 5 years of coronary angiography from 80% of the left anterior descending and 60% of the left anterior descending with mild atherosclerosis. coronary artery disease in both patients.

Abstract 11206: Adipose-Derived Mesenchymal Stem Cells Overexpressing PD-L1 and Akt Confer Myocardial Protection Through Upregulation of CD25 + T Cells in a Rat Model of Acute Myocardial Infarction

Background: Translational studies showed positive results of stem cell therapy against myocardial infarction (MI)-induced cardiac dysfunction. Programmed death ligand 1 (PD-L1) is a key immune receptor, which modulates immune system and maintain the stability of coronary plaques. Akt is one of the signaling that exert its cardioprotective effect through regulating PD-L1. In the present study, we overexpressed PD-L1 and Akt in adipose-derived mesenchymal stem cells (AdMSC) and determined the protection against MI. Methods and Results: Adult Wistar rats were randomly separated into four groups: sham, MI, treatment of AdMSC or AdMSC overexpressed with PD-L1 and Akt (AdMSC-PDL1-Akt) immediately after MI. MI was induced by LAD ligation and ADMSC were injected into the heart around the area at risk. After 4 weeks, rats were examined by echocardiography, pressure-volume analysis, infarct size measurement, and immunohistochemistry to evaluate the efficacy of the ADMSCs on myocardium. Results demonstrated AdMSC-PDL1-Akt was more resistant to ROS in vitro , and could restore MI-induced contractile dysfunction in vivo by increasing ESPVR (P=0.048) and PRSW (P=0.015). AdMSC-PDL1-Akt could also protect hearts from MI-increased infarct size (P=0.002). Immunohistochemistry staining with caspase 3 and NFκB were upregulated in MI hearts and significantly reversed in AdMSC-PDL1-Akt group (P&lt;0.001 and P=0.036). To clarify mechanisms underlying the effect of AdMSC-PDL1-Akt, we found it could induce normal T cells into CD25 + regulatory T cells in vitro , which is in parallel with the data shown in our in vivo immunohistochemistry study that CD25 was upregulated in AdMSC-PDL1-Akt tissues (P=0.03). Conclusions: Overexpression of PD-L1 and Akt in AdMSC could increase its resistance to ROS-related apoptosis in vitro and enhance the protective effects against MI-induced cardiac dysfunction through modulation of T cells in vivo . Keywords: AdMSC; PD-L1; myocardial infarction; regulatory T cells

Relationship between nonalcoholic fatty liver disease and coronary plaque stability and risk factors for composite cardiovascular adverse events

Relationship between nonalcoholic fatty liver disease and coronary plaque stability and risk factors for composite cardiovascular adverse events

Circulating long non-coding RNA Coromarker expression correlated with inflammation, coronary artery stenosis, and plaque vulnerability in patients with coronary artery disease.

The aim of the study was to assess the correlation between circulating long non-coding RNA (lncRNA) OTTHUMT00000387022 (named Coromarker) expression and disease severity, inflammatory cytokine levels, and plaque vulnerability in patients with coronary artery disease (CAD). A total of 134 participants who received coronary angiography were enrolled and classified them as CAD patients (N=89) and controls (N=45). Blood samples were obtained from all subjects. Quantitative polymerase chain reaction was used to evaluate Coromarker expression. The enzyme-linked immunosorbent test was used to measure inflammatory cytokines including high sensitivity C reactive protein (hsCRP), interleukin (IL)-1β (IL-1β), IL-6, NOD-like receptor protein 3 (NLRP3), and markers of coronary plaque stability including matrix metallopeptidase 9 (MMP-9) and soluble CD40 ligand (sCD40L). The severity of coronary stenosis was determined from the Gensini Score. LncRNA Coromarker expression was elevated to a greater extent in CAD patients than in control subjects before and after adjustments for age/gender (both p < 0.001); it was an independent predictor of CAD risk (area under curve: 0.824, 95% CI: 0.732-0.915). Additionally, Coromarker expression was significantly associated with Gensini Score (r=0.574, p < 0.001), hsCRP (r=0.221, p=0.015), IL-1β (r=0.351, p < 0.001), IL-6 (r=0.286, p < 0.01), and NLRP3 levels (r=0.312, p < 0.001). Coromarker expression was found to be linked with MMP-9 (r=0.260, p < 0.01) and sCD40L (r=0.441, p < 0.001). Circulating lncRNA Coromarker expression correlates with increased disease severity and inflammation as well as plaque vulnerability in patients with CAD.