CARDIOVASCULAR PATHOLOGY心血管病理学
CARDIOVASCULAR PATHOLOGY(英文缩写 CARDIOVASC PATHOL),ISSN 1054-8807,eISSN 1879-1336,中文译名:心血管病理学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.975 | Q2 |
| 2022 | 3.700 | Q2 |
| 2023 | 2.300 | Q2 |
| 2024 | 1.900 | Q3 |
| 2025 | 2.000 | Q3 |
CARDIOVASCULAR PATHOLOGY 最新收录文献
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1. Audit of temporal artery biopsy reporting in South Australia.
PMID:期刊:日期:2026-08-27Despite histopathology playing a central role in the diagnosis of giant cell arteritis (GCA), until recently, there was no guideline for reporting on temporal artery biopsies (TAB). The Society for Cardiovascular Pathology established such consensus guidelines in 2023. The aim of this audit was to assess the extent to which South Australian TAB reports aligned with the reporting guidelines, and whether reporting practices changed across time. All SA Pathology TAB reports from 2010, 2017 and 2024 were assessed against the reporting guidelines, which contain four main areas of reporting (diagnosis, comment, gross descriptions, and microscopic descriptions (with 7 sub-points)). If all areas and microscopic descriptions were reported, the report was classified as 'complete'. Trends were examined over time, where possible using multi-level mixed-effects models to account for the reporting pathologist, with a 5% level of significance. There were 76 TAB reports in 2010, 92 in 2017 and 126 in 2024. No reports were complete in reporting with no statistically significant change over time. The only statistically significant changes over time observed were the decreased reporting of a final diagnosis (p = 0.001), and final diagnosis comment (p = 0.004). In South Australia, no TAB reports fully aligned with the Society for Cardiovascular Pathology reporting statement. Reporting did not improve over time, including after guideline publication. Targeted strategies are needed to standardise reporting and support better diagnostic quality and patient care.
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2. Calcium burden is associated with selective changes in luminal surface topography of cadaveric left anterior descending arteries.
PMID:期刊:日期:2026-08-19Coronary artery calcification is a key feature of atherosclerosis and is routinely quantified as a marker of plaque burden. However, its relationship with luminal surface topography remains poorly defined due to the limited resolution of clinical imaging. We aimed to determine whether increasing calcium burden is associated with measurable changes in luminal surface topography. Left anterior descending artery (LAD) specimens from 27 human cadavers were analyzed using micro-computed tomography (micro-CT) to quantify calcium burden. Luminal surfaces were exposed and scanned using high-resolution optical surface metrology (confocal microscopy), yielding quantitative topographical parameters across 366 surface scans. Associations between calcium burden and surface metrics were evaluated using linear mixed-effects models to account for within-specimen clustering (effect estimates reported as β). Sensitivity analyses were performed with adjustment for coronary segment. Across evaluated parameters, most global and spatial surface metrics were not associated with calcium burden. However, higher calcium burden was associated with reduced dale count (β [95% CI] = -17.22 [-33.0, -1.43]; p = 0.034). This association remained consistent after adjustment for coronary segment (β = -16.80 [-32.73, -0.87]; p = 0.039). Calcium burden in cadaveric LADs is selectively associated with reduced luminal surface dale count, suggesting subtle, localized topographic remodeling rather than global surface changes.
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3. Degenerative histopathology in ascending aortic aneurysms: comparative analysis by aneurysm location.
PMID:期刊:日期:2026-08-15Aortic aneurysms have traditionally been studied as a single pathological entity, with emphasis on valve morphology. While histopathological differences between bicuspid (BAV) and tricuspid (TAV) aortopathy are well documented, less is known about how these mechanisms interact with aneurysm location within the ascending aorta. This gap complicates risk assessment and surgical planning beyond diameter-based criteria. We aimed to evaluate histopathological features of ascending aortic aneurysms across three topographical subgroups-root, tubular, and combined involvement-and assess modification by valve cuspidity. Using systematic criteria from the Society for Cardiovascular Pathology and the Association for European Cardiovascular Pathology consensus statement, the analysis focused on medial degeneration, adventitial alterations and atherosclerosis in patients undergoing ascending aortic surgery at a Finnish tertiary care center. The cohort comprised 296 patients with aneurysms located in the sinus of Valsalva (n = 122), tubular part (n = 130), and both regions (n = 44). Medial degeneration was present in all samples and predominantly moderate, with comparable median severity score of 2 (range 1-3, P = 0.829) across groups. In the overall cohort, no statistically significant differences were observed between topographical groups. Among TAV patients, tubular aneurysms demonstrated significantly higher histopathological scores for medial degeneration, elastic fiber fragmentation and loss, elastic fiber disorganisation, smooth muscle cell disorganization and nuclei loss, laminar medial collapse, medial fibrosis, adventitial fibrosis and atherosclerosis (all P < 0.05). In BAV patients, no statistical differences were found. Tubular aneurysms are characterized by more extensive wall remodeling and adventitial changes compared to root aneurysms, particularly in TAV patients. Notably, female sex emerged as a strong independent predictor of advanced medial and adventitial pathology. These findings underscore the importance of considering anatomical location, valve morphology, and sex in risk stratification and may inform surgical decision-making beyond diameter-based criteria.
