Cardiovascular Anesthesiology: Echo Rounds
A 29-yr-old man with a history of Marfan’s disease presented for a reoperative aortic root reconstruction with aortic valve replacement and coronary re-implantation (Bentall procedure), mitral valve (MV) repair, and a tricuspid valve repair. Initial transesophageal echocardiographic examination revealed a dilated left ventricle with moderate ventricular dysfunction, a calcified degenerated aortic valve homograft with severe insufficiency and moderate stenosis. There was billowing, thickening and elongation of both MV leaflets with associated annular dilation (59 mm measured in the commissural plane; upper limit of normal is 40 mm). The posterior leaflet attached “upstream” to the true annulus into the left atrium, which is known as atrialization. These MV findings are consistent with a diagnosis of Barlow’s disease.1 The posterior MV leaflet had prolapse and excess tissue in all segments with resultant severe mitral regurgitation (MR) (Fig. 1 and Video clip; please see video clip available at www.anesthesia-analgesia.org). There was no evidence of septal hypertrophy or a significant gradient across the left ventricular outflow tract (LVOT).
On direct surgical inspection, the size of the anterior leaflet was 1 cm longer than the largest commercially available annuloplasty ring (40 mm). All segments of the posterior leaflet were resected followed by annular plication and sliding-plasty to decrease the length of coaptation of the entire posterior leaflet to 1 cm. The aortic homograft was replaced with a 29 mm mechanical valve conduit and the tricuspid valve repaired with a ring annuloplasty.
Before separation from cardiopulmonary bypass (CPB), epinephrine 6 μg/min was started. With separation from CPB, his heart rate was 90 bpm and the mean arterial blood pressure was 75 mm Hg. Substantial systolic anterior motion (SAM) of the anterior leaflet of the MV was observed. This resulted in severe MR and LVOT obstruction (LVOTO) with a gradient of approximately 60 mm Hg (Fig. 2 and Video clip). Discontinuation of inotropic support, intravascular volume resuscitation, and 2 boluses of esmolol 40 mg and phenylephrine 160 μg decreased his heart rate to 60 bpm and increased the mean arterial blood pressure to 90 mm Hg. There were no significant changes in the degree of SAM, the severity of MR, or LVOTO. CPB was reinstituted and the anterior mitral leaflet was shortened to reduce the distance from the coaption point to the leaflet tip to 7 mm. Mild SAM was visualized after the second separation from CPB without significant LVOTO (gradient 10 mm Hg). Before hospital discharge, a follow-up echocardiographic examination revealed no MR or evidence of LVOTO.
LVOTO after MV repair may have several etiological causes. Asymmetric septal hypertrophy may result in the development of a high velocity jet that pulls the anterior leaflet of the MV into the LVOT. Decreased preload and afterload in the presence of inotropic support may result in LVOTO and MR not present during the prebypass period.
Alternatively, changes to the MV structure or configuration may result in SAM and LVOTO. Normally, blood enters the left ventricle posteriorly through the MV and exits anteriorly through the LVOT. This anterior-posterior separation of blood flow prevents the forward force of ejected blood from pushing the coapted MV leaflets anteriorly. Tewari and Basu2 reported a retained anterior MV leaflet and chordae after MV replacement. Because of its anterior position, flow-drag forces pushed this leaflet into the LVOT with resultant obstruction.
In an echocardiographic study by Maslow et al.,3 a long posterior leaflet and anterior displacement of the MV coaptation plane were associated with postoperative SAM after MV repair. Patients who developed post-MV repair SAM had a lower preoperative ratio of coapted anterior to posterior leaflet length and a shorter distance between the coaptation point to the ventricular septum (Fig. 3A). Similarly, excessive iatrogenic anterior displacement of the MV leaflet coaptation plane by an implanted annuloplasty ring may be an important etiological factor in the development of post-MV repair SAM.4
In the context of degenerative MV repair, there are three general mechanisms of SAM. Excess posterior leaflet tissue is the classical mechanism of SAM after MV repair and results from excess posterior leaflet length (Fig. 3B). The MV coaption plane is displaced anteriorly, exposing the MV to left ventricular outflow. This form of SAM is prevented by the sliding-leaflet plasty.5 Sliding-leaflet plasty reduces the posterior leaflet length, resulting in a smaller posterior leaflet with less leaflet redundancy and posterior translation of the coaptation plane. The second and third mechanisms of SAM are interrelated; either the anterior leaflet is too long or the annuloplasty ring is too small (Fig. 3C). In each case, excessive anterior leaflet tissue is displaced into the LVOT during systole. It is for this reason that annuloplasty rings are sized to match the length of the anterior leaflet. In our case, there was no commercially available ring large enough to accommodate the giant anterior leaflet and, despite using the largest annuloplasty ring available, SAM still occurred because, in relative terms, the ring was too small for this particular valve. As a larger ring was not an option, and as the posterior leaflet height had already been adequately reduced, the anterior leaflet was shortened to reduce the amount of leaflet available to be displaced into the LVOT during systole (Fig. 3C). Anterior leaflet shortening is a simple and effective method of treating SAM due to valve-ring size mismatch. Some surgeons recommend prophylactic application of this technique in all Barlow valves to prevent occurrence of SAM.6
If SAM is detected after MV repair, structural etiologies of SAM must be differentiated from physiological provocation. While separation from CPB may be difficult without inotropic support, physiologic and pharmacological treatments that minimize the severity of SAM should be instituted. Preload should be optimized, inotropic drugs should be discontinued, and β blockade should be instituted. If SAM resolves, no further surgical treatment is probably necessary.7 The risks versus benefits of continued temporary inotropic support during this period should be evaluated. If SAM persists despite hemodynamic and pharmacological optimization, further surgical repair should be considered particularly where there is resultant hemodynamic compromise.
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