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J Thorac Cardiovasc Surg 1994;107:416-0423
© 1994 Mosby, Inc.

Surgery for Acquired Heart Disease

The effects of complete versus incomplete mitral valve repair in experimental mitral regurgitation

Charleston, S.C.

Supported in part by National Institutes of Health NHLBI R01 HL38185grant (Blase A. Carabello) and medical research funds from the Veterans Administration, Washington, D.C. (Blase A. Carabello, Michael R. Zile, George Cooper IV).

Received for publication Sept. 16, 1992. Accepted for publication July 12, 1993. Address for reprints: Blase A. Carabello, MD, Cardiology Division, Medical University of South Carolina, 816 Clinical Science Building, 171 Ashley Ave., Charleston, SC 29425.

Abstract

Severe mitral regurgitation (regurgitant fraction 0.75 ± 0.02) was created in eight dogs by our closed-chest chordal rupture technique. After 3 months of chronic mitral regurgitation all indices of contractile function were depressed. Mitral valve repair was then attempted. Postoperative regurgitant fraction was reduced compared with the preoperative value in all eight dogs. Concomitantly, forward cardiac output increased in all dogs and pulmonary capillary wedge pressure fell in all dogs. However, in some dogs, significant regurgitation persisted despite repair. Postoperative regurgitant fraction ranged from 0% to 60%. Postoperative residual regurgitant fraction was related significantly to postoperative cardiac output (r = 0.99), pulmonary capillary wedge pressure (r = 0.77), ejection fraction (r = 0.75), and two indices of contractile function—the mass-corrected end-systolic stress volume relationship (r = 0.87) and end-systolic stiffness (r = 0.93). In general, these parameters returned to their normal values before mitral regurgitation when postoperative regurgitant fraction was less than 30%. Myocytes isolated from the ventricles at the end of study also demonstrated normal contractile function when regurgitant fraction was less than 30%. (J THORAC CARDIOVASC SURG 1994;107:416-23)

Chronic mitral regurgitation eventually causes left ventricular dysfunction and heart failure if left uncorrected. ^{1, 2} In this regard, earlier, rather than later, restoration of valvular competence is beneficial in preventing permanent left ventricular damage. ^3-5 Until recently, the standard method for restoring mitral valve competence in the United States was mitral valve replacement. However, recognition of the importance of the valvular apparatus coupled with lower operative mortality and lower postoperative morbidity after mitral valve repair has led to increased efforts to repair rather than replace the mitral valve. ^6-9

Although mitral valve repair often leads to better postoperative left ventricular performance than mitral valve replacement, ¹⁰ some mitral regurgitation may remain after the procedure. It might be assumed that such an incomplete repair would be deleterious. However, the extent to which incomplete repair impairs outcome is unknown largely because the operating surgeon, aware that the repair has been inadequate, then proceeds to revise the repair or to perform mitral valve replacement.

This imperative in man does not apply to the experimental model. During the past 7 years we have developed a canine model of mitral regurgitation that produces severe left ventricular dysfunction that can be reversed with mitral valve replacement. ^{2, 5, 11-13} This model affords the opportunity for careful longitudinal follow-up of left ventricular mechanics and contractile function with the use of accurate indices derived from load manipulation, which are difficult to apply in man. In this report we use this model to assess the effects of complete versus incomplete mitral valve repair on left ventricular mechanics and function, an issue of clinical importance but one that is difficult to assess in the clinical setting.

METHODS

Study design.
The subjects of the study were eight mongrel dogs followed longitudinally from baseline, when they were normal, through acute and chronic (3 months) mitral regurgitation to mitral valve repair and then for 1 to 3 months after operation. Thus each animal served as its own control. Hemodynamics and left ventricular mechanics were studied in the ß-blocked state at baseline, immediately after the creation of mitral regurgitation, after 3 months of chronic mitral regurgitation, and 1 to 3 months after mitral valve repair. ß-Blockade was used to prevent variations in adrenergic tone from obscuring changes in intrinsic contractile function. ^{5, 14}

