Systolic anterior motion of the mitral valve after carpentier ring valvuloplasty for mitral valve prolapse

SystolicAnterior Motion of the Mitral Valve After CarpentierRingValvuloplasty for Mitral ValveProlapse MARK S. KREINDEL, MD, WILLIAM A. SCHIAVONE, DO, HARRY M. LEVER, MD, and DELOS COSGROVE, MD

Between July 1983 and March 1985, 45 patients with severe mitral regurgitation underwent mitral valvuloplasty with insertion of a semirigid Carpentier ring. No patient had echocardiographic evidence of systolic anterior motion (SAM) preoperatively, whereas 5 patients had this echocardiographic finding postoperatively. All 5 had mitral valve prolapse as their underlying disease process and SAM developed at varying intervals after valvuloplasty. The development of SAM is related to insertion of the

D

uring the past 13 years, there has been renewed interest in mitral valve reconstruction. In 1971 Carpentier1 reported a new reconstructive operation and 10 years later2 provided follow-up of 551 patients who had undergone mitral valve repair. In our initial experience with this method of mitral valve repair we describe systolic anterior motion [SAM] of the mitral valve after valvuloplasty and discuss its mechanisms, clinical significance and implications for understanding the origin of SAM in this and other diseases known to have left ventricular (LV] outflow tract obstruction.

Methods Between July 1983 and March 1985,45 patients with severe mitral regurgitation seen at our institution underwent mitral valve reconstruction using a Carpentier ring. The underlying disease was mitral valve prolapse (MVP) in 24 patients, rheumatic heart disease in From the Departments of Cardiology and Cardiothoracic Surgery, Cleveland Clinic Foundation, Cleveland, Ohio. Manuscript received March 28,1985; revised manuscript received July 11, 1985, accepted July 12, 1985. Address for reprints: William A. Schiavone, DO, Department of Cardiology, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44106.

semirigid ring, persistence of a redundant anterior mitral leaflet, narrowing of the left ventricular (LV) outflow tract and the Venturi effect. LV and aortic pressure measurements with simultaneous Doppler echocardiography have confirmed the presence of a significant LV outflow tract gradient in these patients. Although all 5 patients are functionally improved after mitral valvuloplasty, the long-term implications of SAM after valvuloplasty are unknown. (Am J Cardiol 1988;57:408-412)

11, arteriosclerotic coronary artery disease in 7, endocardial cushion defect in 1 patient, mitral valve endocarditis in 1 and idiopathic dilation of the mitral anulus in 1. Twenty-five of the patients had an echocardiogram both before and after mitral valve repair. Preoperatively, no patient had SAM of the mitral valve, whereas 5 patients had SAM postoperatively. We will discuss these 5 patients in detail.

Results The clinical presentation, echocardiographic findings, type of mitral valve surgery, and time to development of postoperative SAM for these 5 patients are listed in Table I. The echocardiographic data and Poppler data are listed in Table II.

Discussion SAM of the mitral valve was initially described as a hallmark echocardiographic finding of hypertrophic obstructive cardiomyopathy.3-7 Although no definitive mechanism for SAM has been proved, the anterior mitral leaflet,3-6v8the chordae tendineae,8 malaligned papillary muscles,g-12and the Bernoulli and Venturi effects have been implicated. Our patients developed SAM indistinguishable from that seen in hypertrophic obstructive cardiomyopathy at varying intervals after mitral valve recon408

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TABLE I Observations in the Five Patients with Mitral Valve Wings for Mitral ~e~ur~ita~io~ Secondary to Mitral Valve Prolapse and Systolic Anterior Uotion Postoperatively Echo Age (yr) & Sex

LV Functional Impairment

Flail PML

Prolapsed AML

Resection PML

Time to SAM

Pt 1 2 3 4 5

56M 52M 46M 5OF 52M

Mild Mild Severe Mild None

+ + 0 + +

0 0 + 0 0

+ + 0 0 0

42 6 300 1 4

AML = anterior mitral leaflet: LV = left ventricle;

TABLE II

Pre- and Postoperative

PML = posterior

Echocardiographic

mitral leaflet; SAM = systolic anterior motion.

