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J Thorac Cardiovasc Surg 2008;135:223-224
© 2008 The American Association for Thoracic Surgery


Brief Communication

Papillary muscle realignment for symptomatic left ventricular outflow tract obstruction

Roosevelt Bryant, III, MD, Nicholas G. Smedira, MD*

Department of Thoracic and Cardiovascular Surgery, Cleveland Clinic, Cleveland, Ohio.

Received for publication June 30, 2007; accepted for publication August 8, 2007.

* Address for reprints: Nicholas G. Smedira, MD, Cleveland Clinic, 9500 Euclid Ave/Desk F24, Cleveland, OH 44195. (Email: smedirn{at}ccf.org).

Left ventricular outflow tract obstruction (LVOTO) in hypertrophic cardiomyopathy typically results from proximal septal hypertrophy and systolic anterior motion (SAM) of the anterior mitral leaflet caused by the Venturi effect.1Go Mitral valve and subvalvular anomalies can also produce LVOTO.2Go Reported are 2 patients with abnormal orientation of the papillary muscles resulting in LVOTO treated with the technique of transaortic papillary muscle realignment.

Clinical Summary

A 35-year-old man presented with exertional dyspnea and a provocable gradient of 100 mm Hg on transthoracic echocardiography. SAM of the mitral leaflet was evident on tranesophageal echocardiography and magnetic resonance imaging. The intraventricular septum was 1.8 cm thick. Intraoperatively, the anterolateral and posteromedial papillary muscles had multiple heads, with the anterior or septal-most head pointing directly along the axis of the aortic valve rather than that of the mitral valve (Figure 1, A). There also was a great deal of laxity of the papillary muscles, with only a small apical attachment.


Figure 1
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Figure 1. Cardiac mitral regurgitation before (A) and after (B) the papillary muscle realignment procedure (see supplemental video clips online).

 
A 53-year-old man presented with shortness of breath and a provocable gradient of 184 mm Hg on transthoracic echocardiography. SAM was evident, and there was moderate (2+) mitral regurgitation. The intraventricular septum was 2 cm thick. In addition to a myectomy, the anterior leaflet was shortened at the free edge of the A2 segment by 1 cm. It was also noted that the medial head of the anterolateral papillary muscle pointed along the aortic valve axis and was also very lax. After the procedure, intraoperative isoproterenol (Isuprel) provocation produced a peak gradient of 64 mm Hg, with severe SAM and mitral regurgitation. The septal thickness was 1.5 cm. An additional 3- to 4-mm myectomy was performed, and the anterolateral papillary muscle was realigned.

The realignment procedure was performed through the aortic valve. A pledgetted mattress suture is placed posterior to the most posterior papillary muscle head, avoiding entanglement with the chordae. It is then passed through the anterior head, avoiding twisting of the papillary muscle. One or more mattress sutures might be necessary to realign the papillary muscles, and both the anterolateral and posteromedial papillary muscles have been realigned (Figure 2). LVOTO was eliminated without the development of mitral regurgitation.


Figure 2
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Figure 2. Papillary muscle realignment procedure. A, Anomalous papillary muscle head directed toward the aortic valve, causing left ventricular outflow tract obstruction by systolic anterior motion of the anterior mitral leaflet. B, Pledgetted mattress stitches are placed to change the orientation of the anomalous papillary muscle. C, Completed procedure.

 
Discussion

Orientation of the papillary muscles and their attachment relative to the left ventricular outflow tract is another possible cause of severe SAM of the mitral valve and LVOTO.3Go Abnormalities of the mitral valve have been reported in as many as 20% of patients undergoing surgical intervention for hypertrophic obstructive cardiomyopathy.4Go In 1991, Klues and colleagues2Go reported anomalous insertion of the left ventricular papillary muscles in 13% of patients. Direct insertion of both or either papillary muscle into the anterior mitral leaflet resulted in left ventricular outflow tract gradients of 70 to 150 mm Hg. The papillary muscle abnormality we have described must be added to the now numerous mitral valve abnormalities associated with hypertrophic cardiomyopathy and should be considered a potential cause of LVOTO.

In the cases presented, the orientation of 1 or more papillary muscle heads along the aortic valve axis appeared to contribute to LVOTO. By realigning the papillary muscle toward the mitral valve axis, we easily eliminated the obstruction (Figure 1, B). Thus the papillary muscle realignment procedure we have described is easily accomplished through the aortic valve, eliminates SAM, and preserves mitral valve function.

Supplementary video

References

  1. Lemke R, Kaltenbach M. Systolic anterior movement of the mitral valve and the Venturi effect: an in vitro study. Z Kardiol 1987;76(suppl 3):87-90.
  2. Klues HG, Roberts WC, Maron BJ. Anomalous insertion of papillary muscle directly into anterior mitral leaflet in hypertrophic cardiomyopathy. Significance in producing left ventricular outflow obstruction. Circulation 1991;84:1188-1197.[Abstract/Free Full Text]
  3. Kon MW, Grech ED, Ho SY, Bennett JG, Collins PD. Anomalous papillary muscle as a cause of left ventricular outflow tract obstruction in an adult. Ann Thorac Surg 1997;63:232-234.[Abstract/Free Full Text]
  4. Minakata K, Dearani JA, Nishimura RA, Maron BJ, Danielson GK. Extended septal myectomy for hypertrophic obstructive cardiomyopathy with anomalous mitral papillary muscles or chordae. J Thorac Cardiovasc Surg 2004;127:481-489.[Abstract/Free Full Text]



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