BRIEF BEPOBTS

Association Between Residual Mitral Regurgitation and Left Ventricular Outflow Obstruction After Carpentier Ring Mitral Annuloplasty Paul A. Tunick, MD, David G. Cziner, MD, Edward S. Katz, MD, John L. Perez, MA, and ltzhak Kronzon, MD 1971, Carpentier et al1 reported the use of a new for mitral valve repair using an annuloplasty Iring.ntechnique Although this technique avoidssomecomplications of prosthetic valves,spatial changesin the mitral apparatus after this operation may result in systolic anterior motion of the mitral valve which may causeleft ventricular (LV) outflow obstruction similar to that seenin hypertrophic cardiomyopathy.2,3In a series of 439 patients, systolic anterior motion wasseenin 6.4%of patients after Carpentier ring repair, and LV outflow obstruction was present in 2.3%.4Although outflow obstruction may be treated successfullymedically,4 it may also be a causeof immediate (intraoperative) failure of the technique.sWe have previously reported a relation betweenmitral regurgitation (MR) and LV outflow obstruction in 2 groups.In those who have undergone aortic valve replacement for aortic stenosis,the relief of outflow obstruction after aortic valve replacement was associatedwith a significant reduction in the degree of MR.6 In the second group, those with hypertrophic cardiomyopathy, the degree.of MR was directly associatedwith the severity of outflow obstruction.7 The current study evaluates the possible mechanismsof LV outflow obstruction after Carpentier ring mitral annuloplasty, and investigatesthe relation, if any, of MR to the presenceof LV outflow obstruction. BetweenJune I987 and July 1991,Doppler echocardiography wasperformed on 352patients following Carpentier ring mitral annuloplasty. Mitral systolic anterior motion waspresent in 43 patients (12%) with agesranging from 21 to 83 (mean 60) years, including 30 men (70%). The studies were donefrom 2 days to 7 years after surgery. These echocardiograms were reviewed. M-mode, 2-dimensional, pulsed, continuous-wave, and color flow Doppler studies were performed on a Hewlett-Packard Sonos 500 system (Andover, Massachusetts). The presenceof LV outflow obstruction was documentedby pulsed Doppler in the outflow tract, and the gradient was measuredfrom the apical view using continuous-wave Doppler and the modified Bernoulli equation. A velocity of 12 mfs wasconsideredabnormal. The degree of MR was graded using previously described methods.8Becausenormal people may have no or mild MR,9 the group with no or mild MR was compared with the group with significant, abnormal degrees of MR (moderate or severe).Since the grading of MR and the measurementof the outflow velocity were done before this retrospective review, they were evaluated blindly. At study, the following additional measureFrom the Department of Medicine, New York University Medical Center, 550 First Avenue, New York, New York 10016.Dr. Tunick’s addressis: Noninvasive Cardiology Laboratory, 560 First Avenue, New York, New York 10016. Manuscript received December 16, 1991; revisedmanuscript receivedand acceptedApril 9, 1992.

ments were also obtained: LV diastolic dimension, LV systolic dimension, LV ejectionfraction, left atria1 size, LVoutjlow size, and Carpentier ring diameter. The outjlow size was measuredfrom the anterior part of the Carpentier ring to the ventricular septum. The ring diameter wasmeasuredas the distancebetweenthe centers of the 2 bright circular echoesconsisting of the anterior and posterior edgesof the ring. The latter 2 dimensions (outflow and ring size) were measuredfrom the parasternal long-axis view. Valuesarepresentedwith meansand standard errors of the mean.A Pearsonproduct-moment correlation coefficient was calculated to assessthe relation between variables. Linear regressionwas done with outflow gradient as the dependentvariable. Theprevalenceof significant (moderateor severe)MR wascomparedinpatients with and without mitral systolic anterior motion by the chi-square test. A p value KO.05was consideredsignificant. Mitral systolic anterior motion was seen in 43 patients after Carpentier ring repair (12%). The distribution of LVoutjlow gradients in these43patients is listed in Table I. There was no gradient in 23 patients (54%), and the gradients in the other 2Opatientsrangedfrom 16 to 140 mm Hg. The mean gradient in the study group was 24 f 5.1. There was a significantly higher incidenceof moderate or severeMR in the group of 43 patients with (33%) than in the 309patients without (19%) systolic anterior motion (p = 0.05) (Table II). In thosewith systolic anterior motion, MR was absent or mild in 29 patients (67%), moderate in 10 patients (23%) and severein 4 patients (9%). In the 309patients without systolic anterior motion, MR was moderate in 41 (I 3%) and severein 19 (6%). In the group with systolic anterior motion, mean LV outflow gradient in thosewith absentor mild MR was 15 f 5 mm Hg. Mean gradient in those with moderateMR TABLE I Distribution of Outflow Tract Gradients Gradient (mm Hg) 0

