Background and aims Plaque phenotype on optical coherence tomography (OCT) is little studied outside East Asian and Western cohorts. We related age to OCT phenotype in a Southeast Asian percutaneous coronary intervention (PCI) cohort. Methods We analysed 306 patients (361 lesions) undergoing OCT-guided PCI in southern Vietnam, December 2023 to January 2026. Features were summarised per patient; age was modelled per decade and in three groups (<60, 60-69, ≥70 years). Models were adjusted for sex, clinical presentation and cardiovascular risk factors, with Holm correction across the eight principal features. Eight sensitivity analyses were performed. Results Acute coronary syndrome (ACS) accounted for 36.6%. Unadjusted, calcification rose from 56.5% to 79.1% across age groups, lipid-rich plaque fell from 79.3% to 59.1% and red thrombus from 17.4% to 4.3%. After adjustment, only calcification remained associated with age (odds ratio 1.64 per decade, 95% CI 1.25-2.16; Holm-adjusted P = 0.003), as did every calcium subtype (nodules 1.77); no other feature showed an independent association. Angiography showed the calcium in 34.4% versus 57.7% of OCT-calcified lesions (youngest versus oldest group). The association was evident in ACS (2.64, 1.59-4.36) but not in CCS, in which about 80% had calcification at every age (P for interaction = 0.002). Conclusions Older age was independently associated with calcification on OCT, more often superficial, nodular and angiographically visible, particularly in ACS. The lower prevalence of lipid-rich and thrombotic features was not independent of sex and presentation. Being cross-sectional, these data describe differences between age groups, not change within individuals.
Background Geographic disparities in U.S. cardiovascular mortality are large, but how readily available county socioeconomic indicators compare in their associations with it is unclear. We compared county poverty and unemployment measures as correlates of an AHRF-defined cardiovascular mortality composite. Methods Cross-sectional ecological analysis of the 2024–2025 Area Health Resources File (AHRF). The outcome was the crude 2021–2023 rate of ischemic heart, cerebrovascular, and other cardiovascular deaths in counties with all three components observed. Measures were 2023 overall, pediatric (ages 0–17), and family childhood (ages 5–17) poverty and 2019–2023 overall, female, and White unemployment. Connecticut was excluded from county-level analyses. We estimated Spearman correlations with bootstrap 95% confidence intervals (CIs), paired comparisons, and partial rank correlations adjusted for age structure, rurality, racial and ethnic composition, and state. Results Among 1982 counties, rates differed across Census divisions (p < 0.001), from 348.5 per 100,000 (East South Central) to 233.9 (Mountain). Unadjusted correlations were larger for poverty (ρ 0.524–0.612; pediatric poverty ρ = 0.612, 95% CI 0.581–0.641) than for unemployment (ρ 0.141–0.209). Pediatric poverty exceeded overall poverty (difference 0.088, 95% CI 0.071–0.107) but differed negligibly from family childhood poverty (0.009). After adjustment, partial correlations were 0.530 (95% CI 0.495–0.563) for pediatric poverty and 0.165–0.209 for unemployment; unemployment adjusted for poverty was near zero (0.029, 95% CI −0.020 to 0.077). Conclusion Poverty measures, including pediatric poverty, showed larger associations with an AHRF-defined cardiovascular mortality composite than unemployment measures, before and after adjustment. These ecological associations with crude rates identify candidate county-level markers, not causal effects.
Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein and a well-established causal risk factor for atherosclerotic cardiovascular disease (ASCVD). Despite increasing recognition in clinical guidelines, Lp(a) testing remains underused, and targeted therapies are only now emerging. This narrative review summarizes the biology, cardiovascular risk, measurement challenges, emerging therapies, and translational barriers of Lp(a), highlighting its role in contemporary cardiovascular prevention. Lp(a) promotes cardiovascular disease through pro-atherogenic, pro-inflammatory, and prothrombotic mechanisms mediated by lipid deposition, oxidized phospholipids, and impaired fibrinolysis. Elevated Lp(a) independently predicts coronary artery disease (CAD), ischemic stroke, peripheral artery disease, and calcific aortic valve disease across diverse populations. However, widespread clinical implementation is limited by apo(a) isoform heterogeneity, assay variability, inconsistent reporting in mg/dL and nmol/L, and low testing rates despite recommendations for once-in-a-lifetime screening. Novel Lp(a)-targeted therapies, including antisense oligonucleotides, small interfering RNAs, and the oral small-molecule inhibitors, have demonstrated sustained reductions in Lp(a) concentrations exceeding 80% in early-phase clinical trials, with favorable safety profiles. Lp(a) is an important residual cardiovascular risk factor with promising targeted therapeutic options. However, important translational gaps remain, including assay standardization, validated treatment thresholds, and definitive cardiovascular outcome data. Recent Lp(a)HORIZON phase 3 evidence has shown that substantial Lp(a) lowering does not necessarily reduce cardiovascular events, while other ongoing phase 3 outcome trials will further determine whether Lp(a)-lowering therapies improve clinical outcomes and establish their role in routine cardiovascular prevention.
Background Preeclampsia is a pregnancy-related cardiovascular risk-enhancing factor associated with increased lifetime cardiovascular disease (CVD) risk. However, long-term cardiovascular risk varies according to postpartum blood pressure, metabolic health, and development of conventional cardiovascular risk factors. Current clinical recommendations Current guidelines recognize preeclampsia as a risk-enhancing factor to support cardiovascular risk assessment and shared decision-making regarding lipid-lowering therapy. However, preeclampsia alone is not an indication for routine statin therapy, and no postpartum low-density lipoprotein cholesterol (LDL-C) target is recommended solely on the basis of previous preeclampsia. Evidence gap Existing evidence is derived mainly from observational studies involving heterogeneous populations. Few studies have evaluated women who remain normotensive with favorable metabolic profiles, and no completed randomized trial has demonstrated that postpartum statin therapy improves long-term cardiovascular outcomes. Main argument Lifelong cardiovascular surveillance is warranted after preeclampsia, but routine statin therapy for all survivors is not supported. Lipid-lowering therapy should be individualized according to overall cardiovascular risk. Future directions Future studies should identify high-risk phenotypes, validate postpartum risk prediction tools such as PREVENT, and determine whether selected women benefit from targeted statin therapy.
Hypersensitivity myocarditis caused by NSAIDs can mimic acute STEMI, yet nimesulide as the trigger of primary myocardial injury has rarely been documented. This article reports a 57-year-old male who developed rash and persistent chest pain after taking nimesulide for fever due to respiratory syncytial virus infection. Electrocardiogram revealed ST-segment elevation in leads V2-V3, and the patient was admitted with acute heart failure and shock. Norepinephrine was administered to maintain circulation. Suspected nimesulide-associated hypersensitivity myocarditis was considered based on elevated eosinophil count, medication history and rash. Following methylprednisolone therapy and hemodynamic stabilization, coronary angiography showed no vascular lesions. Cardiac magnetic resonance demonstrated myocardial edema and mid-wall injury of the interventricular septum. Continued glucocorticoid treatment resulted in marked improvement in the patient's symptoms and laboratory findings, with SCAI shock stage improving from stage C on admission to stage A at discharge.Follow-up cardiac magnetic resonance at 3-month after onset showed complete resolution of myocardial injury without fibrosis. Clinicians should be alert to this rare cardiac adverse reaction of nimesulide.