If there was no significant mitral regurgitation 1 month after mitral valve replacement and all indices of pump and contractile function had returned to normal, it was assumed that further observations would not result in further improvement inasmuch as normalcy had been achieved. Thus two animals were killed after 1 month whereas six were followed up to 3 months. Data are reported for the final observation in all animals. Indices of contractile function were developed from simultaneously recorded pressure (micromanometer-tipped catheter) and volume (cineangiography) data obtained after inferior vena cava balloon occlusion. Inflation followed by deflation of the balloon produced a stepwise change in pressure and volume from which the indices of contractile function were developed. ^{2, 5, 14}

Because no single contractility index has received universal acceptance, several indices were used. We examined ejection fraction (EF), the slope of the end-ejection stress–end-ejection volume relationship (EESVR), ^{2, 5, 15} this slope corrected for left ventricular mass (EESVR_mc), ^{2, 5} and the size-independent end-systolic stiffness constant (k). ^{5, 16} To help validate our assessment of ventricular contractility, contractile function was also studied in cardiocytes taken from these same left ventricles. Cell contractile function was assessed with the viscosity (graded external load)-velocity relation ¹³ and cardiocyte peak sarcomere shortening velocity measured by an investigator who was blinded to the global left ventricular contractile function data.

Study protocol.
Initial study.
Anesthesia was induced with droperidol-fentanyl (Innovar Vet, Pitmen-Moore, Washington Crossing, N.J.), 0.15 mg/kg given intramuscularly. The animals were then intubated and mechanically ventilated (Harvard Apparatus Co., Inc., S. Natick, Mass.) and maintained with incremental doses of droperidol-fentanyl together with inhalation of nitrous oxide and oxygen at a 3:1 nitrous oxide/oxygen ratio, a combination that has been shown to have little effect on contractile function. ¹⁷

Catheters were inserted to monitor left and right heart pressures, to determine cardiac output by thermodilution, and to perform inferior vena cava occlusion as previously described. ^{2, 5, 12} Then, ß-blockade was accomplished by intravenous infusion of esmolol, 0.5 mg/kg for 3 minutes, followed by a constant infusion of 0.3 mg/kg/min for the remainder of the study. Baseline pressure recordings were made and thermodilution cardiac output was determined.

A ventriculogram was performed in the 30-degree right anterior oblique position at 60 frames/sec (Cardio Diagnostics, Philips Medical Systems, Sherton, Conn.) to obtain resting EF and cardiac volumes. After a 15-minute recovery period, the inferior vena cava balloon was inflated, causing decreased venous return and a subsequent decrease in aortic pressure. The balloon was deflated simultaneously with the performance of a second ventriculogram and recording of high-fidelity pressure (contractility ventriculogram). Deflation of the balloon produced a beat-by-beat rise in pressure and thus a beat-by-beat change in loading conditions. ^{2, 5, 14} This procedure was done identically in all animals at baseline, at 3 months of chronic mitral regurgitation, and at 1 month and 3 months (if alive) after mitral valve repair.

Creation of mitral regurgitation.
After the contractility ventriculogram at the baseline examination was done, the pigtail and Millar catheters (Millar Instruments, Inc., Houston, Tex.) were removed and a 30 cm 8F sheath was inserted into the carotid artery and advanced across the aortic valve into the left ventricle. Then a urologic stone-grasping forceps (Cook Urological Inc., Spencer, Ind.) was advanced through the sheath to the mitral valve apparatus and was used to grasp chordae tendineae or the mitral valve leaflets. Forcible retraction of the grasping forceps disrupted the chordae tendineae, producing severe mitral regurgitation as described before. ^{2, 5, 11-13} The vessels and cutdown incision were repaired, and the animals recovered from anesthesia and were followed up longitudinally under the supervision of the veterinary care staff. Furosemide was administered as necessary when resting respiratory rate increased, suggesting clinical heart failure. No other drugs were administered.

At all times animals were cared for in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" prepared by the Institute of Laboratory Animal Resources and published by the National Institutes of Health (NIH Publication No. 86-23, revised 1985).

Mitral valve operation.
One week after the determination of hemodynamics and contractile function at 3 months of chronic mitral regurgitation, the animals underwent mitral valve repair. Anesthesia was induced with intramuscular injection of droperidol-fentanyl (0.15 ml/kg) after which the dogs were intubated and placed on a mechanical ventilator before the start of extracorporeal circulation. Anesthesia was maintained by inhalation of 0.5% isoflurane and constant infusion of sufentanil, 0.2 µg/kg per minute. A radial artery cannula was inserted to monitor arterial blood pressure and a central venous catheter was inserted for infusion of drugs and for the measurement of central venous pressure.

