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  • Title: Myocardial pathology in pulmonary thromboembolism.
    Author: Orde MM, Puranik R, Morrow PL, Duflou J.
    Journal: Heart; 2011 Oct; 97(20):1695-9. PubMed ID: 21791512.
    Abstract:
    OBJECTIVE: 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. RESULTS: 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). CONCLUSIONS: 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.
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