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Fatal myopericarditis complicated with coronary vein perforation under the triple antithrombotic therapy: a case report.

ABSTRACT:

Background

Acute pericarditis generally follows a mild clinical course and is rarely fatal. Coronary vein involvement is rarely reported.

Case summary

We report an autopsy case of cardiac tamponade from idiopathic myopericarditis due to coronary venous perforation under the triple antithrombotic therapy. A 69-year-old man was admitted to our hospital with abnormal findings on electrocardiography, bloody pericardial effusion, and mild elevation of troponin I. Oral anti-inflammatories were started and the patient followed a benign course. However, on hospital Day 5, he suddenly suffered cardiogenic shock with pulseless electric activity due to cardiac tamponade under the combination use of the dual antiplatelet drugs and an anticoagulant drug. He died despite intense medical treatment. Autopsy revealed cardiac tamponade caused by perforation in the coronary venous wall. To the best of our knowledge, this is the first description of fatal myopericarditis as a complication of coronary venous perforation.

Discussion

The aetiology and mechanism remain unknown; however, we should take care for this rare complication in patients with acute myopericarditis and bloody effusion under the triple antithrombotic therapy.

SUBMITTER: Takasaki A

PROVIDER: S-EPMC8188861 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background: Cerebral infarction is a rare neurological complication of Kawasaki disease (KD) and occurs in the acute or subacute stage. There have been no reported cases of late-onset fatal cerebral infarction presenting over 1 year after the onset of KD. Case Presentation: A 5-month-old male patient with KD received timely intravenous immunoglobulin therapy; however, extensive coronary artery aneurysms (CAA) and coronary artery thrombosis (CAT) developed 1 month later. Anticoagulation and thrombolytic agents were suggested, but the child's parents refused. Fifteen months after KD onset, an attack of syncope left him with left hemiplegia; brain computerized tomography (CT) scans revealed cerebral infarction of the right basal ganglion without hemorrhage. Magnetic resonance angiography (MRA) revealed severe stenosis of the right middle cerebral artery, and a series of tests were performed to exclude other causes of cerebral infarction. Considering the cerebral infarction and CAT, combination therapy with urokinase and low-molecular-weight heparin (LMWH) was initiated within 24 h of syncope onset, together with oral aspirin and clopidogrel. Five days later, his clinical symptoms partially regressed and he was discharged. Unfortunately, 5 days after discharge, his clinical condition suddenly deteriorated. Repeat brain CT showed hemorrhagic stroke involving the entire left cerebral area, in addition to the previous cerebral infarction in the right basal ganglion, with obvious secondary cerebral swelling and edema, which might have been caused by previous thrombolysis. Severe cerebral hernias developed quickly. Regrettably, the patient's parents abandoned treatment because of economic factors and unfavorable prognosis, and he died soon after. Conclusions: Cerebral infarction and cerebral artery stenosis can develop late, even 1 year after the onset of KD. Pediatricians should be aware of the possibility of cerebrovascular involvement in addition to cardiac complications during long-term follow-up of KD patients. Prompt anticoagulation therapy and regular neuroimaging evaluation are essential for the management of patients with KD with giant CAA and/or CAT.