Talk:Mitral insufficiency

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Chronic AI vs. chronic MR
MR AI
Pathophysiology Pure volume overload Volume and pressure overload
Preload Increased Increased
Afterload Normal or decreased Increased
Medical management Vasodilators in acute MR Vasodilators in chronic AI

I'm not sure where to put this table. If anyone has any ideas, plese let me know. Ksheka 10:43, Aug 4, 2004 (UTC)

Is Mitral Valve Prolapse a cause of primary mitral regurgitation?[edit]

Just wondering whether it belongs in the list... Doktor 18:17, 2 November 2006 (UTC)


can someone help?[edit]

I am not able to add the reference (http://www.ncbi.nlm.nih.gov/pubmed/17680596 Everest Registryto treatment section. The citation appears but does not seem to be listed at the end. thanks--Imagologist (talk) 14:25, 21 March 2008 (UTC)

A few suggestions...[edit]

This is generally a good page and someone has obviously put a great deal of work into it. I do think that a few bits could be better worded, however, and invite comment on the following. "Acute mitral regurgitation (as may occur due to the sudden rupture of a chorda tendinea or papillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle. The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta (the forward cardiac output or forward stroke volume), but also the blood that regurgitates into the left atrium (the regurgitant volume). The combination of the forward stroke volume and the regurgitant volume is known as the total stroke volume of the left ventricle." I can see what the author is getting at but I'm not sure it makes sense as written. Thinking about the first cycle after the MR has set in, the ventricle ejects the same amount of blood as it would have done on the previous cycle, except this time some enters the left atrium . On the second cycle, the atrium has more volume than normal and so more blood enters the ventricle via gravity and then by a more forceful atrial kick due to the extra distension of the atrium according to the Starling mechanism. This causes more blood to be in the left ventricle when it begins to pump (end diastolic volume) which will lead to an increased total stroke volume (SV) comprising a forward SV and a regurgitant SV. The forward SV may well be lower than that which is produced before the MR has occured.

"In the acute setting, the stroke volume of the left ventricle is increased (increased ejection fraction), this happens because of more complete emptying of heart. However, as it progresses the LV volume increases and the contractile function deteriorates and thus leading to dysfunctional LV and a decrease in ejection fraction.[10] The increase in stroke volume is explained by the Frank–Starling mechanism, in which increased ventricular pre-load stretches the myocardium such that contractions are more forceful." The first sentence implies, to my mind, that SV and ejection fraction (EF) are synomynous, or that the stroke volume increases because the LV is now pumping a greater proportion of its blood out, rather than having more blood in the first place. It is the case that that the LV is pumping harder due to the Starling mechanism but the fact that the left atrium is at a lower pressure than the aorta must surely contribute, giving a lower total afterload. If, however, the MR is secondary to an ischaemic event causing a tendon or papillary muscle rupture (i.e. a heart attack and a very common cause of MR), the LV is very likely to have been affected, causing dysmotility of the wall and possibly reducing the EF.

The 'compensated section is very good. Might I suggest adding at the end "As the left ventricle dilates it stretches the mitral annulus and displaces the papillary muscles, gradually worsening the amount of regurgitation. The gradual effect of this positive feedback predisposes to decompensation."

I am then not sure about the author's claim that decompensation is due to increased calcium in cardiomyocytes and it's not referenced. I don't know how that explains decompensation. Again is mentioned a reduced SV leading to a decreased EF (although this time it's termed end-systolic volume which is slightly unclear as they are related but not synomnyous and I think stylistically it would be clearer to keep using the same term) whereas I think it makes more sense to say that the reduced EF leads to a decreased SV as the LV has stretched beyond the limit where it responds by contracting more forcefully and instead reduces its force of contraction as described by the Starling curve.

The other point I wanted to raise was the radiation of the murmur in the actue phase as described in the table. Has someone vandalised this? I wasn't aware that there was a difference between actue and chronic, but I might be wrong. I thought that it always radiates mostly to the axilla but the medscape page (in the refs) mentions the left subscapular region. I've never seen anyone ausculate someone's head and 'spine' is pretty non-specific. That's plenty for now. I'm happy to make some edits but would like some consensus first as someone has obviously put a lot of good effort into this. This page could be really good with a little polishing. James — Preceding unsigned comment added by Jimbobolaffsson (talkcontribs) 20:42, 19 April 2011 (UTC) -- I'm still planning on sorting this out but I'm in the middle of finals so it'll be a week or two. Jimbobolaffsson (talk) 22:25, 18 May 2011 (UTC)

Catheter-based therapies[edit]

Circulation review - doi:10.1161/CIRCULATIONAHA.114.009881 JFW | T@lk 10:59, 7 November 2014 (UTC)