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4. Adaptive proteomic remodeling and eNOS upregulation in luminal endothelium and perivascular adipose tissue of patent saphenous vein grafts after CABG.
PMID:期刊:日期:2026-08-13Long-term patency of saphenous vein grafts (SVGs) remains a significant challenge in coronary artery bypass grafting (CABG). The biological factors underlying successful human grafts are poorly understood. We aimed to characterize the structural and molecular features associated with successful graft function. Patent and occluded SVG and internal thoracic artery (ITA) grafts were obtained from explanted hearts of CABG patients undergoing heart transplantation for end-stage heart failure not attributable to graft failure, along with freshly harvested ITA and SVG controls. Samples underwent histomorphological analysis, immunohistochemistry (IHC), and liquid chromatography-tandem mass spectrometry (LC-MS/MS) proteomics. Patent ITA (ITA-P) showed minimal intimal hyperplasia with medial reinforcement, whereas patent SVGs (SVG-P) had organized, α-smooth muscle actin (αSMA)-positive myofibroblast-rich neointima. Endothelial nitric oxide synthase (eNOS) was markedly upregulated in patent grafts at two sites-the luminal endothelium and adventitial microvessels within perivascular adipose tissue (PVAT)-and lost at both sites in occluded SVG (SVG-O). Adventitial CD31-positive microvessels were significantly increased in patent grafts. Proteomically, ITA-P and SVG-P shared a largely common adaptive proteome enriched in translation, RNA processing, and extracellular matrix (ECM) organization, with shared upstream activation of NR4A3, EGFR, and STAT1, and conduit-specific signatures (IGF-1/RUNX2 in ITA-P; RETN/SRC/PTGES in SVG-P). PTGES was strongly expressed in the adventitia of SVG-P. Patent arterial and venous bypass grafts exhibited a shared adaptive phenotype characterized by dual-site upregulation of eNOS in both the luminal endothelium and the perivascular microvessels/PVAT. In SVG-P, PTGES was co-upregulated alongside eNOS, indicating a mechanistic link between the proteomic and IHC findings. These findings highlight the perivascular compartment as a site of adaptive, eNOS-associated changes in patent vein grafts.
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5. Proteomic profiling of whole tissue sections in cardiac ATTR amyloidosis reveals increased extracellular matrix remodeling.
PMID:期刊:日期:2026-06-16Cardiac transthyretin amyloidosis (ATTR-CA) is caused by myocardial deposition of misfolded transthyretin, leading to progressive heart failure. Disease pathology, however, extends beyond passive amyloid deposition and also involves active processes such as extracellular matrix (ECM) remodeling and immune activation. Mass spectrometry (MS) is the gold standard for amyloid typing in diagnostics. Here, we applied quantitative MS-driven proteomics on formalin-fixed paraffin-embedded whole cardiac tissue sections from six ATTR-CA cases, ten unaffected controls and four AL-CA controls to investigate protein expression changes. In addition to transthyretin, over 500 proteins were upregulated in ATTR-CA biopsies, including complement and coagulation factors as well as extracellular matrix (ECM) remodeling proteins. Among these, members of the A Disintegrin and Metalloproteinase with Thrombospondin Motifs (ADAMTS) family, metalloproteinases (MMPs), and Tissue Inhibitor of Metalloproteinase-3 (TIMP3) showed significant upregulation. These proteins are key regulators of ECM turnover and structural integrity. Immunohistochemistry confirmed ADAMTS4 enrichment in amyloid deposits, while TIMP3 showed strong expression in cardiomyocytes and weaker staining within amyloid deposits. Together, these findings indicate that ECM remodeling, alongside complement and coagulation activation, represents a reproducible feature of cardiac ATTR amyloidosis. Whole-tissue proteomics provides biological insights that extend beyond amyloid typing, with potential implications for biomarker discovery and therapeutic targeting in ATTR-CA.
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6. A large-scale plasma proteomic study reveals the preclinical evolution and potential biomarkers for coronary atherosclerosis.
PMID:期刊:日期:2026-06-03Coronary atherosclerosis (CA) can remain subclinical for decades before clinical onset, while the complex pathophysiological mechanisms underlying its progression remain poorly understood. Proteomics offers a novel perspective for elucidating its pathogenic mechanisms and improving risk prediction. The plasma proteomic data were from 29,020 UK Biobank participants comprising 2,907 Olink-measured proteins. 1,000 iterations of resampling-based univariable Cox regression were performed to identify robust CA-associated proteins. Locally estimated scatterplot smoothing was used to model the temporal trajectories of CA-associated proteins. Cox proportional hazards models integrating CA-associated proteins with traditional risk factors were constructed to predict incident CA, with model performance evaluated using the area under the curve (AUC) of receiver operating characteristic (ROC). During the 15-year follow-up, 65 proteins were found to be significantly associated with CA risk across the long-term, short-term, and overall follow-up periods. These CA-associated proteins were predominantly involved in collagen-containing extracellular matrix, endoplasmic reticulum lumen, and defense response to bacterium. By integrating multi-stage significance rankings using the robust rank aggregation method, we identified 5 key candidate proteins. Among these proteins, MMP12 remained persistently elevated 15 years before CA diagnosis, whereas GDF15, WFDC2, EDA2R and CST3 exhibited progressive abnormalities approximately 8 to 13 years prior to diagnosis. The model constructed using only the 5 key candidate proteins combined with traditional risk factors achieved high accuracy for 10-year (AUC = 0.749) and 5-year (AUC = 0.722) CA risk prediction. This study provides a temporal proteomic landscape of CA progression and highlights a compact panel of five plasma proteins that effectively predict CA risk. These findings not only advance understanding of the molecular mechanisms driving CA but also offer translational potential for early detection and precision prevention in clinical practice.