A thoracotomy was performed in the fourth intercostal space. After pericardiotomy, the heart was suspended in a pericardial cradle. The right femoral artery and right atrium were cannulated and connected to extracorporeal circulation. Then moderate hypothermia (28° C) was established and the aorta was crossclamped. Cardioplegia was induced identically in all animals by intracoronary perfusion with cold hyperkalemic cardioplegic solution, 20 ml/kg initial dose, then 10 ml/kg every 20 minutes as needed.

Mitral valve repair was done by various combinations of the procedures of Carpentier, ^{18, 19} Kay, ^20,21 and Reed ²² and their associates modified according to the lesions of the valve and subvalvular apparatus (Fig. 1). After mitral valve repair was done, the left ventricle was filled with cold saline to test for residual regurgitation. After repair, mitral regurgitation was thought to be absent or mild in all eight dogs. After removal of the crossclamp, air was evacuated and the left atriotomy was closed. The average crossclamp time for mitral valve repair was 60 ± 8 minute

View larger version (38K): [in this window] [in a new window]   Fig. 1. Type of mitral valvular apparatus damage and its method of repair is demonstrated for eight dogs. Preoperative condition for each group is demonstrated in drawings on left side and postoperative condition is demonstrated in drawings on right side. Bold thick lines shown in preoperative drawings indicate sites of chordal rupture. Small letters on postoperative drawings indicate type of repair: a, Carpentier's modification; b, Kay's modification; c, Reed's modification.

During the next 24 hours the animals underwent constant supervision by one of us. Arterial blood gas and electrolyte analyses were obtained hourly and corrected as necessary. Twenty-four hours after operation all animals were able to be extubated and all intraarterial and intravenous cannulas removed. Butorphanol was administered as necessary for postoperative pain. No cardiac medications were administered postoperatively. The animals were then followed up longitudinally for 1 to 3 months with determinations of hemodynamics and contractile function occurring before termination of the experiments.

Cellular contractile function.
One week after the final evaluation of postoperative left ventricular function, investigators who were blinded to the in vivo results isolated and evaluated cardiocytes from these same left ventricles as described previously in detail. ¹³ Briefly, the hearts were removed quickly via a right lateral thoracotomy under droperidol-fentanyl, nitrous oxide/oxygen anesthesia and placed in cold buffer. The atria and great vessels were removed and the portion of the free wall that was perfused by the left circumflex coronary artery was then dissected free of the heart. This artery was cannulated and perfused with type II collagenase and then minced into 2 mm cubes. The minced tissue was then gently agitated for 5 minutes at 37° C while being gassed with 100% oxygen. The cardiocytes were harvested by drawing off the supernatant in which they were suspended for filtration through 210 µm nylon mesh.

To measure sarcomere motion in isolated cardiocytes we used laser diffraction techniques that are well established. ^23-25 The cardiocytes were stimulated to contract between platinum wire electrodes. Changes in sarcomere length were measured from movement of the first-order diffraction pattern cast by a substage laser light passing through the sarcomeres of a given cardiocyte onto a diametrically opposed optical sensor situated above the microscopic stage. Only cardiocytes with the following characteristics were analyzed: single, rod-shaped cells unattached to adjacent cells, which contracted with each stimulus and were quiescent between stimuli. To apply a viscous load (analogous to afterload) to contracting cardiocytes, we immersed the cells in superfusates of differing viscosities altered by the concentration of inert methyl cellulose.

Calculations.
Regurgitant fraction (RF) was calculated as follows:

RF = (SV_A - SV_t)/SV_A^'

where SV_A is angiographic stroke volume (end-diastolic volume minus end-systolic volume) and SV_t is stroke volume calculated from thermodilution cardiac output divided by heart rate. End-diastolic volume was taken as the largest angiographic volume. End-systolic volume was taken to be the smallest volume, recognizing that, although end-systolic volume and end-ejection volume may not be identical in mitral regurgitation, end-ejection volume has the advantage of exact definition.

