CTV06 - Acute Mesenteric Ischemia Secondary to Left Ventricular Thrombus in a Patient With Subclinical Myocardial Infarction

Introduction/Purpose: Acute Mesenteric Ischemia (AMI) remains a worrisome and life-threatening pathology in which the outcome hinges upon early detection and intervention. In this formidable disease process there are several processes which may lead to ischemia - with the most common culprit being embolism. Emboli typically originate from a cardiac source, more specifically the left atrium or left atrial appendage. Another potential source of embolization that is not well documented is from left ventricular thrombus (LVT) thrombus which occurs in approximately 5% of patients post myocardial infarction. When emboli shower the arterial circulation, they frequently occlude mesenteric vessels, specifically the Superior Mesenteric Artery (SMA). With cessation of blood flow through the SMA, due to poor collateral flow, infarction of the entire distribution of small bowel may ensue with rapid progression to necrosis. Onset of ischemia is typically accompanied by acute onset of unrelenting abdominal pain, nausea, emesis, and diarrhea. Although the symptoms may be nondescript, rapid diagnosis is imperative given that associated mortality is between 60-80%. Given the staggering mortality, rapid diagnosis and intervention are essential. Here we present a case of AMI of the SMA secondary to cardiogenic emboli in a patient who developed left ventricular thrombus following untreated myocardial infarction.

Methods or Case Description: A 55 year-old male presented to our institution with prodromal symptoms consistent with acute mesenteric ischemia which began abruptly 3 hours prior to presentation. His physical exam was notable for stable vital signs with pain out of proportion to palpation, but no peritoneal signs. He was taken for computed tomography with angiography which revealed occlusion of the mid superior mesenteric artery. Additionally, a large thrombus was noted within the left ventricular apex which was further characterized by regional wall motion abnormality and cardiomyopathy on echocardiography. Further history revealed that he experienced anginal symptoms three weeks prior to presentation, however he never sought medical attention. Given his constellation of findings, he was commenced on unfractionated heparin infusion and taken emergently for angiography and placement of SMA catheter for infusion of thrombolytic agent. Unfortunately, the patient had persistent symptoms and repeat CTA revealing progressive thrombosis. Imaging findings paired with worsening metabolic acidosis and lactatemia, prompted emergent laparotomy. Upon laparotomy, there was frank necrosis from the proximal jejunum to distal ileum which was resected and left in discontinuity. The patient was then resuscitated further in the intensive care unit and taken for re-exploration after 24 hours. Repeat laparotomy revealed two short segments of full thickness ischemia at the proximal and distal stapled ends of bowel which were resected prior to primary anastomosis. Upon completion, approximately 150cm of small bowel remained in situ. Post-operatively, the patient had a protracted ICU course, but was subsequently discharged home 23 days after presentation. At follow-up and was well without signs or symptoms of short bowel syndrome and outpatient echocardiography noted improvement in LV systolic function, as well as near resolution of thrombus.

Outcomes: The mortality in AMI is striking and as such, urgent intervention is paramount. In this fascinating case, suffered embolization from an infrequently encountered source, the left ventricle - after myocardial infarction. Although the incidence of left ventricular thrombus after myocardial infarction is seemingly rare, it can have potentially lethal complications as evidenced in this case. The management strategy of LVT relies on the thrombus characteristics including size, mobility, and protrusion into ventricle. The mainstay of treatment for small thrombi is generally anticoagulation, whereas large thrombi pose more challenges in management. Guidelines for management of large thrombi remain sparse as these thrombi are typically seen in patients with acute reduction in cardiac function following myocardial infarction which creates management challenges. While the most common and feared embolic complication of LVT is cerebral emboli, embolization to gastrointestinal circulation can produce equally debilitating effects with similar morbidity. As is well documented, embolic AMI typically results from left atrial or left atrial appendage thrombi which can dislodge and shower systemic circulation. Regardless of the site of origination, emboli that result in ischemia or infarction can create a host of symptoms and create a wide range of physiologic derangements.

Conclusion: This nearly undocumented of LVT causing embolic occlusion of the SMA highlights the embolic potential of LVT and its implications in splanchnic circulation.Timely diagnosis and rapid treatment of acute mesenteric ischemia can lead to clinically excellent outcomes while limiting morbidity and mortality.