Progression Of Coronary Atherosclerosis Research Articles

ASSOCIATIONS BETWEEN SMOKING HABITS AND MAJOR ADVERSE CARDIOVASCULAR EVENTS IN PATIENTS WHO UNDERWENT CORONARY COMPUTED TOMOGRAPHY ANGIOGRAPHY

Abstract Objective: We analyzed that smoking could induce major adverse cardiovascular events (MACE) and the progression of coronary atherosclerosis as assessed by coronary computed tomography angiography (CCTA) as screening for coronary artery disease (CAD). Design and method: We enrolled 443 patients who had all underwent CCTA and either were clinically suspected of having CAD or had at least one cardiovascular risk factor. We divided the patients into smoking (past and current smoker) and non-smoking groups or males and females, and evaluated the presence of CAD and MACE (cardiovascular death, ischemic stroke, acute myocardial infarction and coronary revascularization) with a follow-up of up to 5 years. Results: %CAD in the smoking group was significantly higher than that in the non-smoking group. %MACE in males and smokers were significantly higher than those in females and non-smokers, respectively. Kaplan-Meier curves showed that smokers and females tended to show greater freedom from MACE than non-smokers and males, respectively (log-rank test p = 0.057 and p = 0.073, respectively). More interestingly, Kaplan-Meier curves also showed that non-smokers in females significantly greater freedom from MACE than smokers in females (p = 0.007), whereas there was no significant difference in freedom from MACE between non-smokers and smokers in males (p = 0.984). Although there were no significant predictors of MACE in all patients according to a multiple logistic regression analysis, smoking was useful for predicting MACE in females, but not males. Conclusions: Smoking was significantly associated with MACE in females, but not males, who underwent CCTA as screening for CAD. Various conventional risk factors may be associated with MACE in males.

Effect of GLP-1/GLP-1R on the Polarization of Macrophages in the Occurrence and Development of Atherosclerosis.

Aims To investigate the effect of GLP-1/GLP-1R on the polarization of macrophages in the occurrence and development of atherosclerosis. Methods Totally, 49 patients with coronary heart disease (CHD) and 52 cases of health control (HC) were recruited, all subjects accept coronary angiography gold standard inspection. One or more major coronary arteries (LM, LAD, LCx, and RCA) stenosis degree in 50% of patients as CHD group; the rest of the stenosis less than 50% or not seen obvious stenosis are assigned to the HC group. Flow cytometry were used to detect the percentage of (CD14+) M macrophages, (CD14+CD80+) M1 macrophages, (CD14+CD206+) M2 macrophages, and their surface GLP-1R expression differences in the two groups, using BD cytokine kit to detect the levels of IL-8, IL-1β, IL-6, IL-10, TNF, and IL-12p70. Results GLP-1R expression on the surface of total macrophages and M2 macrophages was different between the CHD group and the HC group (P < 0.05). There was no difference in the percentage of total, M1 or M2 macrophages (P > 0.05). Concentration of IL-8 in the HC group was higher than that in the CHD group (P < 0.05). There is no significant difference in the cytokine IL-1β, IL-6, IL-10, TNF, and IL-12p70 in the two groups (P > 0.05). After controlling for potential confounders including age, gender, smoking status (S.S.), drinking status (D.S.), HR, SBP, DBP, PP, TC, TG, HDL-C, LDL-C, GHbA1c, M, M1, M2, GLP-1R_M, GLP-1R_M1, GLP-1R_M2, IL-8, IL-1β, IL-6, IL-10, TNF, and IL-12p70 by multiple linear regression, decreasing Gensini Score was significantly associated with increased percentage of M1 macrophage. Conclusion GLP-1R agonist is independent of the hypoglycemic effect of T2DM and has protective effect on cardiovascular system. GLP-1R may regulate the polarization of macrophages toward M2, thus playing a protective role in the progression of coronary atherosclerosis.

Regression of human coronary artery plaque is associated with a high ratio of (18-hydroxy-eicosapentaenoic acid + resolvin E1) to leukotriene B4.

