Background: Myocardial fibrosis is an important pathological feature of hypertrophic cardiomyopathy (HCM) and is associated with ventricular arrhythmias, disease progression, and adverse clinical outcomes. Cardiovascular magnetic resonance (CMR) with late gadolinium enhancement (LGE) is the reference non-invasive technique for myocardial fibrosis assessment; however, its availability may be limited. Global longitudinal strain (GLS) derived from transthoracic echocardiography (TTE) has emerged as a sensitive marker of myocardial dysfunction and may provide complementary information regarding myocardial involvement. Aim: The aim of our study was to evaluate the diagnostic value of transthoracic echocardiography (TTE) with 2D global longitudinal strain (GLS) to detect the degree of myocardial fibrosis (LGE) in patients with LV hypertrophy (LVH). Methods: A total of 95 consecutive patients referred for cardiovascular magnetic resonance (CMR) because of suspected hypertrophic cardiomyopathy or left ventricular hypertrophy were screened for eligibility. After applying exclusion criteria and excluding patients with alternative diagnoses or inadequate image quality, 83 patients were included in the final analysis. All the participants underwent both CMR and transthoracic echocardiography with GLS assessment. Results: The final study population included 83 patients (57.5 ± 13 years; 66% males). CMR confirmed HCM in 58 (70%) patients, including 23 with left ventricular outflow tract obstruction (LVOTO). The remaining patients demonstrated varying degrees of left ventricular hypertrophy that did not fulfill established diagnostic criteria for hypertrophic cardiomyopathy. Cardiovascular magnetic resonance studies (58 cases; 69%) showed a non-ischemic LGE in LV (23% of segments with LGE). GLS in patients with LGE was significantly lower than those without LGE (−13.9 ± 3.6 vs. −15.9 ± 2.7%, p = 0.01). The mean GLS was −14.52 ± 3.5% and showed a moderate positive correlation with the extent of myocardial fibrosis (LGE%LV; r = 0.45, p < 0.01). This relationship remained significant in multivariable regression analysis (standardized coefficient = 0.683; p < 0.05). Moreover, the transthoracic echocardiography GLS showed a significant association for LV LGE (−14.3%; AUC 0.658; p = 0.01, sensitivity 39%, specificity 90%) with a better diagnostic performance for LGE in more than four LV segments (−12.1%; AUC 0.867; p < 0.001, sensitivity 72%, specificity 87%). Conclusions: GLS was independently associated with myocardial fibrotic burden assessed by CMR. Although it cannot replace CMR for tissue characterization, GLS may provide adjunctive information and may help identify patients with greater fibrotic burden. Prospective studies are needed to validate its clinical utility.

Background: Familial hypercholesterolemia (FH) is associated with accelerated atherosclerosis and an increased risk of cardiovascular disease. Aims: To evaluate circulating biomarkers of inflammation and atherosclerosis in patients with clinically suspected FH stratified according to the Dutch Lipid Clinic Network (DLCN) criteria. Methods: This cross-sectional study included 80 patients (mean age, 53.4 [13.2] years; 58% women) receiving maximally tolerated lipid-lowering therapy (statins ± ezetimibe). Serum concentrations of lipoprotein-associated phospholipase A₂ (Lp-PLA₂), tumor necrosis factor-α (TNF-α), apolipoprotein B (ApoB), oxidized low-density lipoprotein (oxLDL), and monocyte chemoattractant protein-1 (MCP-1) were measured. Participants were classified as definite FH (DLCN score > 8; n = 45) or non-definite FH (DLCN score ≤ 8; n = 35). Biomarker concentrations were analyzed according to the above subgroups and sex. Results: Patients with definite FH had significantly higher serum Lp-PLA₂ concentrations (62.2 [33.8] vs. 46.5 [19.9] ng/mL; p = 0.03) and TNF-α concentrations (6.94 [4.53] vs. 4.51 [2.93] pg/mL; p = 0.02) compared to non-definite FH, whereas ApoB, oxLDL, and MCP-1 concentrations did not differ significantly between the subgroups. Women had significantly higher TNF-α concentrations compared to men (6.57 [4.74] vs. 4.60 [2.20] pg/mL; p = 0.04) with no differences among other cytokines. Conclusions: Patients with definite FH exhibited persistently higher circulating Lp-PLA₂ and TNF-α concentrations despite maximally tolerated lipid-lowering therapy, suggesting ongoing activation of specific inflammatory pathways. These findings support further investigation of Lp-PLA₂ and TNF-α as candidate biomarkers for cardiovascular risk assessment in FH.

Background: Cardiovascular (CV) risk estimation is usually based on the assessment of classic risk factors and the extent of coronary artery stenosis. However, a substantial rate of acute coronary syndromes (ACS) and sudden cardiac deaths (SCD) is observed in patients with high-risk atherosclerotic plaques (HRP), even in the absence of significant stenosis. Therefore, this study aimed to evaluate the predictive value of traditional clinical risk factors for the presence of HRP in patients scheduled for coronary computed tomography (CCT). Methods: This single-center study included 123 patients undergoing CCT for suspected coronary artery disease (CAD). Atherosclerotic plaque morphology (HRP) and the degree of coronary artery stenosis (CAD-RADS categories) were assessed in all the patients. CV risk factors, including LDL serum levels and CT Calcium score (CS), were analyzed. Results: The study cohort was mostly males (54.5%), with an average age of 60.40 ± 12.45 years and typical risk factors: hypertension (70%), diabetes (22%), obesity (30%), and smoking (20%). Most patients (88%) were found to have coronary atherosclerosis with nonobstructive disease (CAD-RADS 1–2) in 39% of patients. HRP was confirmed in over one-fifth of the participants (22%), with half of the patients in the CAD-RADS 2 category. There were no differences in CV risk factors between patients with and without HRP in CCT. No significant clinical predictor of HRP in CCT was identified. Conclusions: CV risk factors do not predict HRP in CCT, which may underestimate the real risk of ACS and SCD.