Clinical evidence suggests that conventional cardiovascular disease (CVD) risk factors cannot explain all CVD incidences. Recent studies have shown that telomere attrition, clonal hematopoiesis of indeterminate potential (CHIP), and atherosclerosis (telomere–CHIP–atherosclerosis, TCA) evolve to play a crucial role in CVD. Telomere dynamics and telomerase have an important relationship with age-related CVD. Telomere attrition is associated with CHIP. CHIP is commonly observed in elderly patients. It is characterized by an increase in blood cell clones with somatic mutations, resulting in an increased risk of hematological cancer and atherosclerotic CVD. The most common gene mutations are DNA methyltransferase 3 alpha (DNMT3A), Tet methylcytosine dioxygenase 2 (TET2), and additional sex combs-like 1 (ASXL1). Telomeres, CHIP, and atherosclerosis increase chronic inflammation and proinflammatory cytokine expression. Currently, their epidemiology and detailed mechanisms related to the TCA axis remain incompletely understood. In this article, we reviewed recent research results regarding the development of telomeres and CHIP and their relationship with atherosclerotic CVD.

Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein that has been established as an independent and causal risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve disease (CAVD). Structurally composed of a low-density lipoprotein (LDL)-like particle covalently linked to apolipoprotein(a) [apo(a)], Lp(a) exhibits unique atherogenic, thrombogenic, and inflammatory properties, largely due to its role as a carrier of oxidized phospholipids (OxPL). Plasma Lp(a) concentrations are predominantly determined by the number of kringle IV type 2 (KIV-2) repeats in the LPA gene, with minimal influence from lifestyle or environmental factors. Despite substantial evidence linking elevated Lp(a) to cardiovascular risk, clinical testing remains underutilized, especially in East Asian countries. In Taiwan, although population-level Lp(a) concentrations are comparatively low, a significant subset exceeds risk thresholds, with local studies confirming its prognostic value in coronary artery disease and ischemic stroke. Barriers, including limited physician awareness, implementation barriers, and therapeutic nihilism, contribute to its under-recognition. This review highlights the molecular features of Lp(a), its pathogenesis of cardiovascular disorders, epidemiology, and current barriers and future advances in diagnostic testing, with a particular focus on implications for cardiovascular risk management in Taiwan.

Statins are the cornerstone of lipid-lowering therapy for the prevention of atherosclerotic cardiovascular disease (ASCVD); however, many patients are unable to achieve guideline-recommended low-density lipoprotein cholesterol (LDL-C) targets because of suboptimal tolerance to statins. The 2026 Taiwan Society of Lipid and Atherosclerosis (TSLA) Consensus Statement presents an updated, evidence-based framework for the identification and management of patients receiving suboptimally tolerable statins (STS)-a pragmatic concept that extends beyond the traditional and restrictive definition of statin intolerance (SI). STS encompasses patients who are unable to maintain recommended statin intensity because of real or perceived adverse effects, even when formal SI criteria are not met, thereby addressing a major treatment gap in real-world practice in Taiwan. This consensus integrates contemporary international evidence and Taiwanese guidelines, including the 2025 Taiwan cholesterol management pathway, and proposes structured, risk-based algorithms for STS management. A tiered therapeutic strategy is recommended: extremely high-risk patients should receive early combination therapy with ezetimibe and bempedoic acid, with prompt escalation to PCSK9 inhibition-based agents if LDL-C targets (<55 mg/dL) are not achieved. In high- and very high-risk patients, ezetimibe is the first-line add-on therapy, followed by bempedoic acid and PCSK9-targeted agents as needed, while lifestyle intervention and shared decision-making are emphasized in lower-risk groups. Non-pharmacological options are also reviewed; however, robust cardiovascular outcome data remain limited. By bridging conceptual and policy gaps between SI and STS, this consensus promotes a patient-centered, precision-based approach to improving LDL-C goal attainment and reducing residual ASCVD risk.