Inflammation in arterial walls leads to coronary artery disease (CAD). We previously reported that a high omega-3 fatty index was associated with prevention of progression of coronary atherosclerosis, a disease of chronic inflammation in the arterial wall. However, the mechanism of such benefit is unclear. The two main omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are precursors of specialized pro-resolving lipid mediators (SPMs)-resolvins and maresins-which actively resolve chronic inflammation. To explore whether SPMs are associated with coronary plaque progression, levels of SPMs and proinflammatory mediators (leukotriene B4 [LTB4 ] and prostaglandins) were measured using liquid chromatography-tandem mass spectrometry in 31 statin-treated patients with stable CAD randomized to either EPA and DHA, 3.36 g daily, or no EPA/DHA (control). Coronary plaque volume was measured by coronary computed tomographic angiography at baseline and at 30-month follow-up. Higher plasma levels of EPA+DHA were associated with significantly increased levels of two SPMs-resolvin E1 and maresin 1-and 18-hydroxy-eicosapentaenoic acid (HEPE), the precursor of resolvin E1. Those with low plasma EPA+DHA levels had a low (18-HEPE+resolvin E1)/LTB4 ratio and significant plaque progression. Those with high plasma EPA+DHA levels had either low (18-HEPE+resolvin E1)/LTB4 ratios with significant plaque progression or high (18-HEPE+resolvin E1)/LTB4 ratios with significant plaque regression. These findings suggest that an imbalance between pro-resolving and proinflammatory lipid mediators is associated with plaque progression and potentially mediates the beneficial effects of EPA and DHA in CAD patients.

Atherogenic index of plasma and the risk of rapid progression of coronary atherosclerosis beyond traditional risk factors

Background and aimsThe atherogenic index of plasma (AIP) has been suggested as a marker of plasma atherogenicity. This study aimed to assess the association between AIP and the rapid progression of coronary atherosclerosis using serial coronary computed tomography angiography (CCTA). MethodsA total of 1488 adults (60.9 ± 9.2 years, 58.9% male) who underwent serial CCTA with a median inter-scan period of 3.4 years were included. AIP was defined as the base 10 logarithm of the ratio of the concentrations of triglyceride to high-density lipoprotein cholesterol. Rapid plaque progression (RPP) was defined as the change of percentage atheroma volume (PAV) ≥1.0%/year. All participants were divided into three groups based on AIP tertiles. ResultsBaseline total PAV (median [interquartile range (IQR)]) (%) (group I [lowest]: 1.91 [0.00, 6.21] vs. group II: 2.82 [0.27, 8.83] vs. group III [highest]: 2.70 [0.41, 7.50]), the annual change of total PAV (median [IQR]) (%/year) (group I: 0.27 [0.00, 0.81] vs. group II: 0.37 [0.04, 1.11] vs. group III: 0.45 [0.06, 1.25]), and the incidence of RPP (group I: 19.7% vs. group II: 27.3% vs. group III: 31.4%) were significantly different among AIP tertiles (all p < 0.05). In multiple logistic regression analysis, the risk of RPP was increased in group III (odds ratio: 1.52, 95% confidence interval: 1.02–2.26; p = 0.042) compared to group I after adjusting for clinical factors and baseline total PAV. ConclusionsBased on serial CCTA findings, AIP is an independent predictive marker for RPP beyond traditional risk factors.

Cardiovascular risk factors and illicit drug use may have a more profound effect on coronary atherosclerosis progression in people living with HIV.

To assess whether HIV infection directly or indirectly promotes coronary artery disease (CAD) volume progression in a longitudinal study of African Americans. We randomly selected 300 individuals with subclinical CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV infected, 174 cocaine users) from 1429 cardiovascularly asymptomatic participants of a prospective epidemiological study between May 2004 and August 2015. Individuals underwent coronary CT angiography at two time points (mean follow-up: 4.0 ± 2.3 years). We quantified noncalcified (NCP: -100-350HU), low-attenuation noncalcified (LA-NCP: -100-30HU), and calcified (CP: ≥ 351 HU) plaque volumes. Linear mixed models were used to assess the effects of HIV infection, atherosclerotic cardiovascular disease (ASCVD) risk, and years of cocaine use on plaque volumes. There was no significant difference in annual progression rates between HIV-infected and HIV-uninfected regarding NCP (8.7 [IQR: 3.0-19.4] mm3/year vs. 4.9 [IQR: 1.5-18.3] mm3/year, p = 0.14), LA-NCP (0.2 [IQR: 0.0-1.6] mm3/year vs. 0.2 [IQR: 0.0-0.9] mm3/year, p = 0.07) or CP volumes (0.3 [IQR: 0.0-3.4] mm3/year vs. 0.1 [IQR: 0.0-3.2] mm3/year, p = 0.30). Multivariately, HIV infection was not associated with NCP (-6.9mm3, CI: [-32.8-19.0], p = 0.60), LA-NCP (-0.1mm3, CI: [-2.6-2.4], p = 0.92), or CP volumes (-0.3mm3, CI: [-9.3-8.6], p = 0.96). However, each percentage of ASCVD and each year of cocaine use significantly increased total, NCP, and CP volumes among HIV-infected individuals, but not among HIV-uninfected. Importantly, none of the HIV-associated medications had any effect on plaque volumes (p > 0.05 for all). The more profound adverse effect of risk factors in HIV-infected individuals may explain the accelerated progression of CAD in these people, as HIV infection was not independently associated with any coronary plaque volume. • Human immunodeficiency virus-infected individuals may have similar subclinical coronary artery disease, as the infection is not independently associated with coronary plaque volumes. • However, cardiovascular risk factors and illicit drug use may have a more profound effect on atherosclerosis progression in those with human immunodeficiency virus infection, which may explain the accelerated progression of CAD in these people. • Nevertheless, through rigorous prevention and abstinence from illicit drugs, these individuals may experience similar cardiovascular outcomes as -uninfected individuals.