16 20 25 36 40 50 64 70 100 140

Frequency (no. of pts.)

%

23 3 1 2 2 1 2 5 2 1 1

53.5 7 2.3 4.7 4.7 2.3 4.7 11.7 4.7 2.3 2.3

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689

TABLE II Mitral Regurgitation in Patients With and Without Systolic Anterior Motion

SAM No SAM

O-l+ MR

2-3+ MR

29 (67%) 249 (81%)

14 (33%) 60 (19%)

p = 0.05.

MR = mitral regurgitation; SAM = systolic anterior motion.

TABLE Ill Distribution of Gradients with Respect to Mitral Regurgitation 0um0w Gradient

(mm Hg)

O-Mild MR

Moderate MR

Severe MR

140 120 100 80 . .. 60 40 ... .

20 0

***(n = 17)

......

MU = mitral regurgitation. Eachdot representsan individual patient. The 3 asterisks represent

17 patients.

TABLE IV Variables Not Correlated with Gradient

1

Variable Left ventricle (diastole) (mm) Left ventricle (systole) (mm) Ejection fraction (%) Left atrium (mm) Left ventricular outflow tract (mm) Carpentier ring diameter (mm)

was 23 f 10 mm Hg, and in those with severeMR 89 f 20 mm Hg (Table ZZZ). The distributions of LVdiastolic and systolic dimensions, LV ejection fractions, left atria1 sizes, outflow tract diameters, and ring diameters in patients with systolic anterior motion are detailed in Table IV. The determination of correlation coefficientsshowedthat the only significant relation among all of these variables was betweenMR and LV outflow tract gradient (r = 0.54, p = 0.005). Although the r value is not high, this does explain 29%of the effect. There wasno significant correlation between the outflow tract diameter, LV size or ejectionfraction, left atria1 sizeor ring diameter, and the outflow tract gradient. Linear regressionshowedthat the outflow gradient was dependenton the degreeof MR (/3 coefficient = 27.4, constant = 14.9, p = 0.0002). Subsequentechocardiogramswereavailable in I6 of 20 patients (80%) with out’ow gradients, recorded 1 week to 15 months after the first study. Of these 16 patients, half (8) had MR that was moderate or severe. The outflow gradient decreasedover time to zero in 6 of these 8 patients (75%), but there was no predictable 690

THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 70

effect of this decreasein gradient on the degreeof MR (MR decreasedin 3 and increasedin 3 as the gradient decreased). The most frequent complication of the Carpentier ring procedure in our 352 patients was significant MR (74 patients, 21%). Of these, 51 patients (14.5%) had moderateand 23 (6.5%) had severeMR. Mitral systolic anterior motion, present in 43 patients (12%), was the next mostfrequent complication. Other more rare problems were also diagnosedby echocardiography.Abnormal placement of the ring was seenin 2 patients (0.6%). The ring was sewn anterior to the annulus in 1 and attached to the atria1 septum in 1. There was partial dehiscenceof the ring with paravalvular leaks in 3 patients (0.9%). In addition, the following complications werediagnosedin 1 patient (0.3%) each: torn chordae, a 5 X 7 cm left atria1 clot, a vegetation, and a coronary fistula to the lef ventricle after myomectomy. Our previous experience in evaluating the relation betweenLV outflow obstruction and MR in patients with aortic stenosis6and hypertrophic cardiomyopathy7led us to hypothesizethat a similar relation may exist in patients who developmitral systolic anterior motion as a complication of the Carpentier ring repair. The current study doesconlirm that there is such a direct association.It is not possibleto say whether MR causesthe outflow obstruction or vice versa. In fact, both mechanismsmay pertain in different patients.There is a significantly higher incidence of MR in the patients with systolic anterior motion than in those without it. In addition to MR asa causeof outflow obstruction in patients with systolic anterior motion, we looked further to seeif there was a relation betweenother parameters and the degreeof obstruction. Although our laboratory has previously shown that the outflow tract dimension decreasesasa result of the Carpentier repair,‘Othere was no relation between the postoperative diameter of LV outflow tract and degreeof obstruction. In addition, the size of the ring itself had no effect, nor did left atria1 or LV dimensionsor ejection fraction. The incidenceof mitral systolic anterior motion in our seriesis relatively high, 12%.Only 44% of thesepatients had enough systolic anterior motion to result in an LV outflow gradient. This obstruction produced an acute critical problem in only 1 patient. This patient, with the highest gradient (140 mm Hg), had acute deterioration immediately after operation, which respondedto medical management. Severe MR eventually disappearedwith therapy, which resulted in the disappearanceof the outflow gradient. Despitethe associationbetweenthe degree of MR and the degreeof obstruction that we havedemonstrated, our data show that there is no way to predict the change in the degree of MR as the outflow gradient decreasesin an individual patient. This probably indicatesthat there are multiple mechanismsfor the persistence of MR after repair, only someof which are related to the degreeof outflow obstruction. Incomplete correction, leaflet degeneration and suture dehiscencehave been previously suggestedas such mechanisms5 1. Carpentier A, DelocheA, Dauptain J, Sayer R, BlondeauP, Piwnica A, Dubost C, McGoon DC. A new reconstructive operation for correction of mitral and

SEPTEMBER 1, 1992

tricuspid insufficiency. J Thorac Cardiomsc Surg 197 I;6 1:I- 13. 2. Galleatein PE, Berger M, Rubenstein S, Berdoff RI, Goldberg E. Systolic anterior motion of the mitral valve and outflow obstruction after mitral valve reconstruction. Cheer 1983;83:819-820. 3. Kronzon I, Cohen ML, Winer HE, Calvin SB. Left ventricular outflow obstruction: a complication of mitral valvoloplasty. J Am Cot1 Cardiol 1984;4:

825-828. 4. Grossi EA. Galloway AC, Parish MA, Asai T, Gindea AJ, Harty S, Kronzon I, Spencer FC. Calvin SB. Experience with 28 cases of systolic anterior motion after Carpentier mitral valve reconstruction. Ann Thorac Surg 1992;103:466-470. 5. Marwick TH, Stewart WJ, Curie PJ, Cosgrove DM. Mechanisms of failure of mitral valve repair: an cchocardiographic study. Am Hear? J 1991;122:149-156, 6. Tunick PA, Gindea A, Kronzon 1. Effect of aortic valve replacement for aortic

Aortic

Distensibility

in Children

stenosis on severity of mitral regurgitation. Am J Cardiol 1990;65:1219-1221. 7. Tunick PA, Lampert R, Perez JL, Kronzon I. Effect of mitral regurgitation on the left ventricular outflow pressure gradient in obstructive hypertrophic cardiomyopathy. Am J Cordial 1990;66:1271-1273. 8. Helmcke F, Nanda NC, Hsiung MC, Soto B, Adey CK, Goyal RG, Gatewood RP. Color Doppler assessment of mitral regurgitation with orthogonal planes. Circulation 1987;75:175-183. 9. Yoshida K, Yoshikawa J, Shakudo M, Akasaka T, Jyo Y, Takao S, Shiratori K, Koizumi K, Odumachi F, Kato H, Fukaya T. Color Doppler evaluation of valvular regurgitation in normal subjects. Circulation 1988;78:840-847. 10. Galler M, Kronzon I, Slater J, Lighty GW Jr, Politzer F, Calvin S, Spencer F. Long-term follow-up after mitral valve reconstruction: incidence of postoperative left ventricular outflow obstruction. Circulation 1986;74(suppl 1):1-99-I-103.

