Zulfiya Makasheva

Dr. Zulfiya Makasheva

cardiological department 2, Almaty Cardiology Center, Almaty, Kazakhstan
orcid

Research Focus & Metrics

Academic Career Length

1Year (2026-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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12 January 2026 in Diseases
Verified
Journal Article
Open access
PDF file
Dina Amangeldinovna KapsultanovaDina Amangeldinovna Kapsultanova
Dina Amangeldinovna Kapsultanova
Sholpan Bolatovna ZhangelovaSholpan Bolatovna Zhangelova
Sholpan Bolatovna Zhangelova
Nurmukhammad Friba NasrullakyzyNurmukhammad Friba Nasrullakyzy
Nurmukhammad Friba Nasrullakyzy
Zulfiya MakashevaZulfiya Makasheva
Zulfiya Makasheva
OSOrazbek Sakhov
Orazbek Sakhov
BABotakoz Kalenovna Aubakirova
Botakoz Kalenovna Aubakirova
Background: High residual platelet reactivity (HRPR) and persistent dyslipidemia remain important unmet needs in cardiovascular risk management, particularly in patients undergoing coronary revascularization. Despite intensive lipid-lowering and antiplatelet therapy, a substantial proportion of patients fail to reach recommended low-density lipoprotein cholesterol (LDL-C) targets or exhibit inadequate platelet inhibition. Inclisiran, a PCSK9-targeting small interfering RNA, represents an emerging approach for long-term LDL-C reduction. Methods: A narrative review of the literature published between 2009 and 2025 was performed using PubMed, Scopus, Web of Science, and MEDLINE. Studies evaluating the addition of inclisiran to standard lipid-lowering therapy in patients with dyslipidemia and HRPR, assessed using the VerifyNow assay, were included. Illustrative clinical cases from Kazakhstan were analyzed to demonstrate real-world changes in LDL-C levels and platelet reactivity following insufficient response to conventional treatment. The review had a descriptive design. Results: Available evidence indicates that a significant proportion of high- and very-high-risk patients do not achieve LDL-C targets or are unable to tolerate high-intensity statin therapy. Inclisiran consistently induces sustained reductions in LDL-C and circulating PCSK9 levels. Emerging data suggest a potential indirect modulation of platelet reactivity associated with intensive lipid lowering. In patients at extreme cardiovascular risk—including those after coronary artery bypass grafting (CABG) and with long-standing multivessel coronary artery disease—inclisiran therapy was associated with marked LDL-C reduction and a trend toward normalization of platelet reactivity. Conclusions: Assessment of platelet function using the VerifyNow assay may improve identification of residual thrombotic risk in patients with advanced atherosclerotic disease. Inclisiran appears to be a promising adjunctive therapy for dyslipidemic patients with persistently elevated cardiovascular risk and HRPR despite standard treatment. Further prospective studies are warranted to clarify the relationship between intensive LDL-C lowering, platelet reactivity, and clinical outcomes, and to optimize integrated lipid-lowering and antiplatelet strategies.