Kundnani Nilima Rajpal, Di Luca Federico, Meche Vlad, Sharma Abhinav, Popa Mihaela-Diana, Nicula-Neagu Marioara, Voinescu Oana Raluca, Iacob Mihai, Duda-Seiman Daniel-Marius, Dragan Simona Ruxanda
University Clinic of Internal Medicine and Ambulatory Care, Prevention and Cardiovascular Recovery, Department VI-Cardiology, "Victor Babes" University of Medicine and Pharmacy, 300041 Timisoara, Romania.
Research Centre of Timisoara Institute of Cardiovascular Diseases, "Victor Babes" University of Medicine and Pharmacy, 300041 Timisoara, Romania.
Int J Mol Sci. 2025 Apr 28;26(9):4181. doi: 10.3390/ijms26094181.
Secondary dilated cardiomyopathy (DCM) refers to left ventricular dilation and impaired systolic function arising from identifiable extrinsic causes, such as ischemia, hypertension, toxins, infections, systemic diseases, or metabolic disorders. Unlike primary DCM, which is predominantly genetic, secondary DCM represents a diverse spectrum of pathophysiological mechanisms linked to external insults on myocardial structure and function. The increasing prevalence of conditions such as alcohol use disorder, chemotherapy-induced cardiotoxicity, and viral myocarditis underscores the need for heightened awareness and early recognition of secondary DCM. A comprehensive analysis of clinical trial data and observational studies involving secondary dilative cardiomyopathy was conducted, with a focus on mortality, symptom relief, and major adverse events. A systematic literature review was performed using databases, including PubMed, Embase, and ClinicalTrials.gov, following PRISMA guidelines for study selection. Data were extracted on patient demographics, etiology of dilation, trial design, outcomes, and follow-up duration. Advances in diagnostic modalities have refined the ability to identify underlying causes of secondary DCM. For example, high-sensitivity troponin and cardiac magnetic resonance imaging are pivotal in diagnosing myocarditis and differentiating it from ischemic cardiomyopathy. Novel insights into toxin-induced cardiomyopathies, such as those related to anthracyclines and immune checkpoint inhibitors, have highlighted pathways of mitochondrial dysfunction and oxidative stress. Treatment strategies emphasize the management of the causing condition alongside standard heart failure therapies, including RAAS inhibitors and beta-blockers. Emerging therapies, such as myocardial recovery protocols in peripartum cardiomyopathy and immune-modulating treatments in myocarditis, are promising in reversing myocardial dysfunction. Secondary DCM encompasses a heterogeneous group of disorders that require a precise etiological diagnosis for effective management. Timely identification and treatment of the underlying cause, combined with optimized heart failure therapies, can significantly improve outcomes. Future research focuses on developing targeted therapies and exploring the role of biomarkers and precision medicine in tailoring treatment strategies for secondary DCM.
继发性扩张型心肌病（DCM）是指由可识别的外在原因引起的左心室扩张和收缩功能受损，这些原因包括缺血、高血压、毒素、感染、全身性疾病或代谢紊乱。与主要为遗传性的原发性DCM不同，继发性DCM代表了与心肌结构和功能受到外部损伤相关的多种病理生理机制。酒精使用障碍、化疗引起的心脏毒性和病毒性心肌炎等疾病的患病率不断上升，凸显了提高对继发性DCM的认识和早期识别的必要性。对涉及继发性扩张型心肌病的临床试验数据和观察性研究进行了全面分析，重点关注死亡率、症状缓解和主要不良事件。按照PRISMA研究选择指南，使用包括PubMed、Embase和ClinicalTrials.gov在内的数据库进行了系统的文献综述。提取了关于患者人口统计学、扩张病因、试验设计、结局和随访持续时间的数据。诊断方式的进步提高了识别继发性DCM潜在病因的能力。例如，高敏肌钙蛋白和心脏磁共振成像在诊断心肌炎以及将其与缺血性心肌病区分开来方面至关重要。对毒素诱导的心肌病（如与蒽环类药物和免疫检查点抑制剂相关的心肌病）的新见解突出了线粒体功能障碍和氧化应激途径。治疗策略强调在标准心力衰竭治疗（包括RAAS抑制剂和β受体阻滞剂）的同时，对病因进行管理。新兴疗法，如围产期心肌病的心肌恢复方案和心肌炎的免疫调节治疗，在逆转心肌功能障碍方面很有前景。继发性DCM包括一组异质性疾病，需要进行精确的病因诊断以进行有效管理。及时识别和治疗潜在病因，结合优化的心力衰竭治疗，可以显著改善结局。未来的研究重点是开发靶向治疗方法，并探索生物标志物和精准医学在为继发性DCM量身定制治疗策略中的作用。