The case of recurrent tako-tsubo syndrome on the background of coronary atherosclerosis

Takotsubo syndrome (TS) is characterized with a reversible disorder of left ventricular contractility. At present time, it is established that various factors, both psycho-emotional and clinical, can trigger this disease. Notably, according to current opinions, coronary atherosclerosis may accompany TS and not be its exclusion criteria as it was previously thought. This article presents a clinical case of TS relapse in a female patient aged 83 years at 5 years following the first episode associated with progression of coronary atherosclerosis.

Investigation of Lipid Metabolism in Dynamic Progression of Coronary Artery Atherosclerosis of Humans by Time-of-Flight Secondary Ion Mass Spectrometry.

Alterations in lipid metabolites in coronary artery tissues are phenotypic changes in the progression of atherosclerosis (AS). A full picture of the spatiotemporal distribution of lipid metabolites in coronary AS is needed for a deeper understanding of its pathology and the identification of potential biomarkers of disease progression. In this work, the changes in species, quantity, and distribution of lipid metabolites at different stages of AS, which were standardized by the disease areas, were analyzed through the high spatial resolution- and high sensitivity-time-of-flight secondary ion mass spectrometry (ToF-SIMS) under delayed extraction mode. Based on high lateral resolution imaging, we further analyzed the ToF-SIMS data extracted from the subregions of AS lesion tissues at different disease progression stages by semiquantitative comparison, clustering analysis (t-stochastic neighbor embedding and HCA), and KEGG enrichment. Thus, a much-detailed description of lipids' features in coronary AS was achieved. We constructed a ToF-SIMS mass spectrometry database of coronary AS lipids. 40 specific lipid metabolites with distinctive patterns between different pathological stages were obtained. Chemical imaging unveiled further details regarding the spatial distribution of lipids. Moreover, linoleic acid and arachidonic acid metabolic pathway were predicted to be critical in AS progression.

Prognostic value of pericoronary adipose tissue and coronary vascular function by cardiac 82Rb PET/CT imaging in patients with suspected coronary artery disease and normal myocardial perfusion imaging

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Pericoronary adipose tissue, due to its proximity to coronary arteries, has been proposed contribute to the progression of coronary atherosclerosis. Purpose The aim of this study was to evaluate the prognostic value of pericoronary fat thickness (PCFT), coronary artery calcium (CAC) score and myocardial perfusion reserve (MPR) by hybrid 82Rubidium (82Rb) PET/CT imaging in patients with suspected coronary artery disease (CAD) and normal myocardial perfusion imaging (MPI). Methods A total of 640 patients without overt CAD and with normal rest-stress 82Rb PET/CT MPI were studied. PCFT was calculated on CT images as the maximum fat thickness (mm) between heart surface and visceral epicardium surrounding the main coronary arteries. CAC score was categorized as 0, &amp;lt;400 or ≥400. MPR was considered reduced when &amp;lt;2. Endpoints events were cardiac death, nonfatal myocardial infarction and coronary revascularization. Results During a follow-up of 42 ± 13 months, 29 events occurred (cumulative event rate 5%). Patients with events were older (66 ± 13 vs. 60 ± 13 years, p &amp;lt; 0.01), had higher PCFT (13 ± 2 vs 11 ± 2 mm, p &amp;lt; 0.001), higher prevalence of CAC score ≥400 (48% vs. 21%, p &amp;lt; 0.01), and lower MPR (2.1 ± 0.7 vs. 2.7 ± 0.7, p &amp;lt; 0.001) compared to those without. A higher prevalence of MPR &amp;lt;2 was observed in patients with events (48% vs. 18, p &amp;lt; 0.001) compared to those without. Patients with reduced MPR had higher PCFT compared to those with normal MPR (12 ± 2 vs. 11 ± 1 mm, p &amp;lt; 0.01). A PCFT value of 11.2 mm was the best trade-off between sensitivity and specificity to detect a reduced MPR. Event rate was higher in patients above this threshold compared to those below (8% vs. 1.5%, p &amp;lt; 0.001). At Cox univariate analysis, age (p &amp;lt; 0.05), PCFT &amp;gt;11.2 mm (p &amp;lt; 0.001), CAC score ≥400 (p &amp;lt; 0.01), and MPR &amp;lt;2 (p &amp;lt; 0.001) were predictors of events. At multivariate analysis, only PCFT &amp;gt;11.2 mm and MPR &amp;lt;2 were independent predictors of events (both p &amp;lt; 0.01). At incremental analysis, adding PCFT &amp;gt;11.2 to a model including clinical data and MPR &amp;lt;2 increased the global chi-square from 26 to 35 (p &amp;lt; 0.01). Classification tree analysis produced 3 terminal groups. For patients with MPR &amp;lt;2, no further split was needed (event rate 12% vs. 3%, p &amp;lt; 0.001). On the contrary, patients with MPR ≥2 were further stratified by PCFT (event rate 7% in patients with and 0.3% in those without (p &amp;lt; 0.001) PCFT &amp;gt;11.2. Conclusions In patients with suspected CAD and normal stress MPI, coronary vascular dysfunction and high PCFT are associated with increased cardiac risk. PCFT could help in identifying patients at higher risk of events. Combined evaluation of anatomical and functional vascular abnormalities by 82Rb PET/CT might allow a better risk stratification.

