Platelet glycoprotein IIb/IIIa may be involved in the pathogenesis of myocardial infarction as the key element in platelet aggregation and as the binding site of lipoprotein(a) to platelets, inhibiting plasminogen binding and activation. Recently, a strong association between the P1A2 polymorphism of the glycoprotein IIIa gene and acute coronary thrombosis has been reported. although this has not been confirmed. In an associated study, we determined plasma lipoprotein levels, the apo E genotype and the P1A genotype in 250 males under 55 years with myocardial infarction and they were compared with 250 age- and sex-matched controls. Patients showed an over-representation of the epsilon3/4 genotype with respect to the control group. We found that there were no differences in the allelic frequency of P1A2 between case patients and age-matched controls (chi2 = 0.05, P = 0.92) and that subjects bearing the P1A2 allele showed higher plasma lipoprotein(a) concentration than p1A1/P1A1 individuals. Therefore, in this population there is no association between carriage of p1A2 allele and increased risk of myocardial infarction but the carriage of P1A2 is associated with higher plasma Lp(a) concentration.
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http://dx.doi.org/10.1016/s0021-9150(98)00076-8 | DOI Listing |
Circ Genom Precis Med
January 2025
Department of Medicine, Division of Cardiology (M.P., N.J.P., N.P.S.), Duke University, Durham, NC.
Background: Established risk models may not be applicable to patients at higher cardiovascular risk with a measured Lp(a) (lipoprotein[a]) level, a causal risk factor for atherosclerotic cardiovascular disease.
Methods: This was a model development study. The data source was the Nashville Biosciences Lp(a) data set, which includes clinical data from the Vanderbilt University Health System.
Eur Heart J Digit Health
January 2025
Cardiology Department, Dr Balmis General University Hospital, Alicante Institute for Health and Biomedical Research (ISABIAL), C/Maestro Alonso s/n, Alicante 03010, Spain.
Aims: Evidence regarding the safety of early discharge following transcatheter aortic valve implantation (TAVI) is limited. The aim of this study was to evaluate the safety of very early (<24) and early discharge (24-48 h) as compared to standard discharge (>48 h), supported by the implementation of a voice-based virtual assistant using artificial intelligence (AI) and natural language processing.
Methods And Results: Single-arm prospective observational study that included consecutive patients who underwent TAVI in a tertiary hospital in 2023 and were discharged under an AI follow-up programme.
Lancet Reg Health West Pac
January 2025
Department of Epidemiology & Biostatistics, School of Public Health, Peking University, Beijing 100191, China.
Background: Existing studies have not provided robust evidence about the CVD risk of non-smoking patients with restrictive spirometric pattern (RSP) or airflow obstruction (AFO), and how the risk is modified by body shape. We aimed to bridge the gap.
Methods: We used never-smokers' data from the China Kadoorie Biobank (CKB) and performed Cox models by sex (278,953 females and 50,845 males).
Int J Nanomedicine
January 2025
School of Medicine, South China University of Technology, Guangzhou, Guangdong, People's Republic of China.
Background: Exosomes sourced from mesenchymal stem cells (MSC-EXOs) have become a promising therapeutic tool for sepsis-induced myocardial dysfunction (SMD). Our previous study demonstrated that Apelin pretreatment enhanced the therapeutic benefit of MSCs in myocardial infarction by improving their paracrine effects. This study aimed to determine whether EXOs sourced from Apelin-pretreated MSCs (Apelin-MSC-EXOs) would have potent cardioprotective effects against SMD and elucidate the underlying mechanisms.
View Article and Find Full Text PDFRes Pract Thromb Haemost
January 2025
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Background: Reduced effect of antiplatelet therapy has been reported in patients with ST-segment elevation myocardial infarction (STEMI). This could partly be explained by an increase of highly reactive immature platelets.
Objectives: To investigate changes in platelet maturity and reactivity after acute STEMI.
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