Dimensions LVOT

LVESD (cm)

LVEDD (cm)

Pt

Pre

Post

Pre

Post

Pre

Post

Pre

Post

Pre

Post

% Decrease

1 2 3

3.2 3.2 6.0

5.2 5.9 7.4

1.6 1.6 1.2 1.4 1.2 1.9 1.6 1.7 1.6 1.5 1.2 1.1 1.0

4.5 5.8 6.8

3.3 4.4 5.4 4.0 4.5 4.0 4.6

3.5 3.9 4.1

2.8 2.0 3.3

20% 49% 20%

2-3

2.2

5.2 5.3 8.0 6.6 6.2 3.1 3.6 3.8 3.7 3.5 5.8 6.0 6.3

1.6 1.3 1.2

4

3.2 3.1 6.6 5.0 4.5 2.0 2.2 2.2 2.4 2.4 3.8 4.0 4.1

2.7

1.4

48%

.

4.2

2.2

48%

4.2

5

4.1

4.6

6.1

VS (cm)

(days)

1.2

1.0

LA (cm)

5.0

5.3

4.7 5.0 5.0 5.1 5.0

Doppler Ws) 2-3

LA = left atrium; LVEDD = left ventricular end-diastolic diameter; LVESD = left ventricular end-systolic diameter: LVOT = left ventricular outflow tract; Post = postoperatively; Pre = preoperatively; VS = ventricular septum.

struction. Patient 1 was asymptomatic when SAM was found echocardiographically 6 weeks after mitral valve reconstruction. In patient 2 SAM was evident on the sixth postoperative day at which time a moderatesized pericardial effusion was present (Fig. 1). Patient 3 developed early postoperative LV dysfunction with pulsus alternans requiring treatment with digitalis and

FIGURE 1. Mitral valve echocardiograms from patient 2. Leff, fluttering of the posterior leaflet in diastole (arrow) before valvuloplasty. Rigfrf, the left ventricular outflow tract is smaller and systolic anterior motion (SAM) of the mitral valve is present after valvuloplasty. MVP = mitral valve prolapse; PE = pericardial effusion.

furosemide (Fig. 2). With subsequent improvement in LV function and decrease in LV volume, a systolic murmur developed 10 months after surgery and SAM became evident echocardiographically. With the administration of amyl nitrite, the SAM worsened (Fig. 31.Patient 4 had early postoperative SAM with midsystolic notching of the aortic valve. A dramatic early

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FIGURE 2. Mitral valve echocardiograms from patient 3. /.eff, preoperative. Rigftf, early postoperatively, the left ventricle remains dilated and the outflow tract is large. MVP = mitral valve prolapsiz; Ring = Carpentier ring.

postoperative increase in thickness of the ventricular septum was seen on the echocardiogram, and this increase contributed to a decrease in LV outflow tract size, reproducing the pathophysiology of hypertrophic obstructive cardiomyopathy. As the size of the ventricular septum decreased, SAM was evident only after the administration of amyl nitrite. In patient 5 an echocardiogram performed on the fourth postoperative day demonstrated SAM of the anterior mitral leaflet and midsystolic notching of the aortic valve (Fig. 4 and 5). Doppler examination revealed an abnormally high LV outflow tract velocity. Cardiac catheterization with LV and aortic pressures measured simultaneously with Doppler examination confirmed the presence of a LV outflow tract gradient (Fig. 6). In addition, there was postextrasystolic potentiation of the LV outflow tract gradient.

FIGURE 3. Late mitral valve echocardiograms from patient 3. Lett, 10 months after valvuloplasty the left ventricle and left ventricular outflow tract are smaller and systolic anterior motion (SAM) is present at rest. Right, with administration of amyl nitrite SAM occurs earlier and the anterior mitral leaflet contacts the ventricular septum. Ring = Carpentier ring.

