Two cases of right ventricular ischemic injury due to massive pulmonary embolism

doi:10.1016/S0379-0738(00)00367-4

Forensic Science International

Volume 116, Issues 2–3, 15 February 2001, Pages 189-195

https://doi.org/10.1016/S0379-0738(00)00367-4 Get rights and content

Abstract

In general, massive pulmonary embolism induces severe right ventricular overload, but pathological changes in the right ventricle due to pulmonary embolism is rarely seen. In this report, we describe two autopsy cases of massive pulmonary embolism without pre-existing cardiopulmonary disease. Both cases were accompanied by myocarditis-like changes in the right ventricle and infiltration of a number of polymorphonuclear neutrophils and mononuclear cells into the dilated right ventricular wall. Transmural or subendocardial coagulation necrosis was not apparent. Almost all of the mononuclear cells were immunohistochemically revealed to be CD68-positive macrophages. We speculated that these findings resulted from ischemia due to massive pulmonary embolism.

Introduction

Acute pulmonary embolism is a major potential complication in hospitalized patients. During the past 50 years or more, there have been a number of studies of it’s pathophysiology [1], [2], [3], [4], [5], [6], [7], as well as clinical ecocardiographic studies [8], [9], [10], [11]. It is generally accepted that pulmonary embolism causes right ventricular dysfunction. However, pathological change of the right ventricle is rarely seen in cases of pulmonary embolism. Although there have been a few reports suggesting that isolated right ventricular infarction can be induced by massive pulmonary embolism [12], [13], [14], little is known about the detailed pathological findings in human right ventricular damage due to massive pulmonary embolism.

In this report, we describe two autopsy cases of massive pulmonary embolism. Both cases showed a number of cells infiltrating the entire right ventricular wall, but no apparent transmural or subendocardial coagulation necrosis. We demonstrate the result of immunostaining with antibodies against infiltrating cells, and discuss its pathogenesis.

Section snippets

Case 1

A 42-year-old woman without pre-existing cardiopulmonary diseases sustained a fracture of the left fibra in a road traffic accident and her left leg was placed in a plaster cast. About a week later, she complained of periodic chest pain, but this was diagnosed as myalgia and she was treated only medically for trauma. However, the chest pain continued, and on the 12th day after the traffic accident she suddenly became unconscious when she was telephoning. Pulmonary embolism was diagnosed by

Materials and methods

Transverse sections (along the short axis) of the heart were obtained at the following three levels: below the tricuspid valve, at the apex of a heart, and midway between these two points. For microscopical observation, the specimens were fixed in 10% formaldehyde solution and embedded in paraffin. Sections of 2–3 μm thick were prepared with hematoxylin-eosin (HE) stain. Immunostaining with the following antibodies was then performed: anti-human-macrophage-CD68 (clone KP1) antigen (Dako,

Macroscopical findings

In case 1, the patient was 161 cm tall, and in case 2, 185 cm. In case 1, the body weight was 93 kg, and in case 2, 87 kg. In both cases, the pulmonary embolism was massive and the embolus extended into the main pulmonary artery. In both cases, the embolus originated in a deep vein of the left leg.

In case 1, the weight of the heart was 455 g, and in case 2, 498 g. In case 1, the weight of the lung was 409 g (left) and 533 g (right), and in case 2, 811 g (left) and 1069 g (right). Both cases showed

Discussion

In both the cases of massive pulmonary embolism that we examined, we saw neither right ventricular hypertrophy nor stenosis of the coronary arteries. The endocardium of the right ventricle was smooth. Both patients had no history of cardiopulmonary diseases. In case 2, psychiatric drugs were a possible cause of cardiac dysfunction. However, to the author’s knowledge, there has been no report suggesting that such drugs induce myocarditis-like change in limited to the right ventricle. Therefore,

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¹: Present address: National Research Institute of Police Science, Kashiwanoha 6-3-1, Kashiwa City, Chiba 277-0882, Japan.

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Case ReportTwo cases of right ventricular ischemic injury due to massive pulmonary embolism

Abstract

Introduction

Section snippets

Case 1

Materials and methods

Macroscopical findings

Discussion

Am. J. Cardiol.

Am. Heart J.

Am. Heart J.

Am. J. Cardiol.

Am. Heart J.

Am. Heart J.

The physiology of pulmonary embolism as disclosed by quantitative occlusion of the pulmonary artery

Arch. Surg.

The limits of right ventricular compensation following acute increase in pulmonary circulatory resistance

Circ. Res.

Coronary artery pressure and strength of right ventricular contraction

Circ. Res.

Case Report
Two cases of right ventricular ischemic injury due to massive pulmonary embolism