with the Marfan

Syndrome

Aslak Savolainen, MD, Pekka Keto, MD, Pauli Hekali, MD, Liisa Nisula, MD, llkka Kaitila, MD, Matti Viitasalo, MD, Veli-Pekka Poutanen, MSc, Carl-Gustaf StandertskjOld-Nordenstam, MD, and Markku Kupari, MD he Marfan syndromeis a heritable diseaseof connective tissue,which predominantly affects the skeletal, ocular and cardiovascular systems.’Recent immunohistochemical and genetic fmdings suggestthat the ultimate defect is in Iibrillin, a microtibrillar protein abundant in tissuesinvolved in Marfan syndrome.2Clinically and in terms of prognosis,dilatation of the aortic root is the key manifestation of the syndrome,becauseit predisposesthe subjectto the risk of aortic dissectionand fatal rupture, or severe regurgitation and heart failure.3 Although the structural abnormalities of the Marfan aorta have been well described,’ its conduit function was poorly known until Hirata et al4 recently reported on impaired aortic distensibility in adults with the Marfan syndrome.In the present investigation we expanded this approach by studying aortic distensibility with magnetic resonance imaging (MRI)5 in children and adolescentswith this disease. T

Children with the Marfan syndrome (11 boys and I3 girls, aged 3.5 to 16 years) were consecutively evaluated and followed-up in 1990 at the Genetics Clinic, Department of Pediatrics, Helsinki University Central Hospital. The diagnosis was based on criteria established at the 7th International Congress of Human Genetics in 198@ and at the First International Symposium on Marfan Syndrome in 1988. Diagnostic procedures were the same as in our previous study,7 and included history, physical examination, complete echocardiographic study and ophthalmologic consultation. Eighteen patients had a positive family history of the Marfan syndrome. All patients were asymptomatic except one 3.5 year-old child who had compensated heart failure due to mitral regurgitation. No patient was receiving B-adrenoceptor blocking drugs. For a control group, we studied 20 healthy children (9 boys and 11 girls, aged 6.5 to 17 years): they were From the First Department of Medicine, and the Departmentsof DiagnosticRadiology, Pediatrics,and Medical Genetics,Helsinki University Central Hospital, 00290Helsinki, Finland. This study wassupportedby grants from Aame Koskelo Foundation,PaavoNurmi Foundationand Ida Montin Foundation, Helsinki, Finland. Manuscript received December 9, 1991; revised manuscript received March 30, 1992, and acceptedApril 4.

recruited through their parents who were members of the hospital staff. These children underwent a physical and echocardiographic examination in addition to the study of the thoracic aorta by MRI. Verbal parental consent was obtained for each child participating in the study. The protocol was approved by the local ethics committee. The studies were performed using a 1.O Tesla superconducting Siemens unit (Magnetom 42 SP), a body coil and electrocardiogram triggering. To examine changes with the cardiac cycle in the luminal areas of the ascending and descending thoracic aorta, a tine-examination was obtained in a plane transecting the ascending and descending aorta axially at the level ofpulmonary artery bifurcation. We used the 2-dimensional gradient echo sequence with a repetition time of 30 ms and an echo time of I2 ms; the flip angle was 60”, the imaging matrix was 128 X 256, and the slice thickness was 7 mm. Another tine-study was obtained in the coronal direction in the plane of the aortic valve. Diastolic and systolic cross-sectional areas of the ascending and descending thoracic aorta were integrated with a commercially available image analysis system (Radgop/Wiz, Contextvision, Struers Vision AB). The radiologist performing the analyses had no knowledge of the subject under study. Measurements were used to determine the change of the aortic luminal area from end-diastole to end-systole. Aortic distensibility was calculated by the followingformula: distensibility = aortic luminal area change/diastolic luminal area X pulse pressure. This measurement is identical to the echocardiographic distensibility measurement,8 except that aortic luminal areas are substituted for diameters. The pressure-independent aortic stiffness index was calculated by the following formula: stiffness index = In (systolic/diastolic blood pressure)/(aortic diameter changelaortic diastolic diameter)9; diameters were derived from the luminal areas assuming circular geometry. In 4 patients with the Marfan syndrome, MRI measurements suggested a minute reduction of the luminal area of the descending aorta from end-diastole to endsystole, rather than an increase. In calculating aortic distensibility and stiffness index, these measurements BRIEF REPORTS

691

Association between residual mitral regurgitation and left ventricular outflow obstruction after Carpentier ring mitral annuloplasty.

BRIEF BEPOBTS Association Between Residual Mitral Regurgitation and Left Ventricular Outflow Obstruction After Carpentier Ring Mitral Annuloplasty Pa...
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