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Outcomes: The Key West Meeting


World Society of Cardio-Thoracic Surgeons


HSF Meeting @ Croatia
Sept. 07 - 09, 2010

Dynamics and Anatomy of Ischemic Mitral Regurgitation

Robert Frater, MD writes the following in response to a case of mitral regurgitation posted by Giusseppe Resigno MD from Lancisi Hospital, Ancona, Italy:


Click to Enlarge Images
Frater : Figure 1
Fig. 1
Frater : Figure 2
Fig. 2
Frater : Figure 3
Fig. 3
Frater : Figure 4
Fig. 4

Analysis:

This is a case of a man in his 70´s with a previous posterior myocardial infarction, severe mitral regurgitation, and coronary artery disease who underwent CABG X 3 with mitral annulolasty using a 26 mm C shaped annuloplasty device (as opposed to D shaped)which resulted in the patient being left with with significant residual mitral insufficiency.

There are two images from the postoperative echocardiogram which I reviewed (one in diastole and one in systole) which I judge are slices through the central region of the anterior and posterior leaflets slightly to the right of the midline. In systole a faint image (i.e. a thin slice) of the right papillary muscle and first and second order chordae are seen.

The anterior leaflet in systole shows an extreme instance of He´s triangle in operation. There is an abrupt bend in the anterior leaflet at the point where the secondary chordae attach. The primary chorda which originate at the lower end of the secondary chorda is seen to insert into the free edge of the anterior leaflet, completing the triangle. From the base of the anterior leaflet through the insertion of the secondary chorda to the papillary muscle and on through it to the base of the muscle on the posterior LV wall is a straight line giving a graphic confirmation that the apparatus is under tension.

I traced the echo images (Figs 3 & 4) and designated the following points on my hand drawings:

  • a: Base of the anterior leaflet along the intertrigonal line.
  • b: Free edge of the anterior leaflet.
  • c: Base of the posterior leaflet at the AV junction.
  • d: Free edge of the posterior leaflet.
  • e: The point on the posterior LV wall to which the whole anterior leaflet points in diastole and the portion between the base and the secondary chorda points in systole.
  • f: The site of the secondary chorda insertion on the anterior leaflet.

Using the centimer scale on the sides of each echo image, I measured the following distances:

  • a-b: The length of the anterior leaflet in diastole.
  • a-f and f-b which in systole make up the length of the tethered anterior leaflet with its bend at the secondary insertion.
  • c-d: The length of the posterior leaflet.
  • a-c: Anteroposterior annular dimension.
  • c-e Distance from the middle of the posterior annulus to the base of the medial papillary muscle. (This was chosen because the papillary muscle was too hazy in outline to be sure of making good measurements. In addition all the other evidence pointed to a dead posterior wall and a dead papillary muscle, but the hazy outline and the tethering did also show that it was not one of those occasionally seen ischemically elongated muscles).
  • b/d-e : The distance from the free edge of the anterior and posterior free edges to the base of the papillary muscle.
  • a-e The distance from the intervalvar trigone to the base of the papillary muscle.

Interpretation of the echo images indicates the following:

  1. ab = 3.6 and also af + fb = 2.6 + 1.0 = 3.6
  2. ac = 4. The annular anteroposterior diameter (sometimes called septolateral) is greater than the length of the anterior leaflet and thus clearly dilated. (In normal systole the AP annular dimension in the longaxis echo equals the diastolic length of the anterior leaflet. The anterior leaflet length is measured in diastole because then it is in a straight line).
  3. ac is the same in systole and diastole. The muscle of this part of the annulus is for all practical purposes dead.
  4. ce is the same in systole and diastole. The normal systolic shortening and diastolic lengthening of the posterior LV wall is not occurring. It, too, is dead.
  5. af and fb are clearly at an angle in systole and this shows unequivocally that fb, the coapting portion of the anterior leaflet, is not meeting the coapting portion of the posterior leaflet. In the absence of a flail central scallop this is a surefire sign of a ventricular mechanism of the failure of coaptation, together of course with the large upside down "tent" formed by the anterior leaflet , posterior leaflet and AP annular diameter.
  6. b and d meet barely at a point and it is no surprise that there is severe insufficiency.


