INTRODUCTION

The existence of a coronary artery aneurysm (CAA) can pose significant risk for death. It can cause thrombosis, dissection, rupture or myocardial infarction. An exceedingly rare involvement of the left main coronary artery (LMCA), particularly giant-sized is even more catastrophic, a finding seen in only 0.1% of patients. Furthermore, co-existence with significant stenotic coronary artery disease (CAD) portends grim survival. Owing to the rarity of this combination, no data is available locally and only limited case reports are documented internationally. Hence, no consensus guidelines have been published yet. This paper aims to contribute to the sparse medical knowledge on the treatment approach and management of LMCA aneurysm with concomitant CAD.

A 62-year-old male, Filipino, hypertensive and hyperlipidemic sought consult due to one-year exertional chest pain. Coronary angiogram revealed the LMCA to be a diffusely aneurysmal, large-sized vessel measuring 9.7 mm x 7.9 mm with a significant two-vessel CAD affecting the proximal left anterior descending (LAD) and right coronary artery (RCA). As per multidisciplinary decision, the patient underwent surgical revascularization via cardiopulmonary bypass graft (CABG) addressing the CAD and LMCA aneurysm managed conservatively through guideline-directed medical therapy. The patient’s course of treatment was uneventful. He returned for follow-ups for three months post-surgery and remained symptom-free.

Giant coronary artery aneurysms (GCAA) are vessel dilatations that exceed 4x the diameter of a normal adjacent artery. The patient had a unique case of GCAA involving the LMCA combined with two-vessel CAD. Few studies have documented a medical or surgical approach and long-term outcomes are unknown. Without sufficient evidence-based guidelines, the multidisciplinary decision was to perform CABG and manage the LMCA aneurysm conservatively.

Due to extremely limited information available on the giant LMCA aneurysm natural history, definitive management remains controversial. A multidisciplinary team approach is highly recommended for patient-specific needs to achieve favorable outcome and ensure survival.

Introduction: Peripheral arterial disease (PAD) is a common macrovascular complication of type 2 diabetes mellitus (T2DM) and is associated with increased cardiovascular morbidity and mortality. The ankle-brachial index (ABI) is a simple, non-invasive method for detecting PAD; however, Doppler devices are not always available in primary care and resource-limited settings. This study aimed to determine the diagnostic accuracy of ABI measurement using a stethoscope compared with the Doppler method among adults with T2DM. Methods: A diagnostic accuracy study was conducted among 200 adults with T2DM recruited through convenience sampling from a private outpatient clinic in Iloilo City. ABI measurements were obtained using both the stethoscope and Doppler methods. An ABI of ≤0.90 was considered indicative of PAD. Diagnostic accuracy measures, including sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), overall accuracy, and agreement, were calculated. Results: The prevalence of PAD was 30.5% using the stethoscope method and 35.0% using the Doppler method. Compared with Doppler ABI, the stethoscope method demonstrated an overall accuracy of 94.5%, sensitivity of 85.7%, specificity of 99.2%, PPV of 98.4%, and NPV of 92.8%. Agreement between the two methods was excellent (Cohen’s κ = 0.88, p < 0.001). Conclusion Stethoscope-based ABI determination demonstrated high diagnostic accuracy and excellent agreement with Doppler ABI. Given its low cost, accessibility, and non-invasive nature, it may serve as a practical screening tool for PAD among adults with T2DM, particularly in primary care and resource-limited settings where Doppler devices are unavailable
Peripheral arterial disease ; Ankle-brachial index ; Stethoscope ; Doppler ultrasound ; Type 2 diabetes mellitus

INTRODUCTION

Coronary artery disease remains a leading cause of mortality worldwide. Although advances in percutaneous coronary intervention (PCI) and stent technology have improved outcomes, in-stent restenosis (ISR) persists as a significant challenge contributing to repeat revascularization, rehospitalization, increased healthcare costs and adverse outcomes.

A single-center retrospective cohort study reviewed medical records from January 2021 to December 2024 to determine the incidence, risk factors and clinical outcomes associated with ISR.

Among 200 patients, ISR occurred in 58 (29%). Factors significantly associated with ISR included hypertension (p = 0.048), smaller stent diameter (OR=0.23, pCONCLUSION

ISR remains a substantial and multifactorial clinical burden highlighting the need for vigilant post-PCI surveillance, aggressive risk factor management and individualized interventional strategies—including optimal stent sizing, lesion preparation and adjunctive imaging use—to reduce restenosis risk and improve long-term outcomes.

