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It’s another session of CardioNerds Rounds! In these rounds, Dr. Natalie Stokes (Formerly FIT at University of Pittsburgh and now General Cardiology Faculty at University of Pittsburgh) and Dr. Karan Desai (formerly FIT at University of Maryland and now General Cardiology faculty at Johns Hopkins) join Dr. Rick Nishimura (Professor of Medicine at Mayo Clinic) to discuss the nuances of managing mitral regurgitation through real cases. Dr. Nishimura has been an author or Chair of the ACC/AHA valve guidelines going back 20 years and has been recognized internationally as one of the world’s best educators, so you don’t want to miss the #NishFactor on these #CardsRounds! Audio editing by CardioNerds academy intern, Pace Wetstein.
This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.
Speaker disclosures: None
Show notes – Mitral Regurgitation with Dr. Rick Nishimura
Case #1 Synopsis:
A man in his 70s with a history of non-ischemic cardiomyopathy (last known LVEF 15-20%) and atrial fibrillation, presented with decompensated heart failure in the setting of moderate to severe mitral regurgitation. He was diuresed, transitioned to GDMT, and referred to cardiac rehabilitation. Over the next 6 months, he continued to have debilitating dyspnea (NHYA Class IIIa) and his outpatient physicians were limited on titrating GDMT further due to hypotension. A TEE was done which demonstrated EF 15%, severe MR by color and quantitation (EROA of 0.5 cm2; Regurgitant Volume of 65 mL), systolic flow reversal in the pulmonary vein and severe tricuspid regurgitation. We were asked how we would approach this case
Case #1Takeaways
- In attempting to keep the evaluation of chronic mitral regurgitation relatively simple, we should ask ourselves three primary questions: (1) What is causing the MR; (2) How much MR is there; and (3) What is the hemodynamic consequence of the MR.
- To the first question of what is the etiology of the MR – a simple framework is to think of the etiology as an issue of the valve (primary) or an issue of the ventricle/atria (secondary). There is further classification that can be made based on the Carpentier Classification which speaks to the valve leaflet movement and position (normal leaflet motion, excessive leaflet motion [e.g., prolapse], or restricted in systole and/or diastole [e.g., rheumatic heart disease]).
- During rounds, Dr. Nishimura provided some historical context in that the original valve guidelines had recommendations for intervention on primary mitral regurgitation and not secondary – given that it is considered a disease of the ventricle. Trials like the COAPT trial have greatly shifted our practice in treating secondary mitral regurgitation. Though, we have to be familiar with which patients with secondary MR would truly derive benefit from mitral valve intervention
- In regards to the COAPT trial, patients with moderate to severe (3+) or severe (4+) mitral regurgitation who remained symptomatic despite maximally tolerated guideline-directed medical therapy (GDMT) were included. Dr. Nishimura makes the point that about one-third of patients intended to be enrolled in the trial were not included because they improved so much on GDMT. And thus, when evaluating patients for consideration of mitral valve intervention in secondary MR – and specifically transcatheter edge to edge repair (TEER) – every effort to optimize GDMT should be made first before intervening. Other important inclusion and exclusion criteria included that patients had LVEF between 20-50%, LV end-systolic diameter less than or equal to 70 mm, and absence of severe pulmonary hypertension (defined as pulmonary artery systolic pressure > 70 mmHg despite vasodilator therapy) or moderate to severe right ventricular failure.
- Dr. Nishimura asks our audience if the patient is truly on optimal GDMT and/or optimized? There are basic tools that clue us into optimization including chest x-ray (e.g., is there still pulmonary vascular congestion) and physical examination (e.g., what is the venous pressure).
- Dr. Nishimura makes an interesting point in correlating our examination with the echocardiographic findings. In patients with largely secondary MR, where the leaflets have poor coaptation and we have a weak ventricle we may not expect to hear a very loud murmur on examination (e.g., there isn’t enough pump to generate the murmur). However, if we hear a significant murmur (e.g., like our patient described in the case with a loud, 3/6, blowing murmur) with presumed secondary MR, our antennae should be up for a possible primary component.
Case #2 Synopsis:
A man in his early 60s with a history of prior LAD PCI in the setting of an NSTEMI and diabetes presented to your hospital in SCAI Stage C to D Cardiogenic Shock with the background of worsening orthopnea and edema several weeks prior. You are told the patient had a recent echo with LVEF 15%, mild LV dilation, reduced RV function and moderate to severe functional MR. When you meet the patient, he is confused, nauseous and with poor perfusion (e.g., cool extremities and Lactate of 7 mmol/L). The patient is taken for left and right heart catheterization with RHC showing significant elevated filling pressures, large V-waves, and low cardiac index. An IABP is placed and LHC is performed where an acute appearing lesion in the proximal LAD and Mid-RCA are treated with PCI. Over the next week the IABP is weaned and removed and low doses of GDMT started. But once the IABP is removed, nausea returns and lactate starts rising again. Hemodynamics and TEE images are obtained with the IABP at 1:1 and on standby and show significant worsening of the hemodynamics and MR with IABP on standby, with the MR in the severe category, and we are asked to comment on what to do next.
Case #2 Takeaways
- Dr. Nishimura suggests we approach this complex case with a simple question: how much of his shock/congestion is a result of his pump (the LV) versus how much is a result of his valve? Dr. Nishimura notes there is a subset of patients who have dynamic mitral regurgitation, which is primarily related to changes in the structure of the annulus/apparatus that happen with changes in preload/afterload/contractility. These patients can go from mild to severe depending on the loading conditions, as they are exquisitely sensitive to these conditions
- Dr. Nishimura notes the continuous wave doppler of the mitral regurgitation can give us a rich amount of detail. The MR continuous wave doppler signal reflects the instantaneous doppler between the left ventricle and left atrium. If we pay attention to the signal during isovolumic contraction – if there is a rapid rise in the signal, that suggests that we are generating LV systolic pressure rather quickly and contractility may be preserved (e.g., this refers to dP/dT which has several caveats but qualitatively can be informative us).
- These patients with dynamic MR who we cannot control the loading conditions, it may be better to treat the MR itself.
References
- Stone GW, Lindenfeld J, Abraham WT, Kar S, Lim DS, Mishell JM, Whisenant B, Grayburn PA, Rinaldi M, Kapadia SR, Rajagopal V, Sarembock IJ, Brieke A, Marx SO, Cohen DJ, Weissman NJ, Mack MJ; COAPT Investigators. Transcatheter Mitral-Valve Repair in Patients with Heart Failure. N Engl J Med. 2018 Dec 13;379(24):2307-2318.
- Writing Committee Members, Otto CM, Nishimura RA, Bonow RO, Carabello BA, Erwin JP 3rd, Gentile F, Jneid H, Krieger EV, Mack M, McLeod C, O’Gara PT, Rigolin VH, Sundt TM 3rd, Thompson A, Toly C. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2021 Feb 2;77(4):e25-e197.
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