Shah Freya H, Agrawal Siddharth, Tated Ritu C, Maheta Darshilkumar, Naqvi Syed
Internal Medicine, Landmark Medical Center, Woonsocket, USA.
Internal Medicine, Smt. Nathiba Hargovandas Lakhmichand (NHL) Municipal Medical College, Ahmedabad, IND.
Cureus. 2025 Aug 11;17(8):e89794. doi: 10.7759/cureus.89794. eCollection 2025 Aug.
Rheumatic diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), significantly increase the risk of cardiovascular disease (CVD), with affected patients exhibiting a 2-3-fold higher risk compared to the general population. This elevated risk is primarily driven by chronic inflammation and accelerated atherosclerosis, which are not fully captured by traditional cardiovascular risk calculators. RA patients face cardiovascular risks similar to those of type 2 diabetics, while SLE patients, particularly young women, have a dramatically increased risk of myocardial infarction. These conditions challenge the conventional understanding of CVD risk, as traditional factors like hypertension, dyslipidemia, and smoking do not fully account for the excess risk observed. This has led to growing interest in the use of new biomarkers and advanced imaging technologies to improve risk stratification and early detection of cardiovascular involvement. This review examines the pathophysiological mechanisms that link rheumatic diseases with cardiovascular risk. Chronic inflammation, immune dysregulation, and vascular dysfunction are central to the accelerated atherosclerosis and myocardial damage seen in RA and SLE. Key proinflammatory cytokines, including Tumor Necrosis Factor- Alpha (TNF-α), Interleukin (IL) IL-6, and IL-17, contribute to endothelial dysfunction and oxidative stress, exacerbating cardiovascular risk. In addition, biomarkers such as high-sensitivity C-reactive protein (hs-CRP), NT-proBNP, and troponins are valuable for detecting subclinical cardiac involvement and predicting adverse cardiovascular outcomes. Emerging biomarkers like IL-32, Dickkopf-related protein 1 (DKK-1), and galectin-3 also show potential in further refining risk assessment, particularly for atherosclerosis and myocardial fibrosis in rheumatic diseases. Advanced imaging methods, such as transthoracic echocardiography (TTE), carotid ultrasonography, cardiac MRI (CMR), and coronary CT angiography (CCTA), provide key insights into subclinical cardiovascular changes in rheumatic disease patients. These techniques enable the detection of myocardial inflammation, fibrosis, and early atherosclerosis, helping guide clinical decisions and preventive interventions. Despite advancements, traditional cardiovascular risk calculators often underestimate CVD risk in rheumatic disease patients, leading to the use of adjusted models, such as EULAR-endorsed 1.5× risk multiplier for RA patients. These adjustments, along with the integration of biomarkers and imaging findings, can help identify high-risk individuals and prompt early interventions, such as statin therapy. However, challenges remain, including the cost and accessibility of some imaging methods, the heterogeneous risk profiles across different rheumatic diseases, and the need for more prospective trials to evaluate the effectiveness of biomarkers and imaging in clinical practice. In conclusion, incorporating biomarkers and advanced imaging techniques into cardiovascular risk assessment provides a more accurate method for managing CVD in rheumatic disease patients. These approaches allow for more personalized care, helping reduce the increased CVD mortality seen in this population. Future research should focus on refining multi-biomarker algorithms, improving imaging technology, and conducting intervention trials to optimize cardiovascular outcomes in rheumatic disease patients.
类风湿关节炎(RA)和系统性红斑狼疮(SLE)等风湿性疾病显著增加了心血管疾病(CVD)的风险,与普通人群相比,患病患者的风险高出2至3倍。这种风险升高主要由慢性炎症和加速的动脉粥样硬化驱动,而传统的心血管风险计算器并未完全涵盖这些因素。RA患者面临的心血管风险与2型糖尿病患者相似,而SLE患者,尤其是年轻女性,心肌梗死风险则显著增加。这些情况挑战了对CVD风险的传统认识,因为高血压、血脂异常和吸烟等传统因素并不能完全解释所观察到的额外风险。这导致人们越来越关注使用新的生物标志物和先进的成像技术来改善风险分层和心血管受累情况的早期检测。本综述探讨了将风湿性疾病与心血管风险联系起来的病理生理机制。慢性炎症、免疫失调和血管功能障碍是RA和SLE中加速动脉粥样硬化和心肌损伤的核心因素。关键的促炎细胞因子,包括肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)IL-6和IL-17,会导致内皮功能障碍和氧化应激,加剧心血管风险。此外,高敏C反应蛋白(hs-CRP)、N末端脑钠肽前体(NT-proBNP)和肌钙蛋白等生物标志物对于检测亚临床心脏受累和预测不良心血管结局很有价值。白细胞介素-32(IL-32)、Dickkopf相关蛋白1(DKK-1)和半乳糖凝集素-3等新兴生物标志物在进一步优化风险评估方面也显示出潜力,特别是对于风湿性疾病中的动脉粥样硬化和心肌纤维化。先进的成像方法,如经胸超声心动图(TTE)、颈动脉超声检查、心脏磁共振成像(CMR)和冠状动脉CT血管造影(CCTA),为了解风湿性疾病患者的亚临床心血管变化提供了关键见解。这些技术能够检测心肌炎症、纤维化和早期动脉粥样硬化,有助于指导临床决策和预防性干预。尽管取得了进展,但传统的心血管风险计算器往往低估了风湿性疾病患者的CVD风险,因此导致使用调整模型,如欧洲抗风湿病联盟(EULAR)认可的RA患者1.5倍风险乘数。这些调整,以及生物标志物和成像结果的整合,有助于识别高危个体并促使早期干预,如他汀类药物治疗。然而,挑战依然存在,包括一些成像方法的成本和可及性、不同风湿性疾病的异质性风险特征,以及需要更多前瞻性试验来评估生物标志物和成像在临床实践中的有效性。总之,将生物标志物和先进的成像技术纳入心血管风险评估为管理风湿性疾病患者的CVD提供了一种更准确的方法。这些方法允许提供更个性化的护理,有助于降低该人群中CVD死亡率的增加。未来的研究应专注于完善多生物标志物算法、改进成像技术,并进行干预试验以优化风湿性疾病患者的心血管结局。