26A hit that was a miss- a STEMI with a twist

Abstract

A 35 year old gentleman presented after a fall from a motorcycle leading to traumatic injury on the left side of the chest, followed by sudden syncope which lasted for 10-15 minutes. A day later he began to experience severe retrosternal chest pain associated with profuse sweating, vomiting and weakness. He was rushed to the nearby hospital where the ECG showed acute ST elevation indicating an anterior wall myocardial infarction after which he was transferred to our hospital for further management. On arrival, he appeared sick, sweating with cold clammy extremities, in shock with BP 80/60 mmHg, tachycardia 142/minute normal sinus rhythm. Auscultation revealed bilateral basal crepitations up to mid-scapulae with LV S3 suggesting pulmonary edema secondary to left ventricular failure (LVF) with cardiogenic shock. He was planned for Primary PCI. Emergency echocardiographic screening was done which is a routine practice. This revealed a very large variably echogenic structure involving the apex, anterior septum and mid anterior wall. The ejection fraction was 25% with severe mitral regurgitation (MR). There was severe pulmonary hypertension with PASP 60 mmHg., restrictive grade 3 diastolic dysfunction and central venous pressure of 15 mmHg or more. Diagnosis of Intra-Myocardial dissecting hematoma (IMH) was based on the presence of an expansile mass bound by intact endocardium and epicardium which expands into the LV cavity during systole. In view of his chest trauma, CT chest was done which revealed lung contusions and confirmed the findings of IMH. Due to his unstable hemodynamic condition intra aortic balloon pump (IABP) was deployed to stabilize the patient in the ICU. PCI was deferred due to the fact that post PCI compulsory aggressive use of anti-thrombotics (heparin, dual antiplatelet agents) could further increase the IMH and may lead to catastrophic pseudoaneurysm, cardiac rupture, infarct extension, arrhythmias, aggravation of LVF and mortality. The patient was kept on medical management with low dose aspirin. Clopidogrel and heparin were withdrawn. High dose statins were added. He subsequently underwent coronary angiography, which revealed 100% occluded Left Anterior descending artery (LAD) but intervention was deferred due to above mentioned reasons and the fact that the presence of IMH denotes a transmural infarct and not much benefit would have been achieved by PCI at this stage. Gradually he was weaned off the IABP support and optimized on medical therapy and discharged a month later with good functional recovery but with persistent severe LV dysfunction and moderate MR. He came for subsequent follow up 2 months post factum, remains in NYHA class II on medical management. The echocardiogram showed a gradual regression of the hematoma and scar formation in the affected region. The literature on treatment of IMH remains controversial and scant. The unique features of this case are: 1) Suspected traumatic occlusion of LAD masquerading as STEMI anterior wall. The delayed presentation of severe anginal syndrome after a day of trauma supports this etiology. 2) Value of echocardiography in emergency primary PCI setting which helped in diagnosis of IMH and altered the treatment approach completely to medical management over the usual primary PCI. 3) The role of IABP as a bail out treatment modality, prolonged ICU stay and poor LV recovery of function with potentially poor long term outcomes. 4) Need for recognizing this rare entity of IMH and differentiate it from the intraventricular clot. Hallmark of IMH being the presence of an expansile echolucent mass bound by intact endo and epicardium with systolic expansion into LV cavity. (Figure Presented).