INTRODUCTION

Coronary artery disease remains a leading cause of mortality worldwide. Although advances in percutaneous coronary intervention (PCI) and stent technology have improved outcomes, in-stent restenosis (ISR) persists as a significant challenge contributing to repeat revascularization, rehospitalization, increased healthcare costs and adverse outcomes.

A single-center retrospective cohort study reviewed medical records from January 2021 to December 2024 to determine the incidence, risk factors and clinical outcomes associated with ISR.

Among 200 patients, ISR occurred in 58 (29%). Factors significantly associated with ISR included hypertension (p = 0.048), smaller stent diameter (OR=0.23, pCONCLUSION

ISR remains a substantial and multifactorial clinical burden highlighting the need for vigilant post-PCI surveillance, aggressive risk factor management and individualized interventional strategies—including optimal stent sizing, lesion preparation and adjunctive imaging use—to reduce restenosis risk and improve long-term outcomes.

Introduction: Homozygous familial hypercholesterolemia (HoFH) is a rare inherited disorder characterized by markedly elevated low-density lipoprotein cholesterol (LDL-C) from birth, childhood xanthomas, and accelerated atherosclerotic cardiovascular disease. Achieving LDL-C targets remains difficult despite statins, ezetimibe, and lipoprotein apheresis, especially in patients with treatment interruption, poor adherence, or limited access to specialized lipid services. We report a female with genetically confirmed HoFH who developed severe premature coronary artery disease and showed marked lipid reduction after inclisiran therapy. Case: A 28-year-old Malay female with LDL receptor mutationconfirmed HoFH, diagnosed at age 7, had a strong family history of premature cardiovascular death. She underwent biweekly lipoprotein apheresis from ages 8 to 15 years, but later defaulted on follow-up. During pregnancy in 2021, weekly then biweekly apheresis was reintroduced for severe hypercholesterolemia, but she disengaged postpartum. In 2025, she re-presented with exertional chest pain, orthopnea, and palpitations. Examination showed widespread xanthomas. Electrocardiography demonstrated sinus tachycardia with inferolateral ST depression. Echocardiography revealed a left ventricular ejection fraction of 40%, anterior and septal akinesia, severe mitral regurgitation, moderate tricuspid regurgitation, and pulmonary hypertension. Her lipid profile showed total cholesterol 18.1 mmol/L and LDL-C 14.9 mmol/L. Coronary angiography demonstrated triple-vessel disease with left main stem involvement and critical right coronary ostial stenosis. Coronary artery bypass grafting was advised but declined. She was treated with high-dose rosuvastatin, ezetimibe, dual antiplatelet therapy, and inclisiran 284 mg. After one dose of inclisiran, total cholesterol fell to 6.78 mmol/L and LDL-C to 4.71 mmol/L, a reduction of more than 60%. Conclusion This case highlights the aggressive natural history of inadequately controlled HoFH and the importance of sustained lifelong therapy. Inclisiran may provide additional LDL-C reduction in selected HoFH patients, although long-term cardiovascular outcome data remain limited.
ALN-PCS ; Coronary Artery Disease ; Homozygous Familial Hypercholesterolemia ; Lipids

