👤 Efthimios Dimitriadis

Coronary microvascular dysfunction (CMD) constitutes an increasingly acknowledged aspect of coronary artery disease. Even though traditional cardiovascular risk factors have been implicated in CMD pathogenesis, data on lipoprotein (a) [Lp(a)] is limited. This cross-sectional study aimed to investigate whether Lp(a) levels are associated with CMD in patients with angina and nonobstructive coronary arteries. Coronary physiology assessment was performed with the standard bolus thermodilution technique, allowing for coronary flow reserve (CFR) and index of microvascular resistance estimation. Participants were categorized into 3 groups based on Lp(a) levels (<30, [30 to 50], and ≥50 mg/dl) as well as into 2 groups based on the presence of CMD. CMD was defined as CFR ≤2.5 and/or index of microvascular resistance ≥25. A total of 127 patients were recruited. No significant differences in baseline characteristics were observed between the groups. In unadjusted analysis, no significant associations were found. In multivariable analysis adjusting for age and sex, participants with Lp(a) values ≥50 mg/dl displayed a trend for a 4.25 increased CMD risk when compared to participants with Lp(a) values <30 mg/dl (odds ratio 4.25, confidence interval 0.81 to 22.28, p = 0.087). The same group of patients tended to have lower CFR than controls with Lp(a) <30 mg/dl, with a median CFR that was 1.05 units lower (p = 0.086). In conclusion, patients with high Lp(a) levels tended to display a higher prevalence of CMD and lower CFR. More studies are needed in order to better elucidate the relationship between Lp(a) and CMD. Show less

Coronary artery disease (CAD) remains a leading cause of global morbidity and mortality, necessitating continuous refinement in the management of dyslipidemia, one of its major risk factors, to mitigate cardiovascular risks. Previous studies have proven the critical role of immediate and robust low-density lipoprotein cholesterol (LDL-C) reduction in the aftermath of acute coronary syndrome (ACS). Emphasizing the evidence supporting this approach, we delve into the impact of early intervention on cardiovascular outcomes and propose optimal strategies for achieving rapid LDL-C lowering, while also providing the rationale for early proprotein convertase subtilisin/kexin 9 inhibitor use after an ACS. Given the importance of the residual lipidemic risk, we present an overview of emerging therapeutic avenues poised to reshape dyslipidemia management, such as bempedoic acid, lipoprotein(a) inhibition, ApoC3 modulation, and angiopoietin-like protein 3 targeting. This comprehensive review amalgamates current evidence with future prospects, offering a holistic perspective on the management of dyslipidemia in CAD. By exploring both the urgency for immediate post-ACS LDL-C reduction and the exciting advancements on the horizon, this article provides a roadmap for clinicians navigating the intricate landscape of lipid-lowering therapies in CAD. Show less

Medications used to treat acute lymphoblastic leukemia (ALL), such as L-asparaginase, can cause blood lipid disturbances. These can also be associated with polymorphisms of the lipoprotein lipase (LpL) and apolipoprotein E (APOE) genes. We aimed to investigate the association between lipid profile, certain LpL and APOE gene polymorphisms (rs268, rs328, rs1801177 and rs7412, rs429358 respectively) as well as the risk subgroup in 30 pediatric patients being treated for ALL, compared with 30 pediatric ALL survivors and 30 healthy controls. The only APOE gene polymorphism with significant allelic and genotypic heterogeneity was rs429358. Further analysis of this polymorphism showed that genotype (CC, CT, or TT) was significantly associated with (1) changes in the lipid profile at the end of consolidation (total cholesterol, LDL, apo-B100, and lipoprotein a) and during re-induction (total cholesterol and apo-B100), and (2) classification in the high risk-ALL subgroup (for CC genotype/C allele presence). Lipid abnormalities in children being treated for ALL may be associated with the APOE genotype, which is also possibly associated with risk stratification. Further research is needed to confirm the potential prognostic value of these findings. Show less

Proper placentation in the first trimester is essential for a healthy pregnancy in humans. A recent proteomics study of human placental tissue has identified that tripeptidyl peptidase 1 (TPP1) production is reduced in the placenta in early-onset preeclampsia compared to uncomplicated pregnancy. However, it remains to be investigated if TPP1 plays a role in regulating trophoblast cell function during early pregnancy. In this study, immunohistochemistry was used to determine the production and localization of TPP1 in human placenta throughout gestation and the first-trimester decidua/implantation sites. Show less

Secondary peripheral chondrosarcoma is a malignant chondroid tumor arising in a benign precursor, either an osteochondroma or an enchondroma. Multiple osteochondromas syndrome (MO) is an autosomal dominant skeletal disorder associated with bony growths in the form of osteochondromas that occasionally undergo malignant transformation to secondary peripheral chondrosarcomas. We describe the genetic examination of three secondary peripheral chondrosarcomas that had arisen synchronously from osteochondromas in a patient with MO by chromosome banding, high resolution chromosomal comparative genomic hybridization, and mutation analysis of the EXT1 and EXT2 genes. In two of the tumors (the third was not genetically informative), very similar chromosome abnormalities were found, indicating that they must somehow be part of the same neoplastic process in spite of being anatomically distinct. Show less