55. Case Report: Suicide LV post-TAVR – The University of Texas at Austin, Dell Medical School

CardioNerds (Amit Goyal & Daniel Ambinder) join UT-Austin cardiology fellows (Priya Kothapali, Sergio Montano, Travis Benzing, and Michael Grzeskowiak) for a speedboat adventure on Lake Travis! They discuss a fascinating case of Suicide LV post-TAVR. Dr. Mark Pirwitz provides the E-CPR and program director Dr. Clay Cauthen provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai. 

Jump to: Patient summaryCase figures & mediaCase teachingReferencesProduction team

CardioNerds (Amit Goyal & Daniel Ambinder) join UT-Austin cardiology fellows (Priya Kothapali, Sergio Montano, Travis Benzing, and Michael Grzeskowiak) for a speedboat adventure on Lake Travis! They discuss a fascinating case of Suicide LV post-TAVR. Dr. Mark Pirwitz provides the E-CPR and program director Dr. Clay Cauthen provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai.
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 woman in her early 70s, with a history of CAD s/p PCI to LAD & RCA with DES six months prior, to presentation, paroxysmal atrial fibrillation s/p ablation, type 2 diabetes mellitus, hypertension, prior TIA, and severe symptomatic AS was admitted for elective TAVR. She underwent successful implantation of a 29mm Medtronic Evolut Pro valve via left common femoral artery access. Post-valve deployment and following protamine administration for heparin reversal, course was complicated by hypotension with PEA arrest requiring CPR for 4 minutes. Intra-op TEE and angiogram showed a well-seated prosthetic valve with trace paravalvular leak and no evidence of acute aortic regurgitation, significant paravalvular leak, pericardial effusion, coronary obstruction, aortic dissection, or access site complications. She was treated for suspected Protamine reaction with high dose steroids & epinephrine. However, she remained hypotensive with MAP in the 50s on high dose Epinephrine, Norepinephrine, and Vasopressin. Hemodynamics by pulmonary artery catheter demonstrated CVP 7, mPA 26, PCWP 18 mmHg and CO/CI 2.8 L/min and 1.3 L/min/m2. Her lactate was elevated at 5.92 mmol/L and EKG demonstrated normal sinus rhythm. Bedside TTE in the ICU showed hyperdynamic LV function with LVEF 70% and near-complete mid to distal cavity obliteration with significant intracavitary gradient. She was diagnosed with post-TAVR suicide LV and managed with aggressive volume resuscitation and rapid wean of Epinephrine/Norepinephrine with improvement in her hemodynamics. She was eventually extubated and discharged on beta-blocker therapy.

Case Media

A. ECG: Normal sinus rhythm, no evidence of AV block, no ST segment elevation or depression.
B. CXR: Pulmonary vascular congestion, no pneumothorax, ETT at level of carina, PAC in appropriate position

TEE: Mid-Esophageal Three-Chamber View
TEE: Mid-Esophageal Short Axis View
Abdominal aortography showed no evidence of vascular access site complication or contrast extravasation.
Aortic root angiography showed no evidence of AI, coronary obstruction, or dissection.

Episode Schematics & Teaching

The CardioNerds 5! – 5 major takeaways from the #CNCR case

  1. Remind all CardioNerds – how do we define Severe Aortic Stenosis? 
  • By TTE, severe AS is defined as a mean gradient >40 mmHg, a peak velocity >4 m/s, an aortic valve area <1 cm2 and dimensionless index < 0.25. But remember, in HF patients decreased trans-aortic valve flow secondary to LV disease can make the diagnosis challenging! 
  • In HFrEF, patients with severe AS by aortic valve area (AVA) may not meet velocity or gradient criteria in one of four contexts: AVA measurement error, pseudo-severe AS, poor contractile reserve, or true severe Low Flow, Low Gradient AS (LFLG AS). 
  • Similarly, in HFpEF patients, disproportionately low flow or gradient AS may occur due to AVA measurement error or from true severe “paradoxical” LFLG due to decrease stroke volume (stroke volume index <35 mL/m2). 
  • Low gradient AS is a critical subset of patients with generally with a comparatively worse clinical trajectory marked by increased heart failure hospitalizations and mortality compared with high gradient AS. 
  • Enjoy the aortic stenosis series (Ep #1-2) and related figure for a deeper dive! 

2.     This patient received a TAVR for her severe AS. What are the major complications? 

  • Generally there are five relatively important post-TAVR complications – termed the “Big 5” – that contribute to long-term morbidity. These include disabling stroke, acute kidney injury, moderate/severe paravalvular leak, vascular and bleeding complications, and conduction abnormalities with possible need for PPM. 
  • Modern TAVR valves include mechanisms to reduce paravalvular leak (i.e., an outer skirt or a porcine pericardial tissue wrap or cuff), but may lead to more conduction abnormalities 

3.     This case covered Suicide LV. What is the pathophysiology behind this? 

  • Severe AS leads to LV hypertrophy and chronic pressure overload. When the fixed obstruction is relieved, the increased contractility of the LV is “unmasked” and can lead to dynamic LV cavity obstruction or obliteration.  
  • When this compromises cardiac output, these labile hemodynamics are termed “suicide LV”.   

4.     What are risk factors for developing Suicide LV post-AVR? 

  • The major risk factors for Suicide LV with dynamic intracavitary gradient include small LVOT and LV size, hyperdynamic and elevated LVEF, asymmetric septal hypertrophy with an elevated interventricular septal to posterior wall thickness ratio, high valve gradients prior to AVR and small LV wall mass. 

5.     What should be my basic approach to Suicide LV management? 

  • The management of suicide LV is similar to that of Hypertrophic Obstructive Cardiomyopathy (see Ep#3) and related figure for a refresher! 
  • The basics include increasing preload with intravenous fluids, increasing afterload to reduce intra-cavitary gradients (phenylephrine tends to be the vasoactive of choice), avoiding inotropes (e.g., digoxin or beta-agonist infusions) while considering negative inotropes (e.g., beta blockers), and maintaining AV synchrony to ensure adequate LV preload 


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