Show notes
CardioNerds (Amit Goyal & Daniel Ambinder) join University of Connecticut (UCONN) cardiology fellows (Mansour Almnajam, Justice Oranefo, Yasir Adeel, and Srinivas Nadadur) as they enjoy the amazing view from the Heublein tower! They discuss a challenging case of left ventricular free wall rupture & pseudoaneurysm as a complication of a STEMI. Dr. Peter Robinson provides the E-CPR and program director Dr. Joyce Meng provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai.
Jump to: Patient summary - Case media - Case teaching - References
Episode graphic by Dr. Carine Hamo
The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.
We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.
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Patient Summary
A man in his mid 50s with no significant PMH presented with a 10-day history of chest pain that progressed to acute pleuritic pain and shortness of breath in the past 24 hours. On arrival, he was hypothermic, in rapid atrial fibrillation with HR in the 130-150s, and an initial BP was not able to be obtained. He was tachypneic with labored breathing, lethargic, and cyanotic. Exam revealed markedly elevated JVP, cool extremities, and diminished breath sounds with bibasilar rales. Labs demonstrated leukocytosis, significantly elevated liver enzymes, troponin-I at 10.91, elevated NT-proBNP, and lactate at 6. ECG demonstrated tall, broad R-waves in V1-V4 with downsloping STD and upright T-waves concerning for a posterior infarct. He was immediately intubated, cardioverted into NSR, and started on vasopressors. Bedside echocardiogram demonstrated diffuse LV hypokinesis with akinesis of the inferolateral wall, LVEF 25-30%, and pericardial fluid with hyperechoic material adherent to the inferior wall as well as tamponade physiology. Chest CTA was negative for aortic dissection and confirmed hemopericardium. He was taken to the OR where he underwent a subxiphoid pericardial window. They found significant clot burden (both old and new), but no frank rupture. Adherent clot was not removed to prevent further hemodynamic compromise. Intraoperative TEE additionally demonstrated severe eccentric MR with partial posteromedial papillary muscle rupture. An IABP was placed and inotropic and vasoactive support was continued to temporize pending definitive therapy and the patient improved hemodynamically. Repeat TTE prior to surgery demonstrated a large apical and inferolateral pseudoaneurysm. Coronary angiogram revealed proximal occlusion of the LCx and diffuse three vessel coronary disease otherwise. He ultimately underwent CABG, mechanical mitral valve replacement, and pericardial patch repair of the ventricular pseudoaneurysm. Final diagnosis: Free Wall Rupture & Pseudoaneurysm. Thankfully, the patient ultimately made a complete recovery!
Case Media
ABCDEFClick to Enlarge
A. ECG: tall, broad R-waves in V1-V4 with downsloping STD and upright T-wavesB. CXRC. CT angiogram thoracic aorta: Moderate sized hemopericardium with tamponade physiology. Transmural infarction of LV base to mid inferior wall. Circumflex occlusion just beyond the first obtuse marginal. Normal aorta without dissection or aneurysm.D-F. Coronary angiogram: LCx is occluded proximally, distal vessel fills via faint collaterals from the right, OM1: Fills via right to left collaterals. LAD: 70%, mid; 90%, apical, 1st diagonal: 50%, ostial; 60-70%, proximal; 90% of inferior subdivision, bifurcating vessel. RCA: (Dominant); 50%, mid: 40%, distal. PDA: 60%, proximal, small-caliber vessel. PLV: 60-70%, proximal
TEE: Trans-gastric views
TEE
TEE: MV with color
CORS: Occluded Lcx
CORS: Obstructive CAD in LAD
CORS: RCA
TTE: PLA
TTE: A4C
TTE: A4C with contrast demonstrating an LV pseudoaneurysm
Episode Schematics & Teaching
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The CardioNerds 5! – 5 major takeaways from the #CNCR case
