Post-traumatic pseudoaneurysm producing coronary milking

Abstract

Left ventricular pseudoaneurysm is a rare complication of myocardial infarction, but it may also result from cardiac surgery, endocarditis, chest trauma, tumours, electrophysiological studies and congenital defects. An accidentally discovered uncommon case of a post-traumatic pseudoaneurysm that produced a selective compression of the circumflex coronary artery during systole is reported.

CASE PRESENTATION

A 29-year-old Colombian woman was admitted to hospital complaining of oppressive chest pain that had lasted for more than 2 h. The electrocardiogram showed ST-T segment elevation on inferior leads, and cardiac injury enzymes reached values of 1590 μg/L for troponin T and 1195 U/L for creatine kinase. The initial diagnosis was myopericarditis, because the patient was recovering from an influenza process and had no apparent cardiovascular risk factors. On further investigation, a two-dimensional echocardiography showed posterior wall hypokinesis and the patient developed Q waves on inferior leads and R waves on V1. Cardiac catheterization was performed to exclude coronary artery disease. Cardiac angiography showed a contrast-filled protruding mass near the aortic root, with severe milking effect on the circumflex artery and first obtuse marginal branch. Ventricular angiography revealed the mass to be a pseudoaneurysm (Figure 1).

Figure 1.

Ventricular angiography in right anterior oblique (A) and lateral (B) projections showing the pseudoaneurysm (Ps)

A transesophageal echocardiogram confirmed the presence of an anterolaterally located ventricular pseudoaneurysm 2.6 cm × 1.9 cm in diameter, without thrombi (Figure 2). To prevent future events, surgical removal was performed and the pseudoaneurysm was successfully repaired and sealed with a Dacron patch.

Figure 2.

Transesophageal echocardiography showing an anterolateral ventricular pseudoaneurysm (Ps). LA Left atrium

DISCUSSION

Left ventricular pseudoaneurysm is a rare complication of myocardial infarction (1). It originates after a left ventricular rupture following myocardial infarction by adherent pericardium. Thus, a distended thin-walled sac without a myocardial layer is formed. In comparison with a true aneurysm, the risk of rupture of a pseudoaneurysm is high, and these lesions must be surgically repaired as soon as the diagnosis is made (2). Other complications such as heart failure, systemic embolisms and arrhythmias have also been described. A pseudoaneurysm may also result from cardiac surgery, infective endocarditis, chest trauma, tumours, electrophysiological studies and congenital defects (3).

A pseudoaneurysm has a narrow connecting orifice, whereas a true aneurysm has a wide orifice. Therefore, all imaging techniques focus on assessing the size of the neck to distinguish a true from a pseudoaneurysm (4). Surgery revealed that the ventricular lesion was a false aneurysm and the neck was not as narrow as those observed postinfarction.

The relationship between acute coronary syndromes and influenza is well established (5), and myocardial infarction due to myocardial bridging has also been reported (6). However, we believe our patient had a myocarditis. Based on her history of chest trauma as a result of a traffic accident when she was a child, the findings in surgery and the fact that toxicological screening tests in urine samples and Trypanosoma cruzi serology were all negative, we concluded that the pseudoaneurysm was of traumatic origin.

No cases of pseudoaneurysm producing selective compression of coronary arteries during systole have been previously published, and this case is, according to our knowledge, the first to be documented in the literature.