Background: The inflammatory response of the immune system plays a major role in the period following an acute myocardial infarction (MI), as it coordinates the formation of the fibrous scar tissue that replaces the infarcted myocardial cells and ultimately leads to healing and remodeling of the affected zone. Along with other pro- and anti-inflammatory cytokines and acute phase proteins, interleukin-6 (IL-6) and C-reactive protein (CRP) are associated with the extent of the infarct size (IS) and may serve as predictors for remodeling and adverse left ventricular (LV) function. Material and methods: A single-center, non-randomized, observational prospective study was conducted, which included 75 patients with primary revascularized ST-elevation myocardial infarction (STEMI). High-sensitivity CRP (hs-CRP) serum levels were determined on day 1 and day 5 following the acute event. IL-6 was also determined on day 1. All patients underwent cardiac magnetic resonance imaging (CMR) at 1-month follow-up with determination of LV function and quantification of the scar tissue using late gadolinium enhancement imaging. The patients were divided into 2 groups based on baseline hs-CRP values. Results: Patients with higher baseline hs-CRP levels presented significantly higher infarct size (p = 0.0003), higher transmural extent (p <0.0001), lower LV ejection fraction (p = 0.0024), end-systolic (p = 0.0021) and end-diastolic (p = 0.0065) volumes. Small IS (<10%) recorded the lowest levels of hs-CRP, while IS >20% presented the highest levels of hs-CRP, at baseline and day 5 (p = 0.4 and 0.001). IL-6 levels were also associated with the magnitude of infarct scar: 2.17 pg/mL for IS <10%, 15.52 pg/mL for IS between 10% and 20%, and 24.52 pg/mL for IS >20%, p = 0.002. Conclusion: hs-CRP and IL-6 serum levels following an MI are correlated with IS, transmurality extent of the scar tissue, as well as with altered systolic and diastolic LV function determined by CMR at 1-month follow-up.

Background: The independent role of each plaque feature in relation to plaque vulnerability is still the subject of ongoing research. This study aimed to compare the morphologic characteristics of vulnerable atheromatous coronary plaques with the ones of stable, non-vulnerable plaques, and in plaques with different locations in the coronary tree, in order to identify the most relevant imaging-based biomarkers associated with coronary plaque vulnerability. Material and methods: This was a prospective observational, non-randomized study that included 50 patients with unstable angina who underwent computed tomography angiography for assessment of the entire coronary artery tree followed by complex morphologic analysis of all lesions, divided into two groups: group 1 – 25 patients with vulnerable plaque (VP) and group 2 – 25 age- and gender-matched patients with non-vulnerable plaque (NVP). Results: Lesions with a stenosis degree >70% were significantly longer than those with a stenosis degree <70% (8.27 ± 2.74 mm vs. 5.56 ± 4.11 mm, p = 0.04). VP presented significantly higher values of plaque thickness (p = 0.0005), plaque burden (p = 0.0004), and higher total plaque volume (p = 0.0005) than NVP. The remodeling index was not significantly different between the groups (p = 0.6), but the eccentricity index was (0.24 ± 0.14 compared to 0.14 ± 0.17, p = 0.023). Linear regression analysis revealed a significant correlation between plaque burden and plaque components in VP (r = 0.76, p <0.0001 for necrotic core; r = 0.62, p = 0.0008 for fibro-fatty tissue; and r = 0.5, p = 0.01 for fibrotic tissue volume). Culprit plaques located in the right coronary artery presented significantly larger plaque burden volumes (91.17 ± 4.88 mm3 vs. 83.35 ± 8.47 mm3, p = 0.04), larger volumes of necrotic core (82.03 ± 47.85 mm3 vs. 45.84 ± 43.72 mm3, p = 0.02) and fibrofatty tissue (53.23 ± 31.92 mm3 vs. 23.76 ± 20.90 mm3, p = 0.02) than the ones situated in the left coronary artery. Conclusions: VPs from the culprit lesions exhibit a different phenotype than non-vulnerable ones, and vulnerability features are present in a significantly larger extent in VPs from the right coronary artery as compared to those from the left coronary artery.

Background: Epicardial adipose tissue (EAT) has been recently identified as a major player in the development of the atherosclerotic process. This study aimed to investigate the role of EAT as a marker associated with a higher vulnerability of atheromatous coronary plaques in patients with acute myocardial infarction (AMI) as compared to patients with stable angina. Material and methods: This analysis enrolled a total of 89 patients, 47 with stable angina (SA) and 42 with AMI, who underwent echocardiographic investigations and epicardial fat measurement in 2D-parasternal long axis view. The study lot was divided as follows: Group 1 included patients with prior AMI, and Group 2 included patients with SA. Results: There were no significant differences between the two groups regarding cardiovascular risk factors, excepting smoking status, which was recorded more frequently in Group 1 as compared to Group 2 (36.17% vs. 11.63%, p = 0.02). The mean epicardial fat diameter was 9.12 ± 2.28 mm (95% CI: 8.45-9.79 mm) in Group 1 and 6.30 ± 2.03 mm (95% CI: 5.675-6.93 mm) in Group 2, the difference being highly significant statistically (p <0.0001). The mean value of left ventricular ejection fraction was significantly lower in patients with AMI (Group 1 -47.60% ± 7.96 vs. Group 2 -51.23% ± 9.05, p = 0.04). EAT thickness values showed a weak but significant positive correlation with the level of total cholesterol (r = -0.22, p = 0.03) and with the value of end-systolic left ventricle diameter (r = 0.33, = 0.001). Conclusions: The increased thickness of EAT was associated with other serum-or image-based biomarkers of disease severity, such as the left ventricular ejection fraction, end-systolic diameter of the left ventricle, and total cholesterol. Our results indicate that EAT is significantly higher in patients with acute coronary syndrome, proving that EAT could serve as a marker of vulnerability in cardiovascular diseases.

Background:The role of periplaque fat (PPF), as a fragment of the total epicardial adipose tissue, measured in the vicinity of a target coronary lesion, more specifically within the close proximity of a vulnerable plaque, has yet to be evaluated. The study aimed to evaluate the interrelation between PPF and coronary plaque vulnerability in patients with stable coronary artery disease (CAD). Secondary objective: evaluation of the relationship between the total pericardial fat and markers for plaque vulnerability. Materials and methods: We prospectively enrolled 77 patients with stable CAD, who underwent 128-multislice computed tomography coronary angiography (CTCA), and who presented minimum one lesion with >50% stenosis. CTCA analysis included measurements of: total pericardial fat and PPF volumes, coronary plaque characteristics, markers for plaque vulnerability -positive remodeling (PR), low attenuation plaque (LAP), spotty calcifications (SC,) napkin ring sign (NRS). Study subjects were divided into two categories: Group 1 -1 marker of plaque vulnerability (n = 36, 46.75%) and Group 2 -≥1 marker of vulnerability (n = 41, 53.25%). Results: The mean age of the population was 61.77 ± 11.28 years, and 41 (53.24%) were males. The analysis of plaque characteristics showed that Group 2 presented significantly longer plaques (16.26 ± 4.605 mm vs. 19.09 ± 5.227 mm, p = 0.02), remodeling index (0.96 ± 0.20 vs. 1.18 ± 0.33, p = 0.0009), and vessel volume (p = 0.027), and more voluminous plaques (147.5 ± 71.74 mm 3 vs. 207.7 ± 108.9 mm 3 , p = 0.006) compared to Group 1. Group 2 presented larger volumes of PPF (512.2 ± 289.9 mm 3 vs. 710.9 ± 361.9 mm 3 , p = 0.01) and of thoracic fat volume (1,616 ± 614.8 mm 3 vs. 2,000 ± 850.9 mm 3 , p = 0.02), compared to Group 1, but no differences were found regarding the total pericardial fat (p = 0.49). Patients with 3 or 4 vulnerability markers (VM) presented significantly larges PPF volumes compared to those with 1 or 2 VM, respectively (p = 0.008). There was a significant positive correlation between PPF volume and the non-calcified (r = 0.474, 95% CI 0.2797-0.6311, p <0.0001), lipid-rich (r = 0.316, 95% CI 0.099-0.504, p = 0.005), and fibro-fatty (r = 0.452, 95% CI 0.2541-0.6142, p <0.0001) volumes. The total pericardial fat was significantly correlated only with the volume of lipid-rich plaques (p = 0.02). Conclusions: Periplaque fat volume was associated with a higher degree of coronary plaque vulnerability. PPF was correlated with lipid-rich, fibro-fatty, and non-calcified plaque-related volumes, as markers for enhanced plaque vulnerability. PPF volume, assessed with native cardiac computed tomography, could become a novel marker for coronary plaque vulnerability.

Atrial fibrillation (AF) is the most frequent form of supraventricular arrhythmia in medical practice. It is characterized by chaotic electrical activity in the atria, which often leads to irregular and fast ventricular contractions. Pulmonary veins (PV) play an essential part in the genesis of AF. There are a series of risk factors that trigger the development and recurrence of AF after PV isolation. Despite advanced medical technology, the success rate of AF ablation is not satisfactory. The purpose of this study is to assess the preprocedural imaging and serum biomarkers linked to an increased recurrence of AF after PV isolation. The primary endpoint is represented by AF recurrence after PV isolation. In addition, the rate of cardiovascular death and the rate of major adverse cardiovascular events will be assessed in relation to the enlargement of the left atrium and the volume of epicardial adipose tissue surrounding the heart.

Funding Acknowledgements PlaqueImage Background The relationship between the degree of pulmonary hypertension (PH) and left ventricular performance in patients with systemic sclerosis is still a controversial issue in the literature. We aimed to conduct a comparative analysis of indexes characterizing left ventricular systolic and diastolic function, in two etiological types of pulmonary hypertension involving different pathophysiological mechanisms: PH caused by systemic sclerosis and PH caused by myocardial ischemia. Material and method We performed a prospective study on 83 patients (36 patients with documented PAH with a systolic pulmonary arterial pressure – sPAP of &gt;35 mmHg and 47 subjects with normal sPAP), out of which group 1 – with systemic sclerosis (n = 48); group 2 – significant coronary artery disease - CAD (n = 35). Patients of each group were divided in two subgroups based on the diagnosis of PH: group 1A - subjects with scleroderma and associated PH (n = 20), group 1B - subjects with scleroderma without PH (n = 28), group 2A - ischemic patients with associated PH (n = 16) and subgroup 2B - patients with ischemic disease without PH (n = 19). Results Patients in group 1 presented a significantly higher number of female subjects (p = 0.001) and a higher mean age (p = 0.009) compared to group 2. Patients with associated PH presented a significantly lower left ventricular ejection fraction (LVEF) compared to those without PH within the ischemic group (p = 0.023). There was a significant inverse correlation between the sPAP and LVEF in ischemic patients (r=-0.52, p = 0.001) as well as for scleroderma patients without PH (r=-0.51, p = 0.04). Tissue Doppler analysis of the left ventricular function indicated a significant negative correlation between the septal E’ value versus the sPAP and lateral E’ value versus the sPAP (r=-0.49, p = 0.002; r=-0.43, p = 0,008). Conclusions Intrinsic myocardial damage plays an important role in left ventricular systolic function even in the absence of PAH. Scleroderma patients present a less pronounced deterioration of the LVEF in response to pulmonary hypertension, indicating that in this group, additional compensatory mechanisms could be involved in the complex response of myocardium to elevated pulmonary pressures.

These authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.

Background: The impact of pulmonary arterial hypertension (PAH) on left ventricular performance in patients with scleroderma is still unknown. This study aims to perform a comparative echocardiographic analysis of left ventricular function between two different etiological varieties of PAH, namely PAH caused by systemic sclerosis as a representative of systemic inflammatory diseases and PAH caused by myocardial ischemia. Material and method: We conducted a prospective observational study on 82 patients, of which 36 were with documented PAH, with the systolic pressure in the pulmonary artery above 35 mmHg, and 46 were patients with normal pulmonary artery pressure. The study population was divided into two groups, based on the etiology of PAH: group 1 included patients diagnosed with scleroderma (n = 48); group 2 included patients with coronary artery disease (n = 35). Patients from each group were divided into two subgroups based on the diagnosis of PAH: subgroup 1A – subjects with scleroderma and associated PAH (n = 20); subgroup 1B – subjects with scleroderma without PAH (n = 28); subgroup 2A – ischemic patients with associated PAH (n = 16); and subgroup 2B – patients with ischemic disease without PAH (n = 19). Results: A significant difference between LVEF values in patients with PAH versus those without PAH in the ischemic group (p = 0.023) was recorded. Compared to scleroderma subjects, ischemic patients presented significantly lower values of LVEF in both PAH and non-PAH subgroups (p <0.0001 and p <0.0001, respectively). Linear regression analysis between sPAP and LVEF revealed a significant negative correlation only for the ischemia group (r = −0.52, p = 0.001) and the scleroderma 2B subgroup (r = −0.51, p = 0.04). Tissue Doppler analysis of left ventricular function revealed a significant impact of PAH on left ventricular diastolic performance in the ischemic group. Conclusions: Compared to patients with coronary artery disease, those with scleroderma present a less pronounced deterioration of LVEF in response to pulmonary arterial hypertension.