OBJECTIVES: In recent years, the role of remnant cholesterol (RC) in the development and progression of cardiovascular diseases has gained increasing attention. However, evidence on the association between RC and subclinical atherosclerosis is limited. This study aims to examine the relationship between RC and atherosclerotic plaques in single and multiple vascular territories. METHODS: This retrospective cross-sectional study used baseline data from participants enrolled between October 2022 and May 2024 in the National Key Research Program "Study on the Prevention and Control System of Risk Factors for Panvascular Diseases". Color Doppler ultrasonography was performed to detect plaques in 4 vascular territories: Bilateral carotid arteries, bilateral subclavian arteries, abdominal aorta, and iliac-femoral arteries. RC was calculated as total cholesterol minus the sum of low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C). Participants were categorized into quartiles (Q1-Q4) according to RC levels. The proportions of participants with ≥2 plaques in a single vascular territory and with plaques in ≥2 vascular territories were compared across RC quartiles. Multivariate ordinal Logistic regression was used to assess the association between RC and the number of plaques in a single vascular territory, as well as the risk of multiple vascular territory involvement. Additionally, the effects of LDL-C/RC concordance on plaque distribution were analyzed. RESULTS: A total of 3 539 participants were included, of whom 2 169 (61.29%) were male, with a age of (51.94±9.22) years. From Q1 to Q4, the proportion of participants with ≥2 plaques in a single vascular territory (bilateral carotid, subclavian, abdominal aorta, and iliac-femoral arteries), as well as those with plaques in ≥2 vascular territories, increased progressively. Compared with Q1, both Q3 and Q4 were significantly associated with higher plaque numbers in a single vascular territory (both P<0.05). When treated as a continuous variable, higher RC levels were associated with an increased risk of greater plaque numbers within a single vascular territory (all P<0.05). RC levels were also significantly associated with multiple vascular territory involvement: Compared with Q1, Q4 had a 1.015-fold higher risk [odds ratio (OR)=2.015, 95% confidence interval (CI) 1.669 to 2.433], and each 1 mmol/L increase in RC corresponded to a 0.160-fold increased risk (OR=1.160, 95% CI 1.073 to 1.271). In LDL-C/RC coordination analysis, compared with the low LDL-C/low RC group, the low LDL-C/high RC group was significantly associated with multiple vascular territory involvement (OR=1.576, 95% CI 1.220 to 2.036). CONCLUSIONS Elevated RC levels are closely associated with atherosclerotic plaques in both single and multiple vascular territories, even among individuals with normal LDL-C, suggesting that RC should be considered in clinical risk assessment and management of atherosclerosis.
Humans ; Plaque, Atherosclerotic/diagnostic imaging* ; Male ; Female ; Cross-Sectional Studies ; Middle Aged ; Retrospective Studies ; Cholesterol/blood* ; Cholesterol, LDL/blood* ; Aged ; Cholesterol, HDL/blood* ; Risk Factors ; Atherosclerosis ; Ultrasonography, Doppler, Color ; Femoral Artery/diagnostic imaging*

Fractional flow reserve (FFR), an established modality for functionally assessing coronary artery disease, is increasingly applied to diagnose and manage lower extremity arterial disease. By incorporating functional parameters, FFR enhances revascularization precision by quantifying the hemodynamic impact of stenotic lesions, thereby overcoming limitations of conventional imaging. Key clinical applications in lower extremity disease include functional assessment in moderate intermittent claudication, post-vascular preparation strategy optimization, and predicting revascularization outcomes and complications. Advances in pressure wire and microcatheter systems, alongside non-invasive imaging-derived FFR techniques, are improving its feasibility and applicability. However, widespread adoption is challenged by the complex anatomy of the lower extremity arterial system, frequent severe calcification and diffuse disease, and a current lack of standardized FFR cutoff values. Promoting the standardized use of FFR is crucial for shifting the clinical management paradigm from anatomy-based repair toward functional reconstruction.
Humans ; Lower Extremity/blood supply* ; Peripheral Arterial Disease/diagnosis* ; Fractional Flow Reserve, Myocardial ; Endovascular Procedures/methods* ; Intermittent Claudication/physiopathology*

OBJECTIVES: To investigate the role of activating transcription factor 3 (ATF3) in atherosclerotic plaques for regulating inflammatory responses during atherosclerosis (AS) progression. METHODS: Human coronary artery specimens from autopsy cases were examined for ATF3 protein expression and localization using immunofluorescence staining and Western blotting. Apolipoprotein E-deficient (ApoE^-/-) mouse models of AS induced by high-fat diet (HFD) feeding for 12 weeks were subjected to tail vein injection of adeno-associated virus serotype 9 (AAV9) to knock down ATF3 expression. After an additional 5 weeks of HFD feeding, the mice were euthanized for analyzing structural changes of the aortic plaques, and the expression levels of ATF3, inflammatory factors (CD45, CD68, IL-1β, and TNF-α), and NF-κB pathway proteins (P-IKKα/β and P-NF-κB p65) were detected. In the cell experiment, THP-1-derived foam cells were transfected with an ATF3-overexpressing plasmid or an ATF3-specific siRNA to validate the relationship between ATF3 and NF‑κB signaling. RESULTS: In human atherosclerotic plaques, ATF3 expression was significantly elevated and partially co-localized with CD68. ATF3 knockout in ApoE^-/- mice significantly increased aortic plaque volume, upregulated the inflammatory factors, enhanced phosphorylation of the NF‑κB pathway proteins, and increased the expressions of VCAM1, MMP9, and MMP2 in the plaques. In THP-1-derived foam cells, ATF3 silencing caused activation of the NF‑κB pathway, while ATF3 overexpression suppressed the activity of the NF-κB pathway. CONCLUSIONS AS promotes ATF3 expression, and ATF3 deficiency exacerbates AS progression by enhancing plaque inflammation via activating the NF-κB pathway, suggesting the potential of ATF3 as a therapeutic target for AS.
Animals ; Activating Transcription Factor 3/metabolism* ; Signal Transduction ; NF-kappa B/metabolism* ; Humans ; Mice ; Plaque, Atherosclerotic/metabolism* ; Inflammation/metabolism* ; Apolipoproteins E ; Atherosclerosis/metabolism* ; Diet, High-Fat