All 5 patients in whom SAM developed after mitral valvuloplasty had MVP as the underlying cause for mitral regurgitation. Since none of these patients had echocardiographic evidence of SAM preoperatively, the development of postoperative SAM is related to. surgery. However, SAM did not develop in every patient with MVP who underwent Carpentier ring valvuloplasty, and it did not develop in any patient with mitral regurgitation owing to either rheumatic heart disease or any of the other causes in our series. Furthermore, several of our patients underwent mitral valvuloplasty without insertion of a semirigid ring and none has had SAM postoperatively. This suggests that SAM after mitral valvuloplasty is dependent upon the presence of the Carpentier ring as well as redundant valvular tissue. Even when segmental leaflet resection

FIGURE 4. Dual cursor echocardiogram from patient 5. Top, aortic valve echocardiogram showing midsystolic notching. l30ffom, mitral valve echocardiogram showing SAM with narrow LV outflow tract.

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FIGURE 5. Parasternal long axis 2-dimensional echocardiogram from patient 5. During this systolic frame the anterior mitral leaflet (al) is abnormally situated in the left ventricular outflow tract. Note that the posterior mitral leaflet (pl) is in its normal closed position.

is part of the reconstruction, it is limited to the posterior leaflet. The anterior leaflet remains redundant and predisposes to SAM as a result of the Venturi effect. As a result of restoring competency to the mitral valve, LV diastolic size and left atria1 size often diminishI (Table 111.With the decrease in LV end-diastolic diameter, the mitral valve may occupy a more anterior position in the LV cavity. In fact, the size of the LV outflow tract, measured from the closure point of the mitral valve to the ventricular septum, decreased by 20 to 50% after valvuloplasty in our 5 patients who developed SAM. With the narrowed LV outflow tract, an increased flow velocity occurs by virtue of the Bernoulli principle and as a result of the Venturi effect there is SAM of the anterior leaflet of the mitral valve. This has been supported by studies by Hatle14 and Yock et all5 who demonstrated by Doppler echocardiography that there is an increase in flow velocity in the LV outflow tract before the onset of SAM in patients with hypertrophic obstructive cardiomyopathy. The SAM seen in patient 5 was localized to the medial aspect of the anterior mitral leaflet, further supporting the concept of the Venturi effect. Thus, it is the localized SAM of the anterior mitral leaflet that results in hemodynamically significant LV outflow tract obstruction. Kronzon et all6 reported 3 cases of SAM after valvuloplasty and theorized that the semirigid ring prevents the normal systolic decrease in the anteroposterior size of the mitral anulus and its subsequent posterior movement during ventricular systole. One must question, however, the theory of inhibition of posterior displacement of the mitral anulus. Since the Carpentier ring is sewn to the anulus, its movement must follow that of the anulus. Resistance to systolic compression of the anulus, however, is plausible in that the semirigid ring tends to keep the mitral valve apparatus in the LV outflow tract during systole. The

t-- I see ---4 FIGURE 6. Continuous-wave Doppler recording of left ventricular (LV) outflow tract velocity with simultaneous LV and aortic pressure tracings in patient 5 after inhalation of amyl nitrite. There is good correlation between the Doppler estimated gradient and the instantaneous peak gradient across the LV outflow tract. Note the postextrasystolic potentiation of the gradient.

size of the Carpentier ring itself does not appear to play a role in the development of SAM. In conclusion, all cases of SAM after mitral valvuloplasty have occurred in patients with MVP. Hemodynamic and echocardiographic data prove that this is a significant obstructive phenomenon caused by the insertion of a semirigid mitral anular ring, diminished LV outflow tract size, and redundant mitral valve tissue. Despite the development of SAM, all 5 of our patients were functionally improved by this procedure. The long-term implications of SAM after valvuloplasty are not known. Doppler echocardiography is useful in assessing the degree of LV outflow tract obstruction, correlates well with invasive hemodynamic measurements, and may be useful in long-term followup of these patients. All patients undergoing mitral valve reconstruction with a Carpentier ring for mitral regurgitation because of mitral valve prolapse should be evaluated echocardiographically both pre- and postoperatively so that the true incidence of this phenomenon and its long-term consequences can be better defined. Acknowledgment: We appreciate the help of Paula LaManna in preparation of this manuscript.

