Localized absence of myocardium mimicking a contained left ventricular rupture.

We present the case of a 42-year-old man with a remarkably thin left ventricular (LV) wall in whom a covered rupture of the LV was suspected. Because of the suggestive imaging and the unusual history, the decision to explore through sternotomy was made. Intraoperative inspection revealed a limited area with a lack of myocardial tissue but did not confirm perforation of the LV. We would like to report this case because of the rarity of such a presentation and to critically discuss our decision.

This young patient collapsed during sport exercise and was found with a ventricular tachycardia that was converted successfully by the emergency team. He had never suffered from cardiac symptoms or arrhythmias in the past. At admission, he was conscious without any symptoms; even immediately prior to collapse, he had no pains, dyspnoea, or palpitations. Electrocardiogram and cardiac markers were normal. Computed tomography was performed to exclude aortic dissection or pulmonary embolism. This examination raised the suspicion of a covered perforation of the lateral wall of the LV with a contrast agent observed immediately under the epicardial surface ( and ). No leakage into the pericardial cavity was observed. Echocardiography confirmed this finding and showed a limited area with a very thin LV wall with some signs of fibrosis but no pericardial effusion. The picture was not typical for a LV diverticulum or a congenital aneurysm but also not for sinusoids or ventricular dysplasia ( and ). Coronary angiography was normal. Since covered rupture could not be excluded, the decision to proceed with explorative sternotomy was taken by the interdisciplinary team at 10 p.m. in the night.

Computerized tomography scan and transoesophageal echocardiography. (A) Sub-epicardial contrast medium without remaining visible left ventricular wall structure. (B) Communication of the defect with the left ventricular cavity. (C) Trans-gastric left ventricular view with the communication between the left ventricle and the sub-epicardial cavity visible (right with colour Doppler). (D) Very thin interventricular septum under the aortic valve with somewhat hyperdense echo signal (subendocardial fibrosis?).

At exploration, no pericardial effusion nor any haemorrhage within the wall of the LV was observed but palpation allowed to confirm a very thin left ventricular area of 4 × 4 cm with the absence of myocardial tissue, just anteriorly to the marginal branch of the circumflex artery. To avoid a potential injury of the marginal artery, a bovine pericardial patch was sutured to the epicardium over an area of 6 × 8 cm to cover the whole thinned area and reinforce the LV wall. Before tying the suture, BioGlue® (CryoLife, Inc., Kennesaw, GA, USA) was injected between the patch and the epicardium to provide additional mechanical stability to the weakened area. Additionally, a TachoSil® (Baxter, Deerfield, IL, USA) sealant patch was applied over the xeno-pericardial patch to induce adhesions of the cardiac surface with the pericardium. The postoperative course was favourable. According to the guidelines, the patient received an implantable cardioverter-defibrillator and was discharged on Day 6.

This very rare case with an obvious deficiency in the parietal left ventricular wall close to the base of the lateral papillary muscle of the mitral valve is difficult to classify into a particular group of diseases. The surgical inspection confirmed that the LV cavity was covered by the epicardium and a thin fibrotic tissue layer. Myocardial tissue was completely missing in this limited area. At echocardiography, the ventricle itself looked somewhat heavily trabeculated, but did not show the classical picture of sinusoids or LV non-compaction; this was excluded by postoperative magnetic resonance.[1,2] The finding did also not look like a congenital diverticulum nor like a congenital LV aneurysm.[3] At intraoperative inspection, the finding appeared like a localized agenesia of the LV myocardial wall but no similar case was found in the literature. In retrospect and considering the absence of pericardial effusion more critically, conservative treatment with intensive care monitoring, permissive hypotension, and repeated echocardiography would also have been probably safe.

The author provided an informed consent for his case to be published.