OBJECTIVES: To explore the molecular mechanism of Jiangzhi Huaban Decoction (JZHBD) for improving atherosclerosis through the "qi meridian-blood channels" pathway. METHODS: ApoE^-/- mouse models of atherosclerosis were established by high-fat diet feeding for 8 weeks, with C57BL/6 mice on a normal diet as the controls. Forty ApoE^-/- mouse models were randomized into model group, low-, medium-, and high-dose JZHBD treatment groups, and atorvastatin treatment group (n=8) for their respective treatments for 8 weeks. The changes in body weight and overall condition of the mice were monitored weekly. After the treatments, serum levels of TC, TG, HDL-C, LDL-C, TBA, ALT, and AST of the mice were measured, pathological changes in the liver and aortic root plaques were examined with HE staining, and lipid accumulation in the liver and aortic wall was assessed using Oil Red O staining. The core molecular mechanism was studied through transcriptomics, and the expressions of the key pathway proteins were confirmed using Western blotting and immunohistochemistry. RESULTS: Treatment with JZHBD significantly reduced blood lipid and total bile acid levels, improved liver function and hepatic steatosis, and decreased aortic lipid deposition and plaque area in the mouse models of atherosclerosis. Transcriptomic analysis suggested that the therapeutic mechanism of JZHBD involved reverse cholesterol transport, PPAR signaling, and the inflammatory pathways. In atherosclerotic mice, JZHBD treatment obviously up-regulated hepatic expressions of PPARγ, LXRα, ABCA1, ABCG1, and CYP7A1, down-regulated hepatic expressions of p-p65/p65, IL-6, IL1β in the liver, increased ABCG5 and ABCG8 expressions in the intestines, and decreased ICAM-1 and VCAM-1 expressions in the aortic plaques. CONCLUSIONS JZHBD improves atherosclerotic vascular damage and plaque formation possibly by regulating hepatic reverse cholesterol transport and inflammation via modulating the hepatic PPARγ/LXRα/NF-κB signaling pathway.
Animals ; Drugs, Chinese Herbal/therapeutic use* ; Mice, Inbred C57BL ; Plaque, Atherosclerotic/metabolism* ; Liver/metabolism* ; Mice ; Atherosclerosis/metabolism* ; Cholesterol/metabolism* ; PPAR gamma/metabolism* ; Male ; Diet, High-Fat ; Biological Transport

The host-microbe co-metabolism system, generating diverse exogenous and endogenous bioactive molecules that influence the host's immune and metabolic functions, plays a crucial role in the pathogenesis of atherosclerosis. Recent studies have elucidated the interaction between natural medicines and this co-metabolism system. Upon oral administration, natural medicine ingredients can undergo transformation by gut microbiota, potentially enhancing their bioavailability or anti-atherogenic efficacy. Furthermore, natural medicines can exert anti-atherogenic effects via modulation of endogenous host-microbe co-metabolism. This review presents an updated understanding of the dual association between natural medicines and host-microbe co-metabolites. It explores the critical function of microbial exogenous metabolites derived from natural medicines and uncovers the mechanisms underlying natural medicines' intervention on key nodes of endogenous host-microbe co-metabolism. These insights may offer new perspectives for cardiovascular disease (CVD) treatment and guide future drug discovery efforts.
Humans ; Atherosclerosis/metabolism* ; Gastrointestinal Microbiome/drug effects* ; Biological Products/therapeutic use* ; Animals ; Host Microbial Interactions/drug effects*