Multislice computed tomography in the evaluation of coronary atherosclerosis dynamics: data three-year observation in patients with myocardial infarction-segment elevation ST and stenting of coronary arteries

The aim – to use multislice computed tomography (MSCT)-coronary angiography data to determine the presence of atherosclerotic process progression in coronary vessels in the dynamics of the three-year follow-up period in patients after STEMI and coronary artery stenting.Materials and methods. 66 MSCT-coronary angiography studies were performed in 19 men after primary myocardial infarction with ST-segment elevation (STEMI) and coronary artery stenting. All patients were male, ranging in age from 38 to 66 years, with a mean (Me 55.6; (Q1–Q3 (49–64)) years, and 18 of 19 (94.0 %) patients developed Q-MI. 1 patient (6 %) had non-Q-MI. A month after acute MI, patients underwent MSCT of the heart with coronary vascular contrast. Re-examination was performed one, two and three years after the development of STEMI. According to the results of MSCT coronary angiography determined the functional status of stents, as well as the presence or exclusion of signs of restenosis (about 50 % or more) or thrombosis 100 % – occlusion) in the stent coronary artery and in non-infarction-causing arteries. With the progression of atherosclerotic plaque, an increase in atherosclerotic plaque of more than 20 % was taken into account compared to the previous study.Results and discussion. By the end of the first year after MI in 11 of 19 (57.9 %) patients according to MSCT-coronary angiography, no progression of atherosclerotic lesions of the coronary arteries was observed. 1 patient (5.6 %) had stent restenosis, which was confirmed by CAG data. Progression of atherosclerotic lesions was observed in 7 patients (36.8 %), 3 of them (16.6 %) in the stent artery, and in 4 patients in the non-infarction-causing artery. In the second year after myocardial infarction, compared with the annual examination, in 6 of 14 (42.9 %) no progression of atherosclerosis was observed, and in 7 of 14 (50 %) progression of atherosclerotic lesions not in the stent artery, and only in 1 of 14 – progression of atherosclerosis in the stent artery. In the third year after the development of MI, 10 of 14 (71.4 %) had no progression of atherosclerosis, and 4 patients showed progression in both IOA and other arteries.Conclusions. MSCT coronary angiography is an informative method in assessing the functional status of stents and determining the progression of coronary atherosclerosis in the infarct-causing artery and other coronary arteries in patients after MI and coronary artery stenting in the dynamics of three-year follow-up. The lack of progression of atherosclerosis was accompanied by slightly lower levels of low-density lipoprotein cholesterol, compared with patients with progression of atherosclerosis.

Heart transplantation in diabetic recipients

Introduction . Heart transplantation (HT) in patients with preexisting type 2 diabetes (T2D) is associated with high risk of infectious and non-infectious complications (renal dysfunction, multifocal atherosclerosis, transplant coronary artery disease, etc.) that can negatively affect recipient survival in the early and late periods after HT. Objective: to assess the effect of pre-transplant T2D on early and long-term outcomes of HT based on a singlecenter retrospective study. Materials and methods . The study enrolled 891 recipients who underwent HT within the period 2011 to 2018, and were divided into two groups: main group (T2D) – recipients with pretransplant T2D (n = 80, 9.0%) and the control group (T2D-free) – recipients without T2D (n = 811, 91.0%). Recipients from both groups did not differ in terms of HT urgency (UNOS status) and the need for pre-transplant mechanical circulatory support (MCS). Results . At the time of the HT, recipients from the T2D group were older than the T2D-free recipients (54 [46; 59] years vs 48 [35; 56] years, p &lt; 0.001), they had a higher weight (p &lt; 0.001) and body mass index (p &lt; 0.001), coronary heart disease was more often their main disease (65.0% vs 36.5%, p &lt; 0.001), they had higher transpulmonary gradient (10.0 [7.0; 12.0] mm Hg vs 9.0 [6.0; 12.0] mm Hg, p = 0.024) and pulmonary vascular resistance (2.9 [2.2; 4.0] Wood units vs 2.5 [1.8; 3.4] Wood units, p = 0.038). In the pre-transplant period, the T2D group had pronounced manifestations of renal dysfunction and increased comorbidity. Recipients in both groups did not differ in terms of cardiac donor parameters, graft ischemia time, cardiopulmonary bypass time, and incidence of severe early heart graft dysfunction requiring MCS (12.5% vs 10.7%, p = 0.74). In the early post-transplant period, the T2D group had high requirements (100% vs 28.0%, p &lt; 0.001) and higher doses of insulin therapy. More pronounced manifestations of renal dysfunction and a greater need for renal replacement therapy (51.4% vs 27.9%, p = 0.003) did not affect artificial ventilation and ICU duration (6 [5; 10] days vs 6 [5; 10] days, p = 0.098), as well as hospital mortality ( 8.8% vs 8.5%, p = 0.895). The presence of pre-transplant T2D had no negative effect on the incidence of acute cardiac graft rejection, progression of transmissible coronary atherosclerosis, incidence and severity of cardiac graft vasculopathy, structure and severity of distant infectious and non-infectious complications, and post-transplant survival. Conclusion . With correct selection of recipients and choice of optimal tactics for their post-transplant management, the presence of pre-transplant T2D has no negative effect on early and long-term outcomes of HT.

Association of PHACTR1 intronic variants with the first myocardial infarction and their effect on PHACTR1 mRNA expression in PBMCs.

Myocardial infarction (MI) and underlining atherosclerosis are the main causes of death worldwide. Phosphatase and actin regulator 1 (PHACTR1) variants have been associated with early onset MI, coronary artery disease and carotid dissection. PHACTR1 mRNA expression has been detected in tissues and cells related to atherosclerosis. Nonetheless, the true effect of PHACTR1 on vascular diseases is still unknown. Our aim was to examine the association of PHACTR1 intronic variants, rs9349379, rs2026458 and rs2876300, with MI and multi-vessel disease (MVD) and to assess their effect on PHACTR1 and EDN1 mRNA expression in PBMCs of patients six months after MI. The study enrolled 537 patients with the first MI and 310 controls. Gene expression was assessed in 74 patients six months after MI and 37 healthy controls. Rs9349379, rs2026458, rs2876300 and relative mRNA expressions were detected by TaqMan® technology. The significant association between PHACTR1 variants and MI was not found, either individually or in haplotype. A higher frequency of rs2876300G-allele in MVD was rendered not significant after Bonferroni correction. PHACTR1 mRNA was significantly increased in PBMCs of patients six months after MI compared to controls (p=0.02). Patients that carry ACG haplotype have increased PHACTR1 mRNA expression in PBMCs (p=0.04). There was no effect of PHACTR1 variants on EDN1 mRNA expression. Our findings suggest that PHACTR1 intronic variants may have a role in severity and progression of coronary atherosclerosis. Future research is needed to clarify the mechanism underlying the role of PHACTR1 in coronary atherosclerosis and MI.

Hypertrophy and Insulin Resistance of Epicardial Adipose Tissue Adipocytes: Association with the Coronary Artery Disease Severity.

Changes in the structural and functional characteristics of the epicardial adipose tissue (EAT) are recognized as one of the factors in the development of cardiometabolic diseases. However, the generally accepted quantitative assessment of the accumulation of EAT does not reflect the size of adipocyte and presence of adipocyte hypertrophy in this fat depot. Overall contribution of adipocyte hypertrophy to the development and progression of coronary atherosclerosis remains unexplored. Objective: To compare the morphological characteristics of EAT adipocyte and its sensitivity to insulin with the CAD severity, as well as to identify potential factors involved in the realization of this relationship. The present study involved 24 patients (m/f 16/8) aged 53–72 years with stable CAD, who underwent coronary artery bypass graft surgery. Adipocytes were isolated enzymatically from EAT explants obtained during the operation. The severity of CAD was assessed by calculating the Gensini score according to selective coronary angiography. Insulin resistance of EAT adipocytes was evaluated by reactivity to insulin. In patients with an average size of EAT adipocytes equal to or exceeding the median (87 μm) the percentage of hypertrophic adipocytes was twice as high as in patients in whom the average size of adipocytes was less than 87 μm. This group of patients was also characterized by the higher rate of the Gensini score, lower adiponectin levels, and more severe violation of carbohydrate metabolism. We have revealed direct nonparametric correlation between the size of EAT adipocytes and the Gensini score (rs = 0.56, p = 0.00047). The number of hypertrophic EAT adipocytes showed a direct nonparametric correlation with the Gensini score (rs = 0.6, p = 0.002). Inverse nonparametric correlations were found between the serum adiponectin level and size (rs = −0.60, p = 0.001), hypertrophy of adipocytes (rs = −0.67, p = 0.00), and Gensini score (rs = −0.81, p = 0.00007). An inverse nonparametric correlation was found between the Gensini score and sensitivity of EAT adipocytes to insulin, estimated by the intracellular redox response (rs = −0.90, p = 0.037) and decrease in lipolysis rate upon insulin addition (rs = −0.40, p = 0.05). The intracellular redox response of adipocytes to insulin was directly correlated with fasting insulin and inversely with postprandial insulin. Our data indicate that the size and degree of hypertrophy of the epicardial adipocytes are related to the CAD severity. According to our results, insulin resistance of adipocytes may be considered as one of the factors mediating this relationship.

Analysis of the causes of repeat stenosis of the coronary arteries after elective stenting in patients with stable angina pectoris

Coronary stenting is the evidence-based treatment approach of stable angina. The objective was to determine the incidence of restenosis or atherosclerosis progression which led to the need for coronary angiography according to a single center registry data. The procedure and clinical data of 3732 (2897 males) consecutive stable coronary artery disease patients undergoing coronary stenting, over five years between March 2010 and September 2014, were subject of this study. Over the next 4 years, 1487 (1173 males) patients were re-evaluated due to angina reoccurrence. 699 patients demonstrated the indications for coronary angiography. The restenosis of the previously stented segment was detected in 84 (12%) cases, the progression of coronary atherosclerosis in 306 (44%), the combination of restenosis and atherosclerosis progression in 63 (9%), and the absence of these complications in 245 (35%) cases. The progression of coronary atherosclerosis was the leading indication for the repeat angiography and revascularization (44 and 58%, respectively); p0.05. The basal level of hsCRP2 mg/l had a prognostic significance for the development of combined event (the restenosis and atherosclerosis progression): AUC 0.65 (0.500.75), OR 3.0 (1.17.9), p0.05. The progression of coronary atherosclerosis was the leading indication for the repeat angiography and repeat revascularization during 2 years after coronary stenting. The hsCRP level 2 mg/l at baseline had a prognostic significance for the development of restenosis in previously stented segment and coronary atherosclerosis progression.

Early Progression of Coronary Atherosclerosis in Patients Following Liver Transplantation: Results From the Coronary Atherosclerosis Following Liver Transplant (CALT) Study

Sudden cardiac death is a leading cause of late mortality following liver transplantation (LT).

Epicardial Adipose Tissue Thickness as a Reliable Marker of Increased Cardiovascular Risk in Patients With Type 2 Diabetes Mellitus

Background: Epicardial adipose tissue (EAT) is a distinct visceral adipose tissue that is present in between the visceral pericardium and myocardium, in which the coronary arteries are lodged. This tissue releases several inflammatory and atherogenic mediators which lead to the initiation and/or progression of coronary atherosclerosis and its thickness is related to the presence and severity of atherosclerotic coronary artery disease (CAD). In this study, we aimed to evaluate the EAT thickness in type 2 diabetes mellitus (T2DM) patients by non-contrast computed tomography (NCCT) of the chest and to correlate its value with HbA1c levels, duration of T2DM and carotid intima-media thickness (CIMT). Methods: This was a cross-sectional study comprising of 40 patients with T2DM who underwent NCCT of chest and ultrasonographic estimation of CIMT. Ten individuals with equivalent age and sex were included as controls, in whom NCCT of chest was done for other purposes. All the individuals underwent thorough history, clinical examination and certain investigations based on a predesigned proforma. Results: The EAT thickness was significantly increased in patients with T2DM as compared to controls (8.7 ± 2.94 mm vs. 3.48 ± 0.99 mm, P < 0.001) and also strongly correlated with duration of diabetes (P = 0.02), HbA1c (P is less than or equal to 0.001), total cholesterol (P is less than or equal 0.001), serum triglyceride levels (P is less than or equal 0.001) and body mass index (BMI) (P is less than or equal 0.001). Conclusion: EAT thickness can be regarded as a sensitive and non-invasive marker for risk stratification of CAD. J Endocrinol Metab. 2020;10(6):173-181 doi: https://doi.org/10.14740/jem710

Current state-of-the-art knowledge on the role of omega-3 fatty acids in the prevention of cardiovascular disease.

