**Introduction/Hypothesis:**
Ventricular free wall rupture is an exceedingly rare, but devastating complication of acute myocardial infarction, occurring in .01 percent of patients presenting with both NSTEMI and STEMI.1 Infrequently, the rupture of the ventricular free wall is contained by epicardial clots or pericardial adhesions; when this happens, it can lead to the formation of a pseudoaneurysm.2 Presentation of patients with pseudoaneurysm is widely variable, with the most commonly reported symptoms being congestive heart failure (36%), chest pain (30%), dyspnea (25%), and up to 12% of patients are asymptomatic at the time of diagnosis.3

**Methods**
An 85 year-old female with a past medical history of hypertension, hyperlipidemia, non-alcoholic steatohepatitis, and chronic kidney disease presented to the Emergency Department with fatigue and sudden onset of shortness of breath. She was normotensive, tachycardic at 110 bpm, saturating at 90% on room air, and mildly tachypneic in the 30s. She appeared nontoxic and further physical exam was largely unremarkable. Labs were pertinent for a troponin of 106, NT proBNP of 10,548, and lactate of 1.5. EKG revealed new T wave inversions in the inferior and lateral leads, septal Q waves, and slight ST-depression in V5 and V6. She[RJ1] was given IV Lasix, 81 mg aspirin, started on heparin, and admitted for potential NSTEMI. TTE revealed a severely reduced ejection fraction of 24.4% and a large mid to apical pseudoaneurysm along the inferolateral wall of the left ventricle contained within the pericardium measuring 5.7 x 8.4 cm with free flow of blood between the LV cavity and the pseudoaneurysm. She was transferred to the CICU and an emergent cardiothoracic surgery consult was placed.

**Results**
The patient underwent emergent coronary catheterization, revealing 100% occlusion of the distal circumflex and 99% occlusion of the middle right coronary artery, which were suspected to be the culprit of the patient’s transmural infarct and subsequent myocardial rupture. An EKG gated CT cardiac angiogram was obtained for evaluation for surgery. Following the catheterization, the patient underwent intra-aortic balloon pump placement for persistent hypotension. The subsequent day, the patient underwent a primary median sternotomy and patch repair of the free wall rupture and coronary artery bypass grafting of the SVG to LAD. Following surgery, the IABP was able to be removed. The patient was discharged to a cardiac rehabilitation facility before ultimately returning home after 3 weeks.

**Conclusion**
Clinical suspicion should be high for mechanical complications following a myocardial infarction, with the preferred method of diagnosis being transthoracic echocardiography. If a pseudoaneurysm is identified, prompt surgical intervention with either direct defect closure with sutures or patch closure over an area of viable myocardium is key. In poor surgical candidates, percutaneous closure methods may be considered. The estimated risk of pseudoaneurysm rupture is between 30 to 45% without intervention.2



**Introduction/Hypothesis:**
Ventricular free wall rupture is an exceedingly rare, but devastating complication of acute myocardial infarction, occurring in .01 percent of patients presenting with both NSTEMI and STEMI.^1^ Infrequently, the rupture of the ventricular free wall is contained by epicardial clots or pericardial adhesions; when this happens, it can lead to the formation of a pseudoaneurysm.^2^ Presentation of patients with pseudoaneurysm is widely variable, with the most commonly reported symptoms being congestive heart failure (36%), chest pain (30%), dyspnea (25%), and up to 12% of patients are asymptomatic at the time of diagnosis.^3^

**Methods**
An 85 year-old female with a past medical history of hypertension, hyperlipidemia, non-alcoholic steatohepatitis, and chronic kidney disease presented to the Emergency Department with fatigue and sudden onset of shortness of breath. She was normotensive, tachycardic at 110 bpm, saturating at 90% on room air, and mildly tachypneic in the 30s. She appeared nontoxic and further physical exam was largely unremarkable. Labs were pertinent for a troponin of 106, NT proBNP of 10,548, and lactate of 1.5. EKG revealed new T wave inversions in the inferior and lateral leads, septal Q waves, and slight ST-depression in V5 and V6. She[RJ1] was given IV Lasix, 81 mg aspirin, started on heparin, and admitted for potential NSTEMI. TTE revealed a severely reduced ejection fraction of 24.4% and a large mid to apical pseudoaneurysm along the inferolateral wall of the left ventricle contained within the pericardium measuring 5.7 x 8.4 cm with free flow of blood between the LV cavity and the pseudoaneurysm. She was transferred to the CICU and an emergent cardiothoracic surgery consult was placed.

**Results**
The patient underwent emergent coronary catheterization, revealing 100% occlusion of the distal circumflex and 99% occlusion of the middle right coronary artery, which were suspected to be the culprit of the patient’s transmural infarct and subsequent myocardial rupture. An EKG gated CT cardiac angiogram was obtained for evaluation for surgery. Following the catheterization, the patient underwent intra-aortic balloon pump placement for persistent hypotension. The subsequent day, the patient underwent a primary median sternotomy and patch repair of the free wall rupture and coronary artery bypass grafting of the SVG to LAD. Following surgery, the IABP was able to be removed. The patient was discharged to a cardiac rehabilitation facility before ultimately returning home after 3 weeks.

**Conclusion**
Clinical suspicion should be high for mechanical complications following a myocardial infarction, with the preferred method of diagnosis being transthoracic echocardiography. If a pseudoaneurysm is identified, prompt surgical intervention with either direct defect closure with sutures or patch closure over an area of viable myocardium is key. In poor surgical candidates, percutaneous closure methods may be considered. The estimated risk of pseudoaneurysm rupture is between 30 to 45% without intervention.^2^



Left Ventricular Pseudoaneurysm Presenting as an Acute Heart Failure Exacerbation

This course will explore basic and cutting-edge imaging techniques to improve patient care and hone individual skills in performance and interpretation of echocardiography, nuclear cardiology, cardiac computed tomography, and cardiovascular magnetic resonance imaging. Days will reinforce how cardiovascular imaging may improve comprehension in ischemic heart disease, structural heart disease, cardiomyopathies, and heart failure. Experts will utilize novel techniques to reinforce key topics including taped interventional cases and a strong emphasis on case presentations.