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Mitral Regurgitation - 8/22/2012

posted Aug 22, 2012, 7:47 AM by Rohit Das   [ updated Dec 27, 2012, 7:03 AM by Purnema Madahar ]

Ahhhh…Chief of Service – another weekly gathering for our interns and residents to learn about an interesting topic. Today, Aman Shah presented a woman in her 30s who has a history of endocarditis leading to severe MR à St. Jude’s MV Replacement in 5/2012 à Now with severe perivalvular leak and associated hemolytic anemia. Very complicated case, and Dr. Garcia was kind enough to give us a nice overview.

This topic brings to light a few questions – What causes MR? How do we manage it, and particularly, when should we consider surgery? Finally, how frequent are the above complications from mitral valve prostheses? Well, let’s get to it.

  • Regarding etiology, it’s first important to differentiate from primary and secondary causes of MR. For the former, Mitral Valve Prolapse, Endocarditis, Rheumatic Heart Disease, and valve calcification (older adults – usually doesn’t lead to severe MR) are the most frequent examples. Secondary causes include ischemia and dilated left ventricles.
  • Epidemologically, in the so-called “developed” world, MV Prolapse/Degenerative Causes and Ischemic Heart Disease (70%, 20% respectively) are the most common causes of MR. In the so-called “underdeveloped” world, RHD remains, by far, the most common cause, mainly effecting a younger population..

How can we diagnose MR? Well, you can always cheat and get a TTE, but here are some useful physical findings:

  • The characteristic, holosystolic murmur best heard at the apex has a decent +LR (about 5), but perhaps more importantly, a compelling –LR (0.2). Be wary of radiation to the axilla, as patients who isolated posterior leaflet disease may have murmurs radiating to the base (and may mimic aortic stenosis). On the other hand, anterior leaflet issues may have radiation to the back.
  • One of the reasons the +LR is not sooo great is because MR may be confused with AS, as described above. One very effective way to differentiate between the two is by increasing systemic vascular resistance (handgrip, or arterial occlusion with a blood pressure cuff) – seeking the path of least resistance, with increased afterload, the volume of blood going through left-sided regugitant lesions will increase with the above exercises.
    • Increased intensity of a left-sided murmur with increased afterload is very predictive of MR, with a LR of around 40!!

Severity of MR is really based on TTE findings, with criteria being ≥ 60cc/beat regurgitant volume, or ≥50% regurgitant fraction, or ≥0.4 cm2 orifice area…yea…hard to remember. Figure 3 in the attached article displays a nice algorithm showing when to consider surgical therapy – some key points:

  • Anyone who’s symptomatic should be evaluated for surgical management, unless they have severe LV dysfunction (in which case LV function does not generally improve, or at least enough so to make the surgery worth it).
  • For asymptomatic patients, surgery should be considered if there is LV dysfunction (EF < 60%), atrial fibrillation or pulmonary hypertension.
  • For all other patients, there is actually NO convincing data that afterload reducing medical therapy has a significant impact on the natural history of MR.

The decision to pursue mitral valve repair versus replacement is a complicated one. In general, repair is preferred over replacement, though this is based on retrospective and prospective cohort data. Also, the etiology of MR, and the anatomy of the valve, plays into the decision…so yea, complicated...In this particular patient, repair was attempted (which has better outcomes for endocarditis-related MR), but failed…which led to a St. Jude’s mechanical valve replacement.

Let’s talk about some of the unique complications of prosthetic heart valves, focused around the patient presented today.

  • Paravalvular leak is actually very common, occurring in 20-50% of patients with mitral or aortic prostheses. However, most of this is very mild leak, does not progress and has no long-term clinical implications.
  • The onset of new, severe MR after replacement is actually very rare. Generally, this is due to either prosthetic valve endocarditis, or structural failure of the prosthesis. The attached review on this topic cites one prospective study of 1200 patients post St. Jude’s replacement, which found a 1-2% incidence of severe paravalvular regurgitation, and the majority of cases being aortic rather than mitral. Furthermore, severe paravalvular regurgitation is more common with bioprosthetic valves as compared to mechanical valves.
  • Due to shearing forces and blood flow turbulence, significant paravalvular regurgitation commonly leads to an increased incidence of intravascular hemolysis (10-15% of cases), with also increasing severity. The presented patient indeed had anemia, reticulocytosis and low haptoglobin levels – all reflective of this phenomenon.

So, what do we do for this lady? Well, reoperation and repair is the only option. Unfortunately, it carries a significant mortality of around 10-11%, which can go as high as 20-25% depending on the degree of their cardiac dysfunction (20-25% in patients with NYHA Class IV heart failure).

Ok - a good overview of a commonly encountered cardiac issue. I’ve attached two good review articles – I particularly favor the Lancet 2009 paper. Keep adding to the library…

Evaluation and Management of Chronic Mitral Regurgitation
Otto, NEJM 2001, Volume 345 (10): 740-746

Enriquez-Sarano et. al., Lancet 2009, Volume 373: 1382-94

Safi et. al., Angiology 2000, Volume 51: 479-487
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