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Ann Thorac Surg 1997;64:1026-1031
© 1997 The Society of Thoracic Surgeons

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Original Article: Cardiovascular

Distortions of the Mitral Valve in Acute Ischemic Mitral Regurgitation

Department of Surgery, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

 
Background. In the absence of papillary muscle rupture, the precise deformations that cause acute postinfarction mitral valve regurgitation are not understood and impair reparative efforts.

Methods. In 6 Dorsett hybrid sheep, sonomicrometry transducers were placed around the mitral annulus (n = 6) and at the tips and bases of both papillary muscles (n = 4). Later, specific circumflex coronary arteries were occluded to infarct approximately 32% of the posterior left ventricle and produce acute 2 to 3+ mitral regurgitation. Before and after infarction, distance measurements between sonomicrometry transducers produced three-dimensional coordinates of each transducer every 5 ms.

Results. After infarction, the annulus dilated asymmetrically orthogonal to the line of leaflet coaptation, but the annular area increased only 9.2% ± 6.3% (p = 0.02). At end-systole, posterior papillary muscle length increased 2.3 ± 0.9 mm (p = 0.005); the posterior papillary muscle tip moved closer to the annular plane and centroid, and the anterior papillary muscle tip moved away.

Conclusions. Small deformations in mitral valvular spatial geometry after large posterior infarctions are sufficient to produce moderate to severe mitral regurgitation. The most important changes are asymmetric annular dilatation, prolapse of leaflet tissue tethered by the posterior papillary muscle, and restriction of leaflet tissue attached to the anterior papillary muscle.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

 
Severe postinfarction mitral insufficiency is a life-threatening, catastrophic event that may be due to either papillary muscle rupture or, more commonly, "papillary muscle dysfunction" [1]. Although they prefer repair, most surgeons replace the valve [2, 3], because in the absence of papillary muscle rupture, the mechanism that causes the intact valve to leak is not understood. A reliable, simple operation to restore valve competence is needed, but annuloplasty often is not efficacious [2, 3]. Unless the heart is chronically enlarged, dilatation of the annulus is not apparent [4].

A sheep model of acute infarction of 32% of the posterior left ventricular (LV) wall produces immediate moderate or severe mitral regurgitation (MR), low cardiac output, and congestive heart failure [5, 6]. The subtle, spatial deformations of the mitral apparatus that cause regurgitation cannot be resolved by two-dimensional echocardiography [7] or other clinical imaging techniques, but they can be studied in laboratory animals by sonomicrometry array localization [8] or marker angiography [9, 10]. This article describes the small deformations that produce moderate or severe MR after acute infarction of 32% of the posterior LV in sheep.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

 
In compliance with guidelines for humane care (NIH Publication No. 85-23, revised 1985), 6 Dorsett hybrid sheep (35 to 45 kg) were induced with sodium thiopental (10 to 15 mg/kg intravenously), intubated, and anesthetized and ventilated with isoflurane (1.5% to 2%) and oxygen (Drager anesthesia ventilator; North American Drager, Telford, PA). The surface electrocardiogram and arterial blood pressure were monitored. The sheep received glycopyrrolate (0.4 mg intravenously), and one dose of cefazolin (1 g intravenously) before operation and one dose afterward.

Through a sterile left lateral thoracotomy, snares were placed around the posterior descending artery and the second and third obtuse marginal branches of the circumflex coronary artery. Sixteen 3-mm hemispheric PZT-5A piezoelectric transducers (Crystal Biotech, Hopkinton, MA) were placed in each sheep before and during cardiopulmonary bypass, as described previously [8]. Three transducers on the chest wall defined a reference plane, two epicardial transducers defined the ventricular minor axis, and one transducer marked the apex. Six transducers were placed around the mitral valvular annulus, and the remaining transducers were sutured to the tips and bases of both papillary muscles [8]. The 16 color-coded transducer wires were brought out through the chest wall and secured externally by a plastic patch sutured to the skin. The three coronary snares were secured under the pectoral muscle.

The animals were studied 5 to 15 days later. The sheep were sedated with thiopental, placed supine, intubated, anesthetized with isoflurane, and mechanically ventilated. A high-fidelity double pressure transducer (SPC-350; Millar Instruments Inc, Houston, TX) for simultaneous measurements of left ventricular and aortic root pressures was passed percutaneously into the LV through a femoral artery. The surface electrocardiogram and LV and aortic root pressures were monitored continuously (Hewlett-Packard 78534C monitor; Hewlett-Packard Inc, Santa Clara, CA). A Swan-Ganz catheter (131H-7F; Baxter Healthcare Corp, Irvine, CA) was introduced through the right internal jugular vein for measurement of duplicate thermodilution cardiac outputs and pulmonary artery and capillary wedge pressures.

