While the causes of acute coronary syndromes (ACSs) have been extensively studied, traditional cardiovascular risk factors do not completely explain the development and severity of ischemic heart disease in all individuals. As a result, incorporating additional biomarkers may improve the accuracy of predicting disease severity and refining risk stratification. This study aims to investigate the predictive value of inflammatory biomarkers—interleukin-1 receptor antagonist (IL-1RA), resistin, and C-reactive protein (CRP)—in assessing the severity of coronary lesions in patients with ACSs. By analyzing their association with coronary multivessel disease (MVD) using advanced imaging techniques and biomarker quantification, we seek to determine whether these markers can enhance risk stratification and improve early clinical decision-making in ACS patients. We assessed the potential role of three inflammatory markers (IL-1RA, resistin and CRP) as independent markers for the severity of coronary lesions in a cohort of patients with ACSs. The inclusion criteria were ACS in the first 7 days after the acute event with at least another coronary lesion apart from the culprit estimated to have a diameter stenosis ≥40% on coronary angiography, in subjects with life expectancy of at least one year. We accessed the severity of the non-culprit coronary lesions extensively with fractional flow reserve and optical coherence tomography. Using enzyme-linked immunosorbent assays method we determined the plasmatic concentrations of biomarkers at baseline (within 48h after the ACS) and at follow-up, at 6 months. Out of the included 93 patients, 59.1% presented with more than one significant coronary lesion and were included in the MVD. In univariate logistic regression, the baseline levels of resistin (OR=1.952, 95% CI=1.466-2.597, p=0.001) and CRP (OR=1.831, 95% CI=1.352-2.248, p=0.008) proved to be independent predictors for coronary multivessel disease. We categorized patients into four groups based on the number of biomarkers exceeding the established cut-off values (cut-offs for CRP 1583 ng/ml, resistin 12.2 ng/ml, IL-1RA 483.8 pg/ml). A statistically significant difference was observed between the SVD and MVD concerning the number of elevated biomarkers (p<0.001). Receiver Operating Characteristic curve (ROC) analysis showed that the two cytokines (AUC 0.92, p=0.001) have a better predictive value for MVD than each individual of these (CRP, AUC=0.81, p=0.004 and resistin, AUC=0.87, p=0.001). Baseline plasma levels of resistin and CRP serve as strong individual and combined predictors of coronary multivessel disease in patients with acute coronary syndrome (ACS). Their significant association with disease severity suggests that these inflammatory biomarkers could enhance early risk stratification and aid in identifying high-risk patients who may benefit from more intensive monitoring and therapeutic interventions

La cardiomyopathie hypertrophique est une maladie cardiaque génétique fréquemment rencontrée avec un développement continu depuis le premier rapport il y a plus de 60 ans. Le diagnostic de la maladie repose principalement sur l’échocardiographie, mais la résonance magnétique joue un rôle émergent apportant des informations précieuses pour le pronostic et la planification chirurgicale. Le traitement a évolué progressivement vers de nouvelles molécules prometteuses, les défibrillateurs cardiaques implantables, la myomectomie personnalisée et la plastie de la valve mitrale. Cette revue générale est concentrée sur le rôle de l’imagerie multimodale dans le diagnostic et la stratification de la maladie ainsi que sur le traitement personnalisé ayant comme but la baisse du risque de mort cardiaque subite afin d’atteindre une survie comparable à celle de la population générale de même âge.

Multiple causes of myocardial thickening may mimic hypertrophic cardiomyopathy (HCM) phenotypes. We present the case of a previously undiagnosed severe hypertensive patient with an incidentally discovered morphological and electrical HCM phenotype. The potential overlap of HCM, hypertensive heart disease, and other HCM phenocopies may lead to ambiguity in the absence of an adequate multi-modal differential diagnosis. Accurate diagnosis is mandatory for prognosis-tailored treatment, especially regarding the risk of sudden cardiac death and the complex decision of internal cardioverter-defibrillator implantation.

Abstract Funding Acknowledgements This work was supported by CREDO Project - ID: 49182, financed through the SOP IEC -A2-0.2.2.1-2013-1 cofinanced by the ERDF Background Echocardiographic assessment of diastolic dysfunction and left ventricular (LV) filling pressures is a complex and challenging process, requiring a multiparameter analysis. In recent years strain imaging has been emerging as a promising method for evaluation of left atrium (LA) function, being correlated with LV systolic dysfunction. Purpose We sought to evaluate LA mechanics in a cohort of patients with ischemic heart failure (HF) at one month after ST elevation myocardial infarction (STEMI) Material and methods 40 patients were enrolled in this study: 30 consecutive patients with ischemic HF after STEMI, with LVEF < 50% and 10 healthy age- and sex-matched controls. All patients had standard echocardiographic examination; also LA strain curves were obtained using speckle tracking with measurement of peak LA systolic strain. Categorization of diastolic dysfunction severity into 3 grades was realized according to 2016 guidelines. Results 2D and 3D LVEF (33% vs 55%, p = 0.00), LV global strain (-10 vs -19, p = 0.00) and peak LA systolic strain (16 vs 33, p = 0.00) were significantly reduced in HF patients compared to controls. In both groups LA strain correlated with the following parameters: 2D EF (p = 0.024), 3D EF (p = 0.02), LV global strain (p = 0.00), E/A (p = 0.05), septal e’ (p = 0.00), lateral e’ (p = 0.00), E/septal e’ (p = 0.006), E/lateral e’ (p = 0.003), E/mean e’ (p = 0.014), LA volume (p = 0.014) and LV filling pressures (p = 0.001). Peak LA systolic strain (PALS) values progressively decreased with worsening of diastolic function showing significant differences between all diastolic dysfunction grades. Using ROC analysis we identified 3 PALS thresholds to distinguish between normal diastolic function and the 3 diastolic dysfunction grades. The optimal cut off values were as follows: between normal diastolic function and grades 1-3 with PALS cut off value of 26.5 (Sb 90%, Sp 87%), AUC 0.963, CI 95%, p = 0.00; between grades 0-1 and grades 2-3 with peak LA strain cut off value of 17.2 (Sb 75%, Sp 93%) AUC = 0.828, CI 95%, p = 0.002; between grade 0-2 and grade 3 with peak LA strain cut off value of 11 (Sb 85%, Sp 93%), AUC 0.942, CI 95%, p = 0.00. Also, PALS value differed significantly between patients with normal vs high LV filling pressures. Using ROC analysis we determined a cut off value for LA of 15.1 to differentiate between the two subgroups with excellent discrimination power AUC 0.902, CI 95%, p = 0.00, Sb 88.9%, Sp 83% thus making LA strain an accurate surrogate estimate of LV filling pressures. Conclusions Global peak LA systolic strain is significantly correlated with LV systolic and diastolic function. PALS is a feasible option for detection and categorization of diastolic dysfunction in patients with HF and depressed LVEF after STEMI. Incorporating LA strain into noninvasive assessment of LV diastolic dysfunction may improve the detection of elevated LV filling pressures. Further large scale studies are needed to validate this data.