Oozing-type rupture caused by right ventricular intramural hematoma after right ventricular infarction

Abstract

An 81-year-old man was admitted to the hospital because of decreased level of consciousness. He had bradycardia (27 beats/min). Electrocardiography showed ST-segment elevation in leads II, III, and aVF and ST-segment depression in leads aVL, V1. Transthoracic echocardiography (TTE) visualized reduced motion of the left ventricular (LV) inferior wall and right ventricular (RV) free wall. Coronary angiography revealed occlusion of the right coronary artery. A primary percutaneous coronary intervention was successfully performed with temporary pacemaker backup. On the third day, the sinus rhythm recovered, and the temporary pacemaker was removed. On the fifth day, a sudden cardiac arrest occurred. Extracorporeal cardiopulmonary resuscitation was performed. TTE showed a high-echoic effusion around the right ventricle, indicating a hematoma. The drainage was ineffective. He died on the eighth day. An autopsy showed the infarcted lesion and an intramural hematoma in the RV. However, no definite perforation of the myocardium was detected. The hematoma extended to the epicardium surface, indicative of oozing-type RV rupture induced by RV infarction. The oozing-type rupture induced by RV infarction might develop asymptomatically without influence on the vital signs of the patient. Frequent echocardiographic evaluation is essential in cases of RV infarction taking care of silent oozing-type rupture.

Learning objective: Inferior left ventricular infarction sometimes complicates right ventricular (RV) infarction. The typical manifestations of RV infarction include low blood pressure, low cardiac output, and elevated right atrium pressure. Although the frequency is low, fatal complications of oozing-type RV rupture might progress asymptomatically. Frequent echocardiographic screening is necessary to detect them.

Keywords: Cardiac arrest; Intramural hematoma; Oozing-type right ventricular rupture; Primary percutaneous coronary intervention; Right ventricular infarction; Transthoracic echocardiography.

Fig. 1

(A) 12-lead electrocardiography on admission shows an atrioventricular block with a junctional escape rhythm. ST-segment elevation in leads II, III, and aVF, and ST-segment depression in lead aVL, V1 is seen. His heart rate was 29 beats/min. (B) Coronary angiography (CAG) shows complete occlusion of right coronary artery (RCA) without collateral flow (white arrowhead). (C) A drug-eluting stent is implanted in the RCA segment two. Final CAG shows reperfusion of RCA. (D) On the fifth hospital day, sudden cardiac arrest is detected by monitor electrocardiography. LAO, left anterior oblique view.

Fig. 2

(A, B) On the third hospital day, transthoracic echocardiographic apical four-chamber view (A4C) just after sinus conversion shows an enlargement of the right ventricle (RV) and right atrium (RA), suggestive of RV infarction. The parasternal short-axis view (PSAX) shows no pericardial effusion. LV, left ventricle; LA, left atrium. (C) On the fifth hospital day, transthoracic echocardiographic PSAX reveals high echoic effusion in the pericardial side, indicating a hematoma (orange arrowheads). (D) Computed tomography revealed a high-density lesion around the pericardium on the fifth hospital day, indicating a pericardial hematoma (orange arrowheads). The white arrowhead shows a pericardial drainage catheter, which is ineffective because of pericardial hematoma.

Fig. 3

(A, B) Macroscopical findings of the autopsy show intramural hematoma extension to the epicardium around the posterior side of the RV free wall (yellow arrowheads). However, no obvious perforation was detected on the epicardial surface. (C) Hematoxylin-eosin staining demonstrates coagulative necrosis (black arrow), indicative of the early stage myocardial infarction within 12 h. (D) Masson staining demonstrates contraction band necrosis (black arrow), indicative of the early stage myocardial infarction within 24 h. (E) Masson staining demonstrates infiltration of inflammatory cells, fibroblast, and collagen fibers (black arrow), indicative of more than a few days after myocardial infarction. The mixed lesions of Fig. C, D, and E are detected around the intramural hematoma, indicative of hemorrhagic infarction more than a few days after myocardial infarction. (F, G) Hematoxylin-eosin staining demonstrates intramural hematoma, which extends to the epicardium surface, where might be an oozing site (yellow arrowheads), indicative of an oozing-type rupture as a clinical diagnosis.