This patient presented with EKG showing a posterior myocardial infarction. Why was he not taken to the cath lab immediately for revascularization? Duration of ischemia, its relationship to infarct size, and the mortality benefit from reperfusion therapies are crucially related to time in the very early course of STEMI. However, this relationship breaks down in patients presenting late after a STEMI. In OAT (Occluded Artery Trial), hemodynamically stable patients who presented late (3-28 days) after a myocardial infarction with high risk features (e.g., proximal LAD occlusion with TIMI 0 to 1 flow) were randomized to PCI + optimal medical therapy (OMT) within 24 hours or OMT alone. There was no difference in the primary endpoint of all-cause mortality, nonfatal MI, or NYHA class III to IV heart failure. These findings are reflected in the ACC/AHA guidelines, where delayed PCI of a totally occluded infract artery 24 hours after STEMI in hemodynamically and electrically stable patients is given a Class III recommendation (no benefit). Although the patient presented with EKG findings concerning for a posterior STEMI, this was likely 10 days after his acute insult. In addition, his hemodynamic instability and bedside POCUS raised the concern for a mechanical complication of a STEMI. In a patient with suspected mechanical complication of acute MI, such as free wall rupture and acute MR, the priority of therapy is to rapidly identify the mechanical problem and perform emergency surgical therapy. Furthermore, the need for antiplatelet therapy following any PCI would complicate surgical planning. PCI may be helpful in patients with ischemia induced papillary muscle dysfunction ("ischemic MR"). However there is no role for immediate PCI when the mechanical integrity of the mitral valve has been compromised. This patient presented with hemodynamic instability and bedside POCUS revealed pericardial fluid with tamponade physiology. What are some causes of acute hemorrhagic pericardial effusion? When thinking about hemorrhagic pericardial effusions, expedited evaluation is critical. While there is overlap with traditional causes of pericardial effusion, some causes may need immediate intervention. Amongst these considerations are iatrogenic complication of cardiac surgery, cardiac catheterization, or electrophysiologic procedures. Other etiologies include complications of myocardial infarction including free wall rupture/pseudoaneurysm, complication of aortic dissection, and trauma. As with serous pericardial effusions, malignancy should remain on the differential, as well as tuberculosis in endemic areas. A CTA of the aorta ruled out dissection but showed a moderate sized hemopericardium raising concern for a mechanical complication of posterior MI, specifically a free wall rupture (FWR). What are the risk factors for a FWR after an MI? Ventricular free wall rupture is quite uncommon in the reperfusion era; however, if it does occur, mortality rates are high. FWR typically occurs acutely or sub-acutely, occurring within 2 weeks for 90% of patients. Risk factors include first myocardial infarction, poor collateralization of the infarcted territory, older age, female sex, persistent ST elevation and delayed presentation/unsuccessful revascularization. When patients present acutely, patients will typically develop tamponade, rapidly progress to pulseless electrical activity, and/or sudden cardiac death. When patients develop subacute FWR or contained rupture (i.e., pseudoaneurysm), they may present with signs and symptoms of pericarditis and subacute hypotension. When FWR occurs, it typically involves the anterior, posterior, or lateral left ventricular wall. The pathophysiology of ventricular free wall rupture is related to the timing of the rupture. Rupture will typically occur at the border of the necrotic and healthy (and often hyperkinetic) myocardium and in areas of the greatest shear stress. In the left ventricle, this tends to be near the anterior and posterior papillary muscles, regardless if they are compromised in the infarct. Note, pericardial effusions can be a common finding in the setting of an acute MI (~15-25% of patients in the acute setting); however, a rapidly expanding pericardial effusion associated with significant wall thinning along the infarcted region should raise the suspicion for LV free wall rupture. The patient was stabilized after surgical evacuation of pericardial fluid in the OR. When should you consider pericardiocentesis vs surgical management? In cases of cardiac tamponade with concern for circulatory collapse there are no absolute contraindications to pericardiocentesis. The goal is urgent drainage of pericardial fluid and how we drain the fluid will depend on the etiology, acuity, and available providers.