Click to Enlarge Images
Frater : Figure 5
Fig. 5
Frater : Figure 6
Fig. 6
Frater : Figure 7
Fig. 7
Frater : Figure 8
Fig. 8
Frater : Figure 9
Fig. 9
Frater : Figure 10
Fig. 10

Discussion::

In Figs 5 through 10, the basic dimensions described above are schematically altered alone or in various combinations in order to observe the effect on the coaptation of the central parts of the anterior and posterior leaflets.

Fig. 5: The bases of the anterior and posterior leaflets, designated by the points a & c, are brought closer together by an annuloplasty. Preoperatively the distance ac (the AP dimension of the annulus) is 4 cm. This is greater than the 3.6 cm of ab or af +fb (the length of the anterior leaflet). Since this is a clear sign that the annulus is dilated, this is a definite indication that the annulus needs to be reduced by annuloplasty. Since there is clearly papillary displacement in this case the situation calls for an undersized annuloplasty. In Fig 5, the effect of reducing a-c by itself, to 2 cm is shown. This is probably close to Dr Rescigno´s use of a 26 size ring but it fails to produce good coaptation in this case.

Fig. 6: Here the annular AP reduction is to 3 cm. This is not as tight but still less than the length of the anterior leaflet and by that fact a "tight" annuloplasty. It too fails to produce good coaptation.

Fig. 7: Annuloplasty reducing a-c from 4 cm to 3cm (ac2). To this is added a shift of the base of the right papillary muscle to the right trigone of 1 cm. This could be achieved by the maneuver described by Kron . The distance a-e is 7cm and a-e2 is 6 cm. There is satisfactory coaptation. Note that in this procedure the tethering of the secondary chordae is lessened by shifting the base of the papillary muscle.

Fig. 8: Annuloplasty is the same as in Fig 7. The secondary chordae are cut. The primary chordae are unchanged and b/d-e stays the same. This too relieves the tethering of the secondary chordae and allows satisfactory coaptation.

Fig. 9: A gusset of pericardium has been inserted in the posterior leaflet between the annulus and the insertion of the 2nd order chordae. Its maximum dimension at the middle of the posterior leaflet is 1.5 cm thus increasing the depth of the posterior leaflet (c-d) from 1.5 cm to 3.0 cm. There is no annuloplasty and the distance f-e remains the same but the posterior leaflet can move towards the center of the orifice and make contact with the anterior leaflet, achieving satisfactory coaptation.

Fig. 10: A gusset of pericardium has been inserted in the anterior leaflet between f where the secondary chordae are inserted and the smooth zone of the anterior leaflet. The maximum depth of the gusset is 1.5 cm thus increasing the depth of the anterior leaflet from 3.6 cm to 5.1 cm. There is no annuloplasty and the distance f-e remains the same. The increased area of the anterior leaflet can move towards the posterior leaflet and make better contact with it, achieving satisfactory coaptation.

Will there be SAM in the situations illustrated by either Figures 9 or 10? SAM typically occurs in degenerative disease when leaflet area exceeds the systolic annular area. SAM does not occur in ventricular mechanism mitral insufficiency when the annular area is reduced to substantially less than the leaflet area.

Presumably in this situation the large midventricular dimension and some residual tethering prevents SAM despite tight annuloplasty. But will there be SAM if we leave the annulus dilated and the leaflet edge to papillary dimensions the same, but increase the leaflet area? I suspect not. Note that there has already been succesful clinical use of posterior leaflet enlargement for ischemic mitral insufficiency cases. We have done anterior leaflet enlargement in a dead pig heart myopathy model. This, of course, is not dynamic but the leaflet always moves to close the mitral orifice when the ventricle is filled under controlled pressure.


References:

  1. Kron IL, Green GR, Cope JT. Surgical relocation of the posterior papillary muscle in chronic ischemic mitral regurgitation. Ann Thorac Surg 2002 Aug; 74(2):600-1

 


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