Ottaviani Giulia, Buja L Maximilian
"Lino Rossi" Research Center for the Study and Prevention of Unexpected Perinatal Death and Sudden Infant Death Syndrome (SIDS), Department of Biomedical, Surgical, and Dental Sciences, University of Milan, Milan, Italy; Department of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Department of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Cardiovasc Pathol. 2016 Nov-Dec;25(6):489-499. doi: 10.1016/j.carpath.2016.08.005. Epub 2016 Aug 28.
Sudden cardiac death (SCD) is defined as the unexpected death without an obvious noncardiac cause that occurs within 1 h of witnessed symptom onset (established SCD) or within 24 h of unwitnessed symptom onset (probable SCD). In the United States, its incidence is 69/100,000 per year. Dysfunctions of the cardiac conduction and autonomic nervous systems are known to contribute to SCD pathogenesis, even if most clinicians and cardiovascular pathologists lack experience with detailed examination of the cardiac conduction system and fail to recognize lesions that are crucial to explain the SCD itself. In this review, we sought to describe the advances over the last 25 years in the study of the anatomopathological changes of the conducting tissue, in SCD, in mature hearts and particularly in sudden infant death syndrome (SIDS) and sudden intrauterine unexpected death syndrome (SIUDS), through the articles published in our journal Cardiovascular Pathology (CVP). We carried out an extensive Medline search to retrieve and review all articles published in CVP in which the sudden unexpected death of one or more subjects believed healthy was reported, especially if associated with lesions of the conducting tissue in settings that revealed no other explained causes of death, particularly in infants and fetuses. The cardiac conduction findings of resorptive degeneration, His bundle dispersion, Mahaim fibers, cartilaginous meta-hyperplasia, persistent fetal dispersion, left-sided His bundle, septation of the bifurcation, atrioventricular node dispersion, sinus node hypoplasia, Zahn node, His bundle hypoplasia, atrioventricular node, and His bundle dualism were similarly detected in SIDS and SIUDS victims.
心脏性猝死（SCD）定义为在出现症状后1小时内发生的无明显非心脏原因的意外死亡（确诊SCD），或在未被目击的症状出现后24小时内发生的意外死亡（可能SCD）。在美国，其发病率为每年69/10万。已知心脏传导系统和自主神经系统功能障碍会导致SCD发病机制，尽管大多数临床医生和心血管病理学家缺乏详细检查心脏传导系统的经验，并且未能识别对解释SCD本身至关重要的病变。在本综述中，我们试图通过发表在我们的《心血管病理学》（CVP）杂志上的文章，描述过去25年中在成熟心脏SCD，特别是婴儿猝死综合征（SIDS）和宫内意外猝死综合征（SIUDS）中传导组织解剖病理学变化研究的进展。我们进行了广泛的医学文献检索，以检索和回顾发表在CVP上的所有文章，其中报道了一个或多个被认为健康的受试者的意外猝死，特别是如果与传导组织病变相关，且在没有其他可解释死因的情况下，特别是在婴儿和胎儿中。在SIDS和SIUDS受害者中同样检测到了吸收性变性、希氏束离散、Mahaim纤维、软骨化生增生、持续性胎儿离散、左侧希氏束、分叉分隔、房室结离散、窦房结发育不全、Zahn结、希氏束发育不全、房室结和希氏束二元性等心脏传导结果。
