Introduction: Cardiovascular diseases are the leading cause of mortality worldwide, with a significant impact on socioeconomic aspects. Various biomarkers have been studied in relation to the diagnosis, progression, and prognosis of atherosclerotic disease, with lipoprotein (a) [Lp (a)] standing out as an important predictor of cardiovascular risk. This observational study aimed to clarify the association between Lp (a) levels and the severity of significant multivessel coronary lesions in acute myocardial infarction (AMI) patients. Materials and Methods: Conducted at the Clinical Emergency County Hospital of Craiova, Romania, the study involved 256 young patients divided into two groups based on Lp (a) levels: Group A (Lp (a) < 30 mg/dL) and Group B (Lp (a) ≥ 30 mg/dL). Patients included young adults up to 55 years for males and 60 years for females, excluding those with familial hypercholesterolemia. Results: The study revealed a significant association between elevated Lp (a) levels and the presence of multivessel coronary lesions. Patients with Lp (a) concentrations ≥ 30 mg/dL exhibited a higher prevalence of multivessel disease compared to those with lower levels. Discussion: The findings suggest that elevated Lp (a) levels are a crucial biomarker for the risk of coronary artery disease, particularly in young patients with AMI. The study emphasizes the need for aggressive lipid management strategies and personalized treatment approaches, considering the significant role of Lp (a) in atherosclerosis and AMI. Conclusions: Lipoprotein A levels above 30 mg/dL are associated with a higher prevalence of multivessel coronary lesions. Multivariate analysis revealed that higher Lp (a) levels and lower HDL levels are linked to an increased risk of multivessel coronary lesions.

Background and Objectives: This observational study investigates the relationship between Lipoprotein (a) (Lp(a)) levels and the risk of acute myocardial infarction (AMI). This study aims to highlight the association of elevated Lipoprotein (a) levels with an increased atherogenic profile and the potential risk of AMI. Materials and Methods: We conducted a case–control study involving 106 individuals, including 64 AMI patients (both STEMI and NSTEMI) and 42 healthy controls. Comprehensive clinical and biochemical assessments, including Lp(a) measurements, were conducted. Results: Patients with Lp(a) levels ≥ 30 mg/dL had a threefold increased risk of AMI compared to those with lower levels, independent of traditional risk factors such as cholesterol, smoking, and body weight. Elevated Lp(a) was observed in 50% of AMI patients compared to 28.57% in controls (p = 0.028). Notably, a multivariate analysis identified high Lp(a) levels, low HDL-C levels, and obesity as significant independent predictors of AMI, indicating these factors may contribute to AMI risk more prominently than other conventional risk factors in patients with elevated Lp(a). Moreover, the association between Lp(a) and AMI risk was consistent across various patient subgroups, with low HDL-C further compounding the risk. Conclusions: Lp(a) is a significant independent risk factor for acute myocardial infarction; therefore, screening for Lp(a) levels can help identify high-risk individuals beyond traditional markers. Therapeutic approaches targeting Lp(a) may reduce AMI incidence. Future research should explore how Lp(a) promotes atherosclerosis and assess Lp(a)-lowering therapies to improve patient outcomes.

Background: The incidence of acute myocardial infarction (AMI) in young adults has been steadily rising, emphasizing the need for new biomarkers to improve risk stratification. Lipoprotein(a) (Lp(a)), a genetically determined lipoprotein with pro-atherogenic and pro-thrombotic properties, has gained increasing attention in this context. Methods: We evaluated serum Lp(a) levels in young patients with AMI and compared them with healthy controls. Associations between elevated Lp(a) levels (≥30 mg/dL) and coronary artery disease patterns were analyzed separately for STEMI and NSTEMI presentations. Results: Elevated Lp(a) levels were significantly more common in young patients with AMI compared with healthy controls. Importantly, Lp(a) ≥ 30 mg/dL was strongly associated with multivessel coronary artery disease in NSTEMI, conferring more than a fourfold increased risk. In STEMI, the effect was weaker and largely influenced by concomitant factors such as diabetes and elevated LDL cholesterol. Conclusions: These findings highlight key pathophysiological differences between infarct phenotypes and position Lp(a) as a particularly relevant biomarker in young NSTEMI patients. The systematic assessment of Lp(a) may enhance coronary risk stratification and support more tailored secondary prevention strategies.

COVID-19 infection often produces cardiovascular complications, which can range from mild to severe and influence the overall prognosis. Imaging is the cornerstone for diagnosing initial COVID-19 cardiovascular involvement as well as treatment guidance. In this review, we present the current state of the literature on this subject while also emphasizing possible algorithms for indicating and executing these investigations.

The incidence of acute myocardial infarction (AMI) in young adults has been steadily rising, emphasizing the need for new biomarkers to improve risk stratification. Lipo-protein(a) (Lp(a)), a genetically determined lipoprotein with pro-atherogenic and pro-thrombotic properties, has gained increasing attention in this context. Our findings show that elevated Lp(a) levels are significantly more common in young patients with AMI compared with healthy controls. Importantly, Lp(a) ≥30 mg/dL was strongly associated with multivessel coronary artery disease in NSTEMI, conferring more than a fourfold increased risk. In STEMI, its effect was weaker and largely influenced by concomitant factors such as diabetes and elevated LDL cholesterol. These results underline key pathophysiological differences between infarct phe-notypes and position Lp(a) as a particularly relevant biomarker in young NSTEMI pa-tients. Systematic assessment of Lp(a) may enhance coronary risk stratification and support more tailored secondary prevention strategies.

Dilated cardiomyopathy (DCM) is a major cause of heart failure and sudden cardiac death, characterized by left ventricular dilation and systolic dysfunction in the absence of significant coronary or valvular disease. Although traditionally viewed as an idiopathic condition, DCM is now recognized as a genetically driven disorder in a substantial proportion of cases. Pathogenic variants affecting structural, cytoskeletal, desmosomal, and nuclear proteins not only initiate myocardial remodeling but also influence disease progression and arrhythmic vulnerability. Importantly, genetic findings do not merely explain disease etiology but also shape its clinical expression. The specific gene involved, as well as the type of mutation, can influence the pattern of ventricular remodeling, the distribution of myocardial fibrosis, and the degree of electrical instability. Cardiac magnetic resonance has emerged as a central tool in bridging molecular insights with clinical assessment. By enabling accurate evaluation of ventricular volumes and function, as well as detailed tissue characterization through late gadolinium enhancement (LGE) and parametric mapping, cardiac magnetic resonance reveals imaging patterns that often mirror the underlying genetic substrate. The integration of genetic testing and advanced imaging provides a more comprehensive understanding of dilated cardiomyopathy, allowing improved risk stratification and supporting a personalized approach to patient management.