Subdiaphragmatic color flow Doppler velocity maps (model 77020A; Hewlett-Packard Inc) to assess the degree of MR were obtained through a sterile, upper midline laparotomy. Transducer wires were connected to a Sonometrics Series 5001 Digital Sonomicrometer (Sonometrics Corp, London, Ontario, Canada) [8]. Ventilation was suspended during sonomicrometry measurements. All 120 distances between the 16 transducers were measured every 5 milliseconds during a 5-second data run. The electrocardiogram and the LV, aortic root, pulmonary capillary wedge, and central venous pressures were recorded simultaneously.

Coronary snares were exteriorized. Before infarction, animals received bolus lidocaine (15 mg/kg) followed by an infusion (2 mg/min). Normal saline solution containing 2 g of MgSO₄ and 40 mEq of KCl per liter also was infused at 70 mL/h. Snares, occluding all three coronary arteries, were pulled up sequentially over a 5-minute period. The subsequent infarction involved 32% of the LV mass and produced immediate 2 to 3+ MR [10]. Subdiaphragmatic color flow Doppler velocity maps, echocardiograms, and hemodynamic measurements were made during coronary occlusion and at 5 and 30 minutes after occlusion. The animals were euthanized with 1 g of thiopental and 60 mEq of KCl. Their hearts were removed and opened to check the placement of cardiac sonomicrometry transducers.

Sonomicrometry distance data were used to determine the three-dimensional coordinates of each transducer at end-diastole, end-isovolumic contraction, end-systole, and end-isovolumic relaxation, as defined [11] and described previously [8]. Two-dimensional views of transducer movements were created by projecting transducer locations in three dimensions onto one of three orthogonal planes: axial or annular (x-y), sagittal (x-z), or coronal (y-z) [11]. At each of the four time points, all 120 preinfarction distances were compared with postinfarction distances using a paired Student's t test.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

 
Occlusion of the three circumflex marginal coronary arteries immediately infarcts 32% of the posterior LV mass [6]. No animal had MR before infarction, but all animals had acute 2+ to 4+ (n = 3) or 3+ to 4+ (n = 3) MR as determined by color flow Doppler velocity mapping after infarction (Fig 1). Thirty minutes after infarction, mean cardiac output decreased from 3.0 ± 0.6 to 2.6 ± 0.9 L/min (p = 0.09); LV end-diastolic pressure increased from 6.8 ± 4.3 to 12.5 ± 4.1 mm Hg (p = 0.01), and mean arterial pressure decreased from 88.2 ± 21.5 to 76.5 ± 20.5 mm Hg (p = 0.03) [12].

View larger version (146K): [in this window] [in a new window]   Fig 1. . Subdiaphragmatic echocardiogram and color-flow Doppler velocity map of 3+ mitral regurgitation in a sheep after acute posterior infarction of approximately 32% of the left ventricle. (AO = aorta; LA = left atrium; LV = left ventricle.)

	Changes in the Mitral Valvular Annulus

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

View larger version (25K): [in this window] [in a new window]   Fig 2. . Mean position of six annular transducers at end-systole before and after infarction. The position of the 1 transducer in the anterior portion of the anterior annulus and the vector between 1 and the anterior commissure (AC) were superimposed to facilitate comparison of changed interrelations of the other transducers after infarction. Because the six annular transducers fall within 3.1 mm in the z axis, no corrections were made for the z axis. The area of infarction is centered between the approximate position of the posterior commissure (PC) and ß2, and is represented by the heavy lines. 1 signifies the transducer near the midpoint of the anterior mitral annulus; ß signifies the transducers around the posterior annulus (also see Table 1).

	Movements of the Tips of the Papillary Muscles

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

 
Changes in distances between the tips of both papillary muscles and specified annular sonomicrometry transducers are shown in Table 2. Of the four time points, changes before and after infarction were most pronounced at end-systole. After infarction, the tip of the APM moves significantly farther from the annular centroid (mean of six annular coordinates), posterior commissure (p = 0.07), and posterior annulus (ß1 to ß3), but is not significantly farther from the anterior commissure and anterior part of the anterior annulus (1). As shown in Figure 3A, the tip of the APM is farther away from the least-squares plane of the six annular transducers in the z direction throughout the cardiac cycle, and is 1.0 ± 0.6 mm farther at end-systole. The amount of APM shortening does not change significantly after infarction. As shown for 1 sheep in Figure 3B, the positions of both papillary muscle tips, when viewed perpendicular to the annulus, do not change consistently from sheep to sheep after infarction, and rotate at most only a few millimeters around the z axis throughout the cardiac cycle.

