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Further Understanding of Myocardial Infarction: Risk Factors, Treatment, and Clinical...
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Further Understanding of Myocardial Infarction: Risk Factors, Treatment, and Clinical Outcomes

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425). This special issue belongs to the section "Cardiovascular Clinical Research".

Deadline for manuscript submissions: 25 December 2025 | Viewed by 466

Special Issue Editor

Prof. Dr. Joanna Sikora

E-Mail Website
Guest Editor
Research and Education Unit for Experimental Biotechnology, Department of Transplantology and General Surgery, Collegium Medicum, Nicolaus Copernicus University, 85-094 Bydgoszcz, Poland
Interests: platelets; coagulation; cardiology; atherosclerosis; heart failure; acute coronary syndromes; hemostasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acute myocardial infarction (AMI), also known as a heart attack, occurs due to decreased coronary blood flow, leading to insufficient oxygen supply to the heart and cardiac ischemia. Decreased coronary blood flow is multifactorial. Atherosclerotic plaques classically rupture and lead to thrombosis, contributing to acutely decreased blood flow in the coronary. Many basic science and clinical studies on new pathomechanisms concerning acute myocardial infarction are extremely important both from a clinical point of view and from a public health perspective.

Further understanding of myocardial infarction by defining new risk factors, proposing new treatment strategies, and conducting new clinical trials is still needed. The prompt recognition, diagnosis, and treatment of AMI are critical to improving patient outcomes and reducing the risk of complications. Moreover, close monitoring and comprehensive post-treatment care are essential for promoting recovery and long-term heart health.

We invite authors to submit original research articles and reviews papers to this Special Issue.

Prof. Dr. Joanna Sikora
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Cardiovascular Development and Disease is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • myocardial infarction
  • antiplatelet therapy
  • acute coronary syndromes
  • cardiovascular risk

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Published Papers (1 paper)

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Research

15 pages, 1035 KB  
Article
The Effects of Inclisiran on the Subclinical Prothrombotic and Platelet Activation Markers in Patients at High Cardiovascular Risk
by Mateusz Maligłówka, Adrianna Dec, Łukasz Bułdak and Bogusław Okopień
J. Cardiovasc. Dev. Dis. 2025, 12(9), 355; https://doi.org/10.3390/jcdd12090355 - 16 Sep 2025
Viewed by 216
Abstract
Atherosclerosis as a multifactorial disease remains the first cause of death worldwide. Current oral lipid-lowering drugs (especially statins) reduce low-density lipoprotein cholesterol (LDLC) levels in the blood, but their clinical efficacy seems to be partially attributed to pleiotropic effects on different pathophysiologic factors [...] Read more.
Atherosclerosis as a multifactorial disease remains the first cause of death worldwide. Current oral lipid-lowering drugs (especially statins) reduce low-density lipoprotein cholesterol (LDLC) levels in the blood, but their clinical efficacy seems to be partially attributed to pleiotropic effects on different pathophysiologic factors of atherosclerosis extending beyond lipid-lowering properties such as anti-inflammatory, antithrombotic and antioxidative features. Novel drugs that interfere with proprotein convertase subtilisin/kexin type 9 (PCSK9) axis of LDL-C receptors (LDLRs) degradation, from the group of monoclonal antibodies (e.g., alirocumab, evolocumab) or small interfering RNA (siRNA), e.g., inclisiran, are effective in reducing LDLC as well. However, data depicting their antithrombotic and antiplatelet activity are scarce, whereas prothrombotic properties of PCSK9 are widely described. Thus, we performed a study to assess the effects of inclisiran on subclinical prothrombotic [fibrinogen, coagulation factor VIII (FVIII), plasminogen activator inhibitor-1 (PAI-1)] and platelet activation markers (platelet factor-4 (PF-4), soluble p-selectin (sCD62P)). Ten patients at high cardiovascular risk with concomitant heterozygous familial hypercholesterolemia (HeFH)—study group 1, and fourteen patients at very high cardiovascular risk without concomitant HeFH—study group 2, were recruited for the study. Lipid profile, subclinical prothrombotic and platelet activation markers were assessed at the beginning and after 3 months of therapy with inclisiran. During therapy, statistically significant reductions in both study groups were seen in total cholesterol levels (study group 1: from 287.6 ± 94.2 to 215.2 ± 89.1 (mg/dL), p = 0.022; study group 2: from 211.7 ± 52.7 to 147.6 ± 55.4 (mg/dL), p < 0.001) and LDL-c (study group 1: from 180.8 ± 73.3 to 114.7 ± 71.5 (mg/dL), p = 0.031; study group 2: from 129.6 ± 46.8 to 63.4 ± 43.6 (mg/dL), p < 0.001). Lipid profile changes were associated with significant decrease in the concentration of FVIII in both groups (study group 1: from 33.3 ± 22 to 22 ± 14.5 (ng/mL), p = 0.006; study group 2: from 37 ±16.9 to 29.3 ±16.4 (ng/mL), p = 0.002) and fibrinogen, but only in study group 2 (from 51.4 (33.2–72.7) to 42.6 (31.3–57.2) (µg/mL), p = 0.035). Among platelet activation markers, a significant decrease in PF-4 in study group 2 was noted (from 286 (272–295.5) to 272 (268–281.5) (ng/mL), p = 0.047). However, there were no statistically significant changes in PAI-1 and sCD62P throughout the study. In our study, inclisiran appeared to be an effective lipid-lowering drug in patients at high cardiovascular risk. Moreover, it was shown that beyond lipid-lowering properties, the drug may also partially affect thrombogenesis and platelet activation. Full article
(This article belongs to the Special Issue Further Understanding of Myocardial Infarction: Risk Factors, Treatment, and Clinical Outcomes)
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