Department of Forensic Medicine, Sydney South West Area Health Service, Sydney, Australia.
Heart. 2011 Oct;97(20):1695-9. doi: 10.1136/hrt.2011.226209. Epub 2011 Jul 26.
To assess the nature of necroinflammatory changes identified in postmortem histological sections of the right ventricular myocardium in cases of fatal pulmonary thromboembolism (PTE).
DESIGN/SETTING: A retrospective study examining coronial autopsy cases (n = 28, age 58 ± 21 years, 9 men/19 women) of PTE in which isolated right ventricular myocardial pathology was encountered. Detailed immunohistological analysis was undertaken on sections of myocardium, and comparison was made to age- and sex-matched controls (n=28, age 57 ± 21 years, 9 men/19 women) without significant cardiorespiratory disease.
The PTE was considered extensive in 86% of cases, and histological features of organisation were observed in 68%. PTE cases had similar body mass indices to controls (32 ± 2 kg/m(2) vs 28 ± 2 kg/m(2), p = 0.13) but greater heart weights (414 ± 17 g vs 358 ± 18 g, p = 0.02) and, where documented, thicker right ventricular walls (4.8 ± 0.3 mm (n = 18) vs 3.4 ± 0.2 mm (n = 15), p = 0.0008). The inflammatory infiltrate in PTE cases comprised predominantly macrophages and T cells, though neutrophilic inflammation was a frequent accompaniment. Myocyte necrosis was identified in association with the inflammatory foci in 64%. There was a 6.6-fold greater amount of diffuse macrophage recruitment within the right ventricle in cases of PTE compared to controls (p<0.0001), and there was a 6.1-fold increase in right ventricular fibrosis (p = 0.01). Right ventricular fatty replacement was similar between the two groups (p = 0.46).
We conclude that PTE may result in right ventricular myocardial inflammation and necrosis, distinct from that seen in typical myocardial infarction due to atherosclerotic coronary artery disease, or myocarditis. This observation may be explained, in part, by local stretch and strain of the right ventricle due to increased afterload, possibly compounded by diminished diastolic blood flow to the right ventricular myocardium and the effects of global myocardial hypoxia.
评估在致命性肺血栓栓塞症(PTE)死后组织学切片中发现的右心室心肌坏死性炎症变化的性质。
设计/设置:一项回顾性研究,检查了 28 例尸检病例(年龄 58 ± 21 岁,9 名男性/19 名女性)的 PTE,这些病例中发现了孤立的右心室心肌病理学变化。对心肌切片进行了详细的免疫组织化学分析,并与年龄和性别匹配的无明显心肺疾病的对照组(n=28,年龄 57 ± 21 岁,9 名男性/19 名女性)进行了比较。
86%的 PTE 被认为是广泛的,68%的 PTE 出现了组织学特征。PTE 病例的体重指数与对照组相似(32 ± 2 kg/m2 对 28 ± 2 kg/m2,p=0.13),但心脏重量更大(414 ± 17 g 对 358 ± 18 g,p=0.02),并且在有记录的情况下,右心室壁更厚(4.8 ± 0.3 mm(n=18)对 3.4 ± 0.2 mm(n=15),p=0.0008)。PTE 病例的炎症浸润主要由巨噬细胞和 T 细胞组成,但中性粒细胞炎症是常见的伴随物。在 64%的病例中,与炎症灶相关的肌细胞坏死被确定。与对照组相比,PTE 病例的右心室弥漫性巨噬细胞募集量增加了 6.6 倍(p<0.0001),右心室纤维化增加了 6.1 倍(p=0.01)。两组的右心室脂肪替代相似(p=0.46)。
我们得出结论,PTE 可能导致右心室心肌炎症和坏死,与典型的因动脉粥样硬化性冠状动脉疾病引起的心肌梗死或心肌炎不同。这种观察结果部分可以解释为由于后负荷增加导致右心室的局部拉伸和应变,可能由于右心室心肌舒张期血流减少和全身心肌缺氧的影响而加剧。