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7. Burden of cardiovascular disease in victims of fatal intoxication: An autopsy study.
PMID:期刊:日期:2026-06-02Previous post-mortem studies in victims of intoxication have typically focused on toxicological and biochemical analyses. This study aimed to assess the prevalence and types of cardiovascular disease in fatal intoxication cases. We included post-mortem autopsy examinations of 865 fatal intoxication cases performed on medico-legal basis at the Gade Laboratory for Pathology at Haukeland University Hospital, Bergen between 2000 and 2013. The mean age at death was 42.1 years (range 13-97) and 72% were males. The cause of death was attributed to intoxication with drugs in 35% cases, combination of drugs and narcotics in 17%, narcotics in 17%, ethanol and drugs in 15%, and ethanol alone in 8% cases. More than a third (36.0%) had concomitant causes of death. The mean heart weight was 387 ± 86 g. A total of 12.3% patients had mild, 8.4% moderate and 9.7% had severe atherosclerosis, while 69.6% had no atherosclerosis or only minor changes in the coronary arteries. A total of 14.9% patients had pathological changes in the brain: cerebral oedema in 23% (n = 29) cases, old ischemic strokes in 22% (n = 28), traumatic brain injury in 13.2% (n = 17) and intracranial hemorrhage in 8.5% (n = 11), while the incidence of acute ischemic stroke was 3.1% (n = 4). Myocardial infarction (old/healed) was evident in 10.3% (n = 89) of the victims. The incidence of left ventricular hypertrophy was nearly 3-fold higher than right ventricular hypertrophy (29.2% vs 10.6%). In victims of intoxication, cerebrovascular disease was found in 15% and heart diseases in up to 30% of cases. It is possible that the acute toxic effects of alcohol and substance abuse are aggravated in patients with underlying cardiac and cerebrovascular diseases. The findings from the current study highlight the importance of enhanced cardiovascular risk assessment in substance use disorders, with major forensic and public health implications.
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8. Immune cells in cardiac homeostasis and disease.
8. 心脏稳态和疾病中的免疫细胞PMID:期刊:日期:2026-05-28Immune cells play key roles in cardiac homeostasis and disease. Although the function and significance of diverse immune cell populations in the heart in health, aging, and in disease is not fully understood, it is clear that these immune populations can be of diagnostic and therapeutic significance. The field of cardio-immunology is vast and evolving constantly. Herein, we aim to focus on a subset of the immune cells that are abundant and significant in healthy and diseased heart, providing relevant biological concept and clinical implications for practicing pathologists.
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9. Genetic Mutations, Pathology, and Single-nucleus Transcriptomic Landscape in LVHT Patients Reveal Differential Progression to Heart Transplantation.
PMID:期刊:日期:2025-12-12Left ventricular hypertrabeculation/non-compaction (LVHT/LVNC) is characterized by a thinned myocardial wall, prominent trabeculations, and deep intertrabecular recesses. It presents with unique cardiac morphology and hemodynamic features but displays considerable clinical heterogeneity. The factors influencing disease progression to heart transplantation remain unclear. No studies have investigated the relationship between transcriptomic or pathological features of LVHT and progression to transplantation. We enrolled 74 patients diagnosed with LVHT, among whom 63 underwent whole-exome sequencing to assess genetic variants. Explanted heart tissue was obtained from 24 patients who received heart transplantation, and single-nucleus RNA sequencing was performed on the compacted and non-compacted layers of the left ventricle in 3 LVHT patients, compared with 3 normal controls. In addition, myocardial composition, fibrosis, fat content, and the extent of non-compaction were evaluated histopathologically. Genetic variants were detected in 46% of patients but were not associated with progression to heart transplantation. The compacted and non-compacted layers of LVHT hearts exhibited highly similar transcriptional profiles. Notch signaling was enriched in LVHT-related cardiomyocyte clusters. MAML3, a Notch coactivator, was significantly upregulated in LVHT compared with other cardiomyopathies and normal myocardium, and was associated with faster progression to transplantation. Histopathological analysis further demonstrated that both myocardial fibrosis and the anatomical distribution of non-compaction were linked to cardiac function and transplant outcomes. LVHT is associated with distinct transcriptomic and pathological features that influence the rate of progression to heart transplantation. The Notch pathway-related molecule MAML3 may serve as a potential marker of disease progression in LVHT.