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The continuum of cardiovascular vulnerability: From premature atherosclerosis to heavily calcified lesions

Heart Science Journal · Vol. 7 No. 4 (2026) · pp. 1–3

DOI
10.21776/ub.hsj.2026.007.04.1
ISSN
2721-9984, 2721-9976
Published
2026-10-13
Publisher
Universitas Brawijaya
Language
en
License
creativecommons.org/licenses/by/4.0

Abstract

Coronary atherosclerosis encompasses premature clinical events and heavily calcified lesions that complicate percutaneous coronary intervention (PCI). This editorial examines overlapping biological and procedural vulnerabilities and implications for prevention and intervention. Cumulative exposure to apolipoprotein B-containing lipoproteins, alongside inherited and acquired risk factors, drives atherosclerosis. Plaque inflammation, disruption, healing, fibrosis, and mineralization are dynamic processes, not an inevitable linear sequence. Biological vulnerability concerns the propensity for rupture, erosion, and thrombosis; procedural vulnerability concerns treatment complexity and complications when PCI is clinically indicated. Calcified nodules may confer both forms of vulnerability. Macrocalcification may reflect an adaptive healing response that stabilizes plaques, whereas microcalcification may promote vulnerability. Extensive coronary calcium nevertheless marks cumulative atherosclerotic burden, and lesion calcification complicates PCI. Risk assessment should integrate systemic risk, plaque burden, morphology, and clinical context. Intensive lipid lowering, risk-factor control, and adherence remain essential. Coronary imaging can refine risk assessment and guide lesion preparation, but neither high-risk plaque features nor heavy calcification alone establishes an indication for PCI. In PREVENT, preventive PCI plus optimal medical therapy reduced a composite endpoint in selected patients with non-flow-limiting, imaging-defined high-risk plaques; this does not establish a definitive reduction in death or spontaneous myocardial infarction. Indonesian priorities include earlier recognition of severe hypercholesterolemia, tobacco control, access to lipid-lowering therapy, and follow-up. Conclusion: This continuum supports lifelong prevention and selectively indicated, imaging-informed intervention, prioritizing patient outcomes over plaque detection or stent implantation.

Keywords

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9 authors · 27 co-authorship links

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Co-authorOrganisationJoint articles
Dian Larasati MunawarAffiliation unknown2
Beny HartonoAffiliation unknown2
Evan Jim GunawanAffiliation unknown1
Johan JohanAffiliation unknown1
Dian Andina MunawarAffiliation unknown1
Muhammad FadilAffiliation unknown1
Fadhil Pratama ApriansyahAffiliation unknown1
Darwin IndraAffiliation unknown1

Affiliations come from OpenAlex; journal OAI-PMH metadata carries none. Authors without an OpenAlex ID are matched by name, which can merge or split people.

Metadata source: OAI-PMH (metadata jurnal) https://heartscience.ub.ac.id/index.php/heartscience/oai, first harvested 8 Nov 2026, last seen 8 Nov 2026.
Original metadata (oai_dc) 
<oai_dc:dc xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/  http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
	<dc:title xml:lang="en">The continuum of cardiovascular vulnerability: From premature atherosclerosis to heavily calcified lesions</dc:title>
	<dc:creator xml:lang="en">Munawar, Muhammad</dc:creator>
	<dc:subject xml:lang="en">Atherosclerosis</dc:subject>
	<dc:subject xml:lang="en">Atherosclerotic</dc:subject>
	<dc:subject xml:lang="en">Plaque</dc:subject>
	<dc:subject xml:lang="en">Percutaneous Coronary Intervention</dc:subject>
	<dc:subject xml:lang="en">Risk Ventricular</dc:subject>
	<dc:subject xml:lang="en">Vascular Calcification</dc:subject>
	<dc:description xml:lang="en">Coronary atherosclerosis encompasses premature clinical events and heavily calcified lesions that complicate percutaneous coronary intervention (PCI). This editorial examines overlapping biological and procedural vulnerabilities and implications for prevention and intervention. Cumulative exposure to apolipoprotein B-containing lipoproteins, alongside inherited and acquired risk factors, drives atherosclerosis. Plaque inflammation, disruption, healing, fibrosis, and mineralization are dynamic processes, not an inevitable linear sequence. Biological vulnerability concerns the propensity for rupture, erosion, and thrombosis; procedural vulnerability concerns treatment complexity and complications when PCI is clinically indicated. Calcified nodules may confer both forms of vulnerability. Macrocalcification may reflect an adaptive healing response that stabilizes plaques, whereas microcalcification may promote vulnerability. Extensive coronary calcium nevertheless marks cumulative atherosclerotic burden, and lesion calcification complicates PCI. Risk assessment should integrate systemic risk, plaque burden, morphology, and clinical context. Intensive lipid lowering, risk-factor control, and adherence remain essential. Coronary imaging can refine risk assessment and guide lesion preparation, but neither high-risk plaque features nor heavy calcification alone establishes an indication for PCI. In PREVENT, preventive PCI plus optimal medical therapy reduced a composite endpoint in selected patients with non-flow-limiting, imaging-defined high-risk plaques; this does not establish a definitive reduction in death or spontaneous myocardial infarction. Indonesian priorities include earlier recognition of severe hypercholesterolemia, tobacco control, access to lipid-lowering therapy, and follow-up.
Conclusion: This continuum supports lifelong prevention and selectively indicated, imaging-informed intervention, prioritizing patient outcomes over plaque detection or stent implantation.</dc:description>
	<dc:publisher xml:lang="en">Universitas Brawijaya</dc:publisher>
	<dc:date>2026-10-13</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
	<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
	<dc:format>application/pdf</dc:format>
	<dc:identifier>https://heartscience.ub.ac.id/index.php/heartscience/article/view/20884</dc:identifier>
	<dc:identifier>10.21776/ub.hsj.2026.007.04.1</dc:identifier>
	<dc:source xml:lang="en">Heart Science Journal; Vol. 7 No. 4 (2026): Navigating High-Risk Cardiovascular Subsets: Premature Disease, Plaque Complexity, and Precision Interventions; 1-3</dc:source>
	<dc:source>2721-9984</dc:source>
	<dc:source>2721-9976</dc:source>
	<dc:source>10.21776/ub.hsj.2026.007.04</dc:source>
	<dc:language>en</dc:language>
	<dc:relation>https://heartscience.ub.ac.id/index.php/heartscience/article/view/20884/612</dc:relation>
	<dc:rights xml:lang="en">Copyright (c) 2026 Muhammad Munawar</dc:rights>
	<dc:rights xml:lang="en">http://creativecommons.org/licenses/by/4.0</dc:rights>
</oai_dc:dc>