View larger version (19K): [in this window] [in a new window]   Fig 3. . Three-dimensional motion of the tips of both papillary muscles relative to the least-squares plane of the six annular transducers before and after infarction in 1 sheep. (A) Trajectory of the tip of the anterior papillary muscle (APM) in the Z direction (negative numbers increase toward the ventricular apex) during the cardiac cycle beginning at end-diastole. (B) Axial view of the annulus at end-systole before and after infarction. The positions of the papillary muscle tips throughout the cardiac cycle are indicated by circles. The viewer is looking at the valve from the atrium. (C) Trajectory of the tip of the posterior papillary muscle (PPM) in the z direction. In both (A) and (C), the heart rate was 90 beats/min before infarction and 95 beats/min afterward. (AC = anterior commissural transducer; EIVC = end-isovolumic contraction; EIVR = end-isovolumic relaxation; ES = end-systole; PC = posterior commissural transducer.)

	Movements of the Bases of the Papillary Muscles

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

 
After infarction, the base of the APM moves away from all transducers attached to the mitral annulus at both end-diastole and end-systole (Table 3; Fig 4), and at nearly all other time points in the cardiac cycle (data not shown). Shortening of the APM increases slightly, but not significantly (Table 2).

View larger version (19K): [in this window] [in a new window]   Fig 4. . Three-dimensional motion of the base of the anterior papillary muscle (APM) and posterior epicardial (PE) transducer relative to the least-squares plane of the six annular transducers before and after infarction in 1 sheep. Because of variation in the placement of transducers at the base of the posterior papillary muscle, the overlying PE transducer is shown. (A) Trajectory of the base of the APM in the z direction (negative numbers increase toward the ventricular apex) beginning at end-diastole. (B) Axial view of the annulus at end-systole before and after infarction. The positions of the APM base and PE transducers throughout the cardiac cycle are indicated by circles. The viewer is looking at the valve from the atrium. (C) Trajectory of the PE transducer over the base of the posterior papillary muscle in the z direction. The PE transducer and base of the posterior papillary muscle (Table 3) move away from the annulus during ejection. (AC = anterior commissural transducer; EIVC = end-isovolumic contraction; EIVR = end-isovolumic relaxation; ES = end-systole; PC = posterior commissural transducer.)

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

 
This study indicates that acute, postinfarction MR is the product of small changes in the spatial relations of the anatomic components of the mitral valve. The study highlights the impact of very small changes in annular shape and in the positions of the tips of both papillary muscles. The study also illuminates the deformation of borderzone myocardium and the contribution of healthy, uninfarcted myocardium. Although the infarction involves only a small section of the annular perimeter, asymmetric dilatation of the annulus also involves the adjacent, border zone myocardium on each side. Further, the unbalanced pull of the anterior ventricle and papillary muscle appears to contribute to distortion of leaflet coaptation. The fact that deformations on the order of 1 to 2.5 mm cause MR implies a very fragile, dynamic balance between the major components of the valve during closure.

Ovine anatomy may contribute to this lack of valvular resilience. In sheep, most of the papillary muscle is integral to the ventricular wall, and only a small (0.5- to 1-cm) nipple is free (Fig 5). Thus, positional changes of sheep papillary muscle tips during ejection primarily reflect passive forces on the noncontracting PPM and changes in ventricular shape before and after infarction. Ovine chordae are much shorter than in humans, but like humans, insert in two or more locations in the tip of the papillary muscle. Human papillary muscles and chordae are longer and more independent, and human ventricles are larger than in sheep; therefore, movements of the papillary muscle tips may be greater, but nevertheless are measured in millimeters and are difficult to discern in vivo [7, 13–15].

View larger version (86K): [in this window] [in a new window]   Fig 5. . Photograph of excised ovine mitral valve showing relatively short chordae attached to two insertion locations on the small tips of the papillary muscles. The majority of both papillary muscles are contiguous with the ventricular wall. The anterior papillary muscle is on the left; the anterior leaflet is below.

Admittedly, the exact deformations in the sheep model cannot be transferred reliably to humans. Nevertheless, the sheep model demonstrates the importance of the uninfarcted papillary muscle, unbalanced regional ventricular forces, expansion of border zone myocardium, asymmetric widening of the annulus, and very small changes in the positions of both papillary muscle tips during ejection on the development of acute postinfarction MR. These data serve to refocus our understanding of the pathogenesis of the human disease and to inspire the development of simple methods to repair the valve.

Two-dimensional echocardiograms cannot resolve the minute changes in anatomic geometry that cause the mitral valve to leak after acute, posterior myocardial infarction. Further, careful analysis of the echocardiograms in these sheep does not reveal a consistent location or pattern of the regurgitant flow between sheep. This inconsistency may be caused by anatomic variations in the serrated free edges of the leaflets or varying impact of valvular spatial deformations on leaflet coaptation between sheep. The precision and reproducibility (0.1 to 0.2 mm) [8, 17] of sonomicrometry array localization resolves changes in the muscular components of the valve, but does not resolve distortions in leaflet coaptation. Marker angiography may provide further information [18–21], although a possible influence of the markers on leaflet coaptation is a concern.

Satisfactory repair of acute, postinfarction MR probably requires the clinical introduction of three-dimensional echocardiography and the ability to visualize asymