Histologic Examination of the Heart in the Forensic Autopsy

Duncanson, Emily; Mackey‐Bojack, Shannon

doi:10.1177/1925362118797736

Cited by 8 publications

(4 citation statements)

References 27 publications

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“…The absence of myocyte injury distant from the sites of inflammation is a key feature in differentiating myocarditis from other pathologies such as ischaemic injury and neurocardiogenic injury. [8] The postmortem histological examination, in this case, was consistent with the above findings which confirmed the presence of myocarditis. Considering all the aspects and the absence of any other aetiology, it was reasonable to assume that this was a case of druginduced myocarditis due to Zoledronic acid.…”

Section: Discussionsupporting

confidence: 87%

“…[7] Although some other reported cases had pericarditis together with myocarditis after the administration of Zoledronic acid, this case did not show the involvement of pericardium. [8] In this case, the patient was suspected to have a plasma cell neoplasm which was later confirmed by the postmortem bone marrow biopsy. He was started on Zoledronic acid in order to control the hypercalcaemia; which resulted in the development of cardiovascular symptoms which were absent previously.…”

Section: Discussionmentioning

confidence: 85%

“…Even though several criteria have been presented for the histological diagnosis of myocarditis, their practical utility in postmortem specimens remains questionable. [8] The myocyte injury patterns consist of myocyte destruction by inflammation or patchy fibrosis associated with residual inflammation. The absence of myocyte injury distant from the sites of inflammation is a key feature in differentiating myocarditis from other pathologies such as ischaemic injury and neurocardiogenic injury.…”

Section: Discussionmentioning

confidence: 99%

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Fatal Myocarditis Following Administration of Zoledronic Acid: A Case Report

et al. 2022

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Myocarditis is a potentially life-threatening condition which occurs due to inflammation of the cardiac muscle. It has a multitude of causes including certain medications. Zoledronic acid is a bisphosphonate given as an intravenous preparation for bone-related diseases. Medical literature provides details about only very few cases of Zoledronic acid-induced myocarditis and all of them were non-fatal. We report a fatal case of myocarditis due to the administration of intravenous Zoledronic acid. A 40-year-old male with a history of multiple joint pain and swelling for one week and right knee joint swelling for three months was administered intravenous Zoledronic acid. One day after the administration of Zoledronic acid patient developed dizziness and eventually became drowsy. His ECG revealed ST depressions in leads I, II, and aVF, as well as leads V3 to V5. Highly sensitive Troponin I was elevated to 2195.3 pg/ml (normal:<26.5 pg/ml) and Echocardiogram showed an ejection fraction of 30% with hypokinetic wall segments and regional wall motion abnormalities. He went into cardiogenic shock and was pronounced dead. At the autopsy, the macroscopic examination did not reveal any noticeable fatal pathology. However histological examination of the myocardium revealed diffuse infiltration of mononuclear cells with myocyte necrosis. Although life-threatening adverse effects of Zoledronic acid such as severe systemic inflammatory response syndrome and myopericarditis have been previously reported, fatalities due to Zoledronic acid-induced myocarditis, like in this case, has not been reported. This case highlights the importance of being vigilant in using this drug.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

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Fatal Myocarditis Following Administration of Zoledronic Acid: A Case Report

et al. 2022

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“… [26] Microscopic changes of acute ischemia were characterized by reversible hydropic degeneration, irreversible contraction band necrosis, hyper-eosinophilic myocytes with nuclear loss, and myocyte necrosis with interstitial neutrophils. [27] Myocarditis was defined as an inflammatory infiltrate consisting of ≥14 lymphocytes/mm 2 including ≤ four monocytes/mm 2 with the presence of CD3-positive T lymphocytes ≥ seven cells/mm 2 in the setting of myocyte degeneration and necrosis. [ 28 , 29 ] COVID-19 pneumonia was defined histologically as diffuse alveolar damage and/or organizing pneumonia.…”

Section: Methodsmentioning

confidence: 99%

Cardiac pathology in COVID-19: a single center autopsy experience

Sang

Burkett

Heindl

et al. 2021

Cardiovascular Pathology

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Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is commonly associated with myocardial injury and heart failure. The pathophysiology behind this phenomenon remains unclear, with many diverse and multifaceted hypotheses. To contribute to this understanding, we describe the underlying cardiac findings in fifty patients who died with coronavirus disease 2019 (COVID-19). Methods Included were autopsies performed on patients with a positive SARS-CoV-2 reverse-transcriptase-polymerase-chain reaction test from the index hospitalization. In the case of out-of-hospital death, patients were included if post-mortem testing was positive. Complete autopsies were performed according to a COVID-19 safety protocol, and all patients underwent both macroscopic and microscopic examination. If available, laboratory findings and echocardiograms were reported. Results The median age of the decedents was 63.5 years. The most common comorbidities included hypertension (90.0%), diabetes (56.0%) and obesity (50.0%). Lymphocytic inflammatory infiltrates in the heart were present in eight (16.0%) patients, with focal myocarditis present in two (4.0%) patients. Acute myocardial ischemia was observed in eight (16.0%) patients. The most common findings were myocardial fibrosis (80.0%), hypertrophy (72.0%), and microthrombi (66.0%). The most common causes of death were COVID-19 pneumonia in 18 (36.0%), COVID-19 pneumonia with bacterial superinfection in 12 (24.0%), and COVID-19 pneumonia with pulmonary embolism in 10 (20.0%) patients. Conclusions Cardiovascular comorbidities were prevalent, and pathologic changes associated with hypertensive and atherosclerotic cardiovascular disease were the most common findings. Despite markedly elevated inflammatory markers and cardiac enzymes, few patients exhibited inflammatory infiltrates or necrosis within cardiac myocytes. A unifying pathophysiologic mechanism behind myocardial injury in COVID-19 remains elusive, and additional autopsy studies are needed.

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