CRY Department of Cardiovascular Pathology, Molecular and Clinical Sciences Research Institute, St. George's University of London, London, UK; NIHR Academic Clinical Fellow, University of Cambridge, Cambridge, UK.
CRY Department of Cardiovascular Pathology, Molecular and Clinical Sciences Research Institute, St. George's University of London, London, UK.
Resuscitation. 2022 Jun;175:6-12. doi: 10.1016/j.resuscitation.2022.04.002. Epub 2022 Apr 9.
Sudden arrhythmic death syndrome (SADS), defined as sudden cardiac death (SCD) with a morphologically normal heart, is an important cause of sudden death. Hypoperfusion due to cardiac arrest followed by successful cardiopulmonary resuscitation (CPR) may induce histologic changes that mimic pathologic conditions. Detailed characterisation of such features and whether they could confound SADS diagnosis are not described.
Retrospective observational study analysing all consecutive cases of sudden death prospectively referred to a UK national cardiac pathology centre between 2017 and 2021. Cases showing hypoperfusion features were identified after review of clinical information and examination by expert cardiac pathologists.
Out of 2,568 SCD cases, 126 (4.9%) were identified with hypoperfusion changes. Macroscopically, the commonest finding was left ventricular focal or diffuse subendocardial haemorrhage (13.5%). Microscopically, haemorrhage and contraction band necrosis (n = 50, 37.7%), subendocardial acute infarction (n = 44, 34.1%), interstitial mixed inflammatory cell infiltrates (n = 31, 24.9%), healing granulation tissue (n = 9, 7.1%) and subendocardial fibrosis (n = 1, 0.7%) were observed. These changes correlated to duration of survival following resuscitation. In a subcohort of 41 cases, autopsy pathologists misinterpreted such changes as ischaemic myocardial infarction (n = 7; 17%), myocarditis (n = 5; 12.1%), or other pathologies (n = 2; 4.8%) in 14 SADS cases.
We provide a comprehensive characterisation of hypoperfusion-related changes in the heart following successful CPR with survival, which are time related. These features can lead to diagnostic confusion among pathologists but knowledge of history of resuscitation with survival should help with general and expert pathology assessment and improve SADS diagnostic yield, prompting genetic screening of decedents' relatives.
猝发性心律失常死亡综合征（SADS）定义为形态正常心脏的心脏性猝死（SCD），是猝死的一个重要原因。心脏骤停后继发的低灌注可引起类似病理情况的组织学改变。目前尚未详细描述这些特征及其是否会混淆 SADS 的诊断。
回顾性观察性研究，分析了 2017 年至 2021 年期间英国国家心脏病理学中心连续前瞻性转介的所有猝死者病例。通过临床信息回顾和专家心脏病理学家检查，确定了存在低灌注特征的病例。
在 2568 例 SCD 病例中，有 126 例（4.9%）被发现存在低灌注改变。大体上，最常见的发现是左心室局灶性或弥漫性心内膜下出血（13.5%）。镜下，可见出血和收缩带坏死（n=50，37.7%）、心内膜下急性梗死（n=44，34.1%）、间质混合性炎症细胞浸润（n=31，24.9%）、愈合性肉芽组织（n=9，7.1%）和心内膜下纤维化（n=1，0.7%）。这些改变与复苏后存活时间相关。在 41 例亚组病例中，尸检病理学家在 14 例 SADS 病例中错误地将这些改变解释为缺血性心肌梗死（n=7；17%）、心肌炎（n=5；12.1%）或其他病理学改变（n=2；4.8%）。
我们提供了成功复苏后与存活相关的低灌注相关性心脏改变的全面描述，这些改变与时间有关。这些特征可能会导致病理学家的诊断混淆，但了解复苏后的存活史应有助于一般和专家病理评估，并提高 SADS 的诊断率，促使对死者亲属进行基因筛查。
