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Archive for the ‘Mitral regurgitation’ Category

Ischemic MR is a critical entity in determining the long-term survival in post MI patients as well as dilated cardiomyopathy. (Originally described  by J. H. Philips Ann Intern Med. 1963;59(4):508-520)

The mechanism of MR  can really be complex .We know mitral apparatus consists of  six components.The sub valvular apparatus plays a key role. LV  free wall especially the inferior and lateral segments which subtends the two papillary muscle has a critical role in maintaining the mitral valve competency .

There seems to me a complex mechano -anatomical behavior of subvalvular structures in progressive LV dysfunction especially so in ischemic cardiomyopathy. The LV size, shape eccentricity in attachment of leaflets to papillary muscle is (Simply called altered geometry ) .The intraventricular desynchrony ,disproportionate  LV dysfunction also make MR more likely .

Beware of a striking  physiological irony in ischemic MR.

While infero basal free wall dysfunction occurs commonly with  LCX/RCA Infarct and  is commonly associated with Ischemic of MR .There is something unique happens . . . when the infarct is larger and involves the head of the papillary muscle .Yes, it attenuates the severity of MR.(Friendly Infarct extension!) The mechanism is , papillary muscle dysfunction  tends to prevent apical tensor effect leading to   improved tethering of leaflets .This may appear a blessing in terms of  prevention of acute pulmonary edema. This also explains why some patients are as cool as cucumbers and lie flat comfortably with silent lungs in spite of severe LV dysfunction .The LV is too weak it doesn’t  have contractile energy to generate acute  severe MR.

Here is an illustration  from circulation .Note: The Infarct extends to pap muscle head, the MR is arrested.

Image courtesy : Emmanuel Messas J. Luis Guerrero, Mark D. Handschumacher, et all  Paradoxic Decrease in Ischemic Mitral Regurgitation With Papillary Muscle Dysfunction Insights From Three-Dimensional and Contrast Echocardiography With Strain Rate Measurement Circulation. 2001; 104: 1952-1957

Further debates 

Papillary muscle dysfunction may be protective against progressive MR.Still ,sudden papillary muscle rupture result in flash pulmonary edema and death is imminent . How ? Complete rupture  causes flail free-floating leaflet that prolapse into LA and result in free MR.While simple dysfunction without flail leaflet is less likely to cause MR . The key determinant seems to be the net force that keeps the alignment of mitral,leaflet at annular level.

In this context , we also realise the impact of primary PCI on the  regression of  Ischemic MR is not uniformly positive.Reasons not clear.

Final message

Ischemic MR  due to LV free wall infarct is a near knockout punch , that may determine the ultimate ACS  outcome. However , a simultaneous lesser punch ( by a friendly devil ! ) on the adjacent head of papillary muscle neutralises the effect of Initial Injury. While such non academic scripts are enjoyable , we are still a long way away to understand this anatomical ,hemodynamic conundrum.

Reference

1.

mechanism of ischemic mitral regurgitation papillary muscle dysfunction

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Regurgitant  lesions of cardiac valves  are often tricky for the heart . Myocardium shows “love- hate” relationship with these  leaky valves.  Some of them are  “sort of”  stress relievers for  LV . A mild MR will make the LV comfortable in terms of wall stress. When the wall stress is reduced the contractility increases and LV EF may raise a little.Hence EF is never going to help us to assess true LV function in MR .

LV end diastolic dimension(LVEDD) is  a preload dependent  parameter .A patient with 6.5cm LV EDD  may still  have good contractility  and he may reach even a  40mm LV ESD, implying an intact LV function.

LV function should be best  assessed  in systole .(After all ,  systole is the prime function of heart) .Further , it should be assessed when the LV is  free from  influence of the all  loading  conditions of heart .  (Note : The initial part of systole  depends on after load. As the systole progresses the influence  of after-load lessens .In the pressure volume loop* , the point at which loading conditions are least operative is end systole.)

* Please realise , heart is a dynamic organ there is no true load independent point in cardiac cycle  as pressure and volume are eternally coupled.

What happens in AR ?

The same rule applies for Aortic regurgitation, but the parameters worsen little later than that of MR. For same degree of regurgitant fraction MR will require early surgery than AR.The reason for better  tolerablity of  AR  is due to largely  intact LA function and compliance till very late stages of AR.(In AR- it’s single chamber volume overload , while in MR  it’s two chambers !)

Final message

LVEDD is not used in assessing MR  as it is a pre-load dependent parameter that will not reflect true myocardial  function /dysfunction. LV ESD is fairly accurate  measure of LV systolic function minus all loading factors .

Watch out  for next topic

Vasodilator therapy in MR and AR : How is it different ?

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