References 1. Carpentier A, Deloche A, Dauptain 1, Sayer R, Blondeau P, Piwnica A, Dubost C. A new reconstructive operation for correction of mitral and tricus-

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pid insufficiency. 1 Thoroc Cordiovasc Surg 1971;61:1-13. 2. Carpentier A. Chauvaud S. Fabiani IN. Deloche A. Relland 1. Lessana A. d’Alla;nes CI, Blondeau P, Piwnica A,‘Dubost C. Reconstructive surgery of mitral valve incompetence. Ten yeor appraisal. 1 Thoroc Cordiovasc Surg 1980;79:338-348.

3. Shah PM, Gramiak R, Kramer DH. Ultrasound localization of left ventricuJar outflow obstruction in hypertrophic obstructive cardiomyopathy. Circulotion 1969;40:3-11. 4. Henry WL, Clark CE, Glancy DL, Epstein SE. Echocardiographic measurement of left ventricular outflow gradient in idiopathic hypertrophic subaortic stenosis. N Engl r Med 1973;288:989-993. 5. Shah PM, Gramiak R, Adelman AC, Wigle ED. Role of echocardiography in diagnostic ond hemodynamic assessment of hypertrophic suboortic stenosis. Circulation 1971;44:891-898. 6. Popp RL, Harrison DC. Ultrasound in the diagnosis and evaluation of therapy of idiopathic hypertrophic suboortic stenosis. Circulation 1969; 40:905-914. 7. Pridie RB, Oakley CM. Mechanism of mitral regurgitation in hypertrophic obstructive cardiomyopathy. Br Heart r 1970;32:203-208. 8. Henry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricuJar outflow obstruction in patients with obstructive asymmetric septal hypertrophy [idiopathic hypertrophic suboortic stenosis]. Am / CardioJ 1975;

inferior septal hypertrophy in IHSS: the fundamental determinant of obstruction (abstr). Circulation 1973;48:suppJIV:IV-6. 10. Reis RL, Bolton MR, King JF, Pugh DM, Dunn MI, Mason DT. Anteriorsuperior displacement of anterior papillory muscle (APM) producing obstruction and mitral regurgitation in IHSS: operative relief by posteromedial realignment of APM following ventricular septal myectomy. Circulation 1974;5o:suppI rr:rr-181srr-188.

11. Rodger JC. Motion of mitral apparatus in hypertrophic cardiomyopathy with obstruction. Br Heart 1 1976;38:732-737. 12. Nag&a S, Nimura Y, Beppu S, Park YD, Sakakibara H. Mechanism of systolic anterior motion of mitral valve and site of intraventricular pressure gradient in hypertrophic obstructive cardiomyopathy. Br Heart J 1983; 49:234-243. 13. Schuler G, Peterson KL, Johnson A, Francis G, Dennish G, Utley J, Daily PO, Ashburn W, Ross J. Temporal response of left ventricular performance to mitral valve surgery. CircuJation 1979;59:1218-1231. 14. Hatle L. Doppler Ultrasound in Cardiologv. -_ PhiJadeJuhia: Lea b Febieer. . 1984:212.

35:337-345.

15. Yock PC, Hatle L, Popp RL. Patterns and timing of Doppler-detected introcavitary and oortic flow in hypertrophic obstructive cardiomyopathy (obstr]. [ACC 1985;5:395. 16. Kronzon I, Cohen ML, Winer HE, Colvin SB. Left ventricular outflow obstruction: o CompJication of mitral vahlophty. IACC 1984;4:825-

9. King JF, Reis RL, Bolton MR, DeMaria A, Zelis R, Mason DT. Superior-to-

828.