The slope of the EESVR was multiplied by the simultaneously determined angiographic left ventricular mass to obtain a mass-corrected relation (EESVR_mc), ^{5, 12} because although the slope of EESVR is relatively load-independent, it is size- and mass-dependent. ^{16, 26, 27} Contractile function was also examined with a size-independent index of active ventricular stiffness, ^{5, 12, 16} relating a change in end-ejection stress (s) to the corresponding change in a measure of strain, the natural logarithm (ln) of the reciprocal of wall thickness (1/H):

s = Ce^kln(1/H).

where C = a constant. The size-independent index (k) is the end-systolic stiffness constant of the myocardium; it was obtained by curve-fitting of the end-systolic s - ln (1/H) relation to the preceding equation. ¹⁶

Statistics.
The mean value and the standard error of the mean are shown for each group of data. When two sets of data were compared, a paired t test was used. When a comparison among more than two data sets was made, statistical inference was made by one-way analysis of variance followed by a Newman-Keuls test if the analysis of variance demonstrated a difference was present. The slope of the EESVR and of the relationship of various parameters to regurgitant fraction was determined by linear regression by the least-squares method. The value of k was obtained by means of a curvilinear fit to the natural logarithm of the reciprocal of wall thickness (ln 1/H) stress coordinates. The correlation coefficient of both EESVR and k exceeded 0.97 in all cases.

RESULTS

After 3 months of mitral regurgitation the average regurgitant volume for the eight dogs was 0.75 ± 0.02. Pulmonary capillary wedge pressure was 8 ± 2 mm Hg at baseline and rose significantly to 28 ± 2 mm Hg at 3 months of mitral regurgitation (p < 0.001). Cardiac output was 1.8 ± 0.2 L/min after 3 months of mitral regurgitation, which was significantly lower than that at baseline, (2.8 ± 0.3 L/min; p < 0.03). EF was 0.49 ± 0.01 at baseline and increased to 0.65 ± 0.01 (p < 0.001) when the favorable loading conditions of mitral regurgitation were created; EF was then depressed (0.47 ± 0.02, p < 0.01) after 3 months of mitral regurgitation compared with values at acute mitral regurgitation.

Both indices of contractile function were depressed after 3 months of mitral regurgitation. The mass-corrected slope of the EESVR had fallen from 567 ± 48 to 301 ± 36 (p < 0.009) and k had fallen from 3.81 ± 0.15 to 2.08 ± 0.11 (p < 0.003).

At termination of the experiments (1 month after mitral valve repair in two dogs, 3 months after mitral valve repair in six dogs), the average regurgitant fraction was 29.5, but there was a wide range from 0% to 60% as shown in Fig. 2. In the three dogs with the highest residual regurgitant fractions (Fig. 2), the forward stroke volume was significantly higher after repair (0.88 ml/kg) than it had been at 3 months of mitral regurgitation (0.69 ± 0.06 ml/kg; p < 0.05). Likewise, wedge pressure was lower in these three dogs after repair (18 ± 2.8 mm Hg) than it had been at 3 months of mitral regurgitation (31.7 ± 3.4 mm Hg; p < 0.01). However, EF was reduced after the failed repair in this group (0.305 ± 0.028) compared with EF at 3 months of mitral regurgitation (0.432 ± 0.012; p < 0.01). Both indices of contractile function showed no improvement after failed repair in these three dogs (EESVR_mc 310 ± 22, k 2.4 ± 0.1) compared with valves for 3 months of chronic mitral regurgitation (EESVR_mc330 ± 35, k 2.5 ± 0.1).

View larger version (32K): [in this window] [in a new window]   Fig. 2. Regurgitant fraction is shown at baseline (Control), after acute mitral regurgitation was created (Acute MR), after mitral regurgitation had been present for 3 months (MR 3mo), and at final postoperative study (PO). Regurgitant fraction fell in all dogs but remained 30% or greater in three dogs. MVP, mitral valve repair.

View larger version (26K): [in this window] [in a new window]   Fig. 3. Postoperative cardiac output is shown as it relates to postoperative regurgitant fraction for eight animals. Horizontal lines at top of graph indicate mean and standard error of cardiac output before mitral regurgitation was created, when dogs were normal. Values in five of eight dogs returned to this normal relationship. These dogs had regurgitant fractions of 30% or less.

View larger version (26K): [in this window] [in a new window]   Fig. 4. Pulmonary capillary wedge pressure as it relates to postoperative residual regurgitant fraction is demonstrated. Horizontal lines represent mean and standard error of wedge pressure before mitral regurgitation was created, when dogs were normal. Values in four dogs returned to this normal relationship. These were animals with regurgitant fractions of less than 20%.

View larger version (23K): [in this window] [in a new window]   Fig. 5. Postoperative EF as it relates to postoperative residual regurgitant fraction is demonstrated. Horizontal lines represent mean and standard error for eight dogs before mitral regurgitation was created, when dogs were normal. Five dogs had EFs in this range or greater. These were dogs with residual regurgitant fractions of 30% or less.

View larger version (56K): [in this window] [in a new window]   Fig. 6. Two indices of contractile function as they relate to postoperative residual regurgitant fraction are demonstrated. Mass-corrected slope of EESVR is demonstrated on left and k is demonstrated on right. Horizontal lines represent mean and standard error of these relationships for dogs before mitral regurgitation was created, when they were normal. Values in four animals returned to this normal relationship and in five animals returned to values that were normal for our laboratory (EESVR greater than 450, k greater than 3.3). These five animals had residual regurgitant fractions of less than 30%.

View larger version (27K): [in this window] [in a new window]   Fig. 7. Myocyte velocity-viscosity relationships are demonstrated in this graph. Cells taken from animals undergoing mitral valve repair with residual regurgitant fractions (RRF) of less than 30% demonstrated contractile function identical to cells taken from normal dogs. Myocytes taken from dogs with regurgitant fractions of greater than 30% demonstrated contractile dysfunction.

A major finding of this study was that postoperative pump and contractile function correlated well with residual regurgitant fraction. For most parameters examined, return to normal did not occur if the regurgitant fraction exceeded 30%. Although it is not surprising that a failed mitral valve repair would fail to lead to improvement in left ventricular function, we believe that these data are important for three reasons.

First, they constitute a detailed observation of the hemodynamic and contractile function consequences of partial but unsuccessful mitral valve repair in a fashion that is unlikely to be obtained in human beings. That is, when it is obvious that mitral valve repair has failed in human beings, subsequent steps will almost always be undertaken to correct the mitral regurgitation unless for some reason the patient is then deemed inoperable.

Second, the indices of contractile function created by load manipulation obtained in our experimental model are accurate ¹³ but difficult to obtain in patients, and the cellular contractile data are impossible to obtain from patients.

Third, our data help address the issue of how satisfactory a repair must be to normalize postoperative contractile function. Some level of mitral valve competence was restored in every case. Yet only when regurgitant fraction was less than 30% was full recovery possible. This level of mitral regurgitation is equivalent to about 2+ on the standard semiquantitative grading scale.

Of interest, forward cardiac output improved in all dogs and wedge pressure decreased in all dogs after repair including the three dogs with the highest residual regurgitant fractions. However, contractile function did not improve in this group. Thus although partial repair may allow improvement in pump function, substantial residual regurgitation may preclude improvement in contractile function.

Table I compares our previous data from mitral valve replacement with chordal preservation ¹² with that from the current repair groups. As can be seen, similar results regarding contractile function and hemodynamics are seen with successful repair and mitral valve replacement with chordal preservation, and both are superior to failed repair. We believe that our new data should be taken in light of these previous experimental results and clinical results, which demonstrate that mitral valve replacement with chordal preservation offers an excellent postoperative result with regard to left ventricular function. ^{28, 29} Pure mitral valve repair is the most desirable of all mitral valve operations because it reduces the prevalence of endocarditis and thromboembolism while it at the same time preserves left ventricular function. ^{9, 10, 30-32} However, in cases in which the risk of failed repair is high, that is, in rheumatic valve disease, mitral valve replacement with chordal preservation appears to be an excellent alternative to a potentially failed repair.

Conclusions.
We conclude that successful mitral valve repair, like successful mitral valve replacement ⁵ and successful mitral valve replacement with chordal preservation, ¹² allows for restoration of left ventricular contractile function if it was depressed before the operation. With regard to pump performance, successful mitral valve repair compares favorably with mitral valve replacement in which chordal preservation is done; both procedures are superior to mitral valve replacement with chordal disruption. ^{5, 12} However, mitral valve repair that partially restores mitral competence but leaves a residual regurgitant fraction of greater than 30% does not permit a return of contractile function to normal even though some indices of pump performance may be improved.

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