Polyunsaturated n-3 fatty acid preparations containing eicosapentaenoic acid (EPA) and docosahexanaenoic acid (DHA), or EPA only, have long been recommended in the management of hypertriglyceridaemia, especially when severe (triglyceride levels ≥500mg/dL), at the dose of 2-4g/d, mostly for the prevention of acute pancreatitis. The presented article reviews clinical trials and their metaanalyses which evaluated the effect of n-3 fatty acids on cardiovascular disease risk, and regulatory agencies' and cardiac societies' positions regarding their use. The findings indicate that only EPA is effective. Particular clinical benefit (25% reduction of cardiovascular events) was observed in the recently published REDUCE-IT trial which evaluated EPA (icosapent ethyl) at the dose of 4 g/d for 4.9 years (median), compared to placebo, in hypertriglycerydaemic patients at high or very high cardiovascular risk. This positive effect has been reflected in the expert opinions which recommend eicosapent ethyl (4 g/d) in patients similar to those participating in the REDUCE-IT trial. Additional data in favour of the above position have been provided by the EVAPORATE trial results which showed reduced progression of coronary atherosclerosis with EPA at the dose of 4 g/d. The clinical studies and metaanalyses strongly point out that only EPA (icosapent ethyl), especially at dose of 4 g/d, is effective in reducing cardiovascular events in very high and high risk patients with hypertriglyceridemia. The use of EPA + DHA preparations in doses up to 1 g/d does not prevent recurrent cardiovascular events.

Beta-2-glycoprotein-I IgA antibodies predict coronary plaque progression in rheumatoid arthritis

ObjectivesTo evaluate whether anti-Beta-2-Glycoprotein-I (anti-β2GPI) IgA antibodies associate with progression of coronary atherosclerosis and cardiovascular disease (CVD) events in rheumatoid arthritis (RA). MethodsOne hundred-fifty patients underwent plaque evaluation (total, non-calcified, mixed and calcified) with coronary computed tomography angiography; 101 were re-imaged within 6.9±0.3 years to assess progression. The Framingham-D'Agostino score assessed cardiovascular risk. Coronary artery calcium (CAC) and segment involvement score quantified plaque burden. ResultsAnti-β2GPI IgA were seen in 45 (30%) patients. Despite no link to baseline plaque burden, anti-β2GPI IgA associated with segment involvement score increase (adjusted-RR=1.64 [95%CI 1.02–2.63]), CAC change (adjusted-β=0.33 [95%CI 0.002–0.656]) and developing new extensive or obstructive plaque at follow-up (adjusted-OR=4.24 [95%CI 1.30–13.87]). Adding anti-β2GPI IgA to logistic regression models with conventional risk factors predicting plaque progression outcomes increased Area under the receiver-operator curve and improved Net Reclassification and Integrated Discrimination Improvement indices (all P<0.05). In per-segment analyses, anti-β2GPI IgA predicted mixed plaque formation (adjusted-OR=3.20 [95%CI 1.01–10.09]) and lower likelihood of transition of mixed to calcified plaque (adjusted-OR=0.19 [95%CI 0.04–0.96]). Anti-β2GPI IgA moderated the effect of C-reactive protein on CAC change such that C-reactive protein associated with CAC change (β=0.26 [95%CI 0.14–0.38]) and CVD risk (adjusted-HR=1.89 [95%CI 1.02–3.51]) only in anti-β2GPI IgA positive patients. ConclusionAnti-β2GPI IgA addition to clinical risk models improved prediction accuracy of CAC, plaque progression and transition to extensive/obstructive disease. They associated with new high-risk mixed plaques and delayed healing to calcified lesions. Anti-β2GPI IgA further modified the effect of inflammation on plaque progression and CVD events.

Combination of chronic myocarditis and progressive coronary artery disease: differential diagnosis and stepwise treatment

Aim. To assess the differential diagnosis in a patient with a combination of coronary artery disease and myocarditis and the results of stepwise treatment (including immunosuppressive therapy (IST), and coronary stenting).Material and methods. A 56-year-old female patient with hypertension, obesity (body mass index, 31,6 kg/m2), diabetes and psoriasis developed shortness of breath after a respiratory viral infection. Primary echocardiography revealed left heart dilatation, ejection fraction (EF) of 21%. Coronary angiography revealed anterior descending artery stenosis of 75%, circumflex artery — 80%, right coronary artery (RCA) — 70%. RCA stenting was performed and cardiovascular and diuretic therapy was started. However, shortness of breath and low exercise tolerance persisted.Results. In the blood test, anti-endothelial cell antibodies were 1:320, anticardiomyocyte and anti-smooth muscle antibodies — 1:80, anti-cardiac conduction system fibers — 1:320 (N≤1:40). During myocardial perfusion scintigraphy with computed tomography, an uneven distribution of the indicator was noted. Signs of myocardial scarring and indications for further revascularization were not revealed. Cardiac magnetic resonance imaging confirmed a decrease in left ventricular (LV) contractility (LVEF 37%) and moderate dilatation. Biopsy was not performed due to dual antiplatelet therapy. The condition is regarded as infectious-immune myocarditis. IST was started with azathioprine 150 mg/day. We noted dyspnea relief and a stable increase in LVEF to 50-52%. The clinical course was complicated by sick sinus syndrome with pauses up to 6 seconds and presyncope; a pacemaker was implanted. After 5 years from the onset of IST, dyspnea episodes reappeared without exacerbation of myocarditis. As their cause, ischemia was diagnosed due to the progression of coronary atherosclerosis. Symptoms regressed after repeated coronary stenting.Conclusion. The presence of moderate coronary atherosclerosis without signs of ischemia and myocardial infarction should not be considered as the only cause of severe systolic myocardial dysfunction. Diagnosis and treatment of myocarditis in combination with coronary artery disease is carried out according to the standard principles and can improve LV systolic function and control the heart failure symptoms.

Epidemiology and pathophysiologic insights of coronary atherosclerosis relevant for contemporary non-invasive imaging.

In the past few years significant changes have taken place in the diagnostic and therapeutic approach to patients with coronary artery disease (CAD) and/or ischemic heart disease (IHD). New discoveries about the development and progression of coronary atherosclerosis have changed the clinical landscape. At the same time a marked decrease in cardiovascular (CV) mortality and CAD incidence have been observed in many Countries but particularly in the most industrialized ones. This fall has been also observed in the incidence of stroke, sudden death, myocardial ischemia, myocardial infarction (MI), and prevalence of CAD. As a consequence, an increasing number of patients with chest pain exhibits non-significant stenosis at both invasive and non-invasive coronary angiography and the rate of coronary vessels revascularizations has greatly reduced. Coronary atherosclerosis and its characteristics have shown to be both diagnostic and therapeutic targets beyond obstructive CAD. The decreased prevalence of CAD in the general population has modified the pre-test probability (PTP) of disease. In this landscape the conventional stress imaging tests appear to have limited accuracy making the diagnosis of obstructive CAD very challenging. These diagnostic tests have been introduced and tested in a population with a much higher probability of disease and therefore the contemporary accuracy of these old tests appear much lower than in the past. In addition, in the past few years the relevance of the traditional ischemia guided coronary intervention strategy has been questioned. Given the low CV events granted by an optimal medical therapy in CAD the major attention has been directed on detecting coronary atherosclerosis. The earlier the better. At the same time, a growing number of data from clinical studies have shown a significant prognostic role for non-obstructive CAD and coronary atherosclerosis. All these facts have shifted the clinicians' attention from the functional evaluation of the coronary circulation to the anatomic burden of disease.

Associations between smoking habits and major adverse cardiovascular events in patients who underwent coronary computed tomography angiography as screening for coronary artery disease.

We analyzed whether smoking was associated with major adverse cardiovascular events (MACE) and the progression of coronary atherosclerosis as assessed by coronary computed tomography angiography (CCTA) as screening for coronary artery disease (CAD). We enrolled 443 patients who had all undergone CCTA and either were clinically suspected of having CAD or had at least one cardiovascular risk factor. We divided the patients into smoking (past and current smoker) and non-smoking groups and into males and females, and evaluated the presence of CAD, severity of coronary atherosclerosis and MACE (cardiovascular death, ischemic stroke, acute myocardial infarction and coronary revascularization) with a follow-up of up to 5years. %CAD and the severity of coronary atherosclerosis in the smoking group were significantly higher than those in the non-smoking group. %MACE in males and smokers were significantly higher than those in females and non-smokers, respectively. Interestingly, Kaplan-Meier curves also showed that female non-smokers enjoyed significantly greater freedom from MACE than female smokers (p = 0.007), whereas there was no significant difference in freedom from MACE between male non-smokers and male smokers (p = 0.984). Although there were no significant predictors of MACE in all patients according to a multiple logistic regression analysis, smoking was useful for predicting MACE in females, but not males. In conclusion, smoking was significantly associated with MACE in females, but not males, who underwent CCTA as screening for CAD.