Mitral Regurgitation

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 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

MR definition 0.4cm or larger, regurgitant volume 60ml or more, vena contracta 0.7cm or larger

Txtmt

- vasodilator - nitroprusside decreases aortic impedence and MR, improving forward cardiac output

IABP decrease afterload and augment coronary perfusion pressures

Chronic Mitral Regurgitation

1) symptomatic patients with LVEF > 30%

2) asymptomatic pts w/ LV dysfunction LVEF 30-60% and/or LV end systolic diameter >/=40mm

3) pts undergoing another cardiac surgical repair

Case #1Takeaways

  1. 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.
  2. 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]).
  3. 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
  4. 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.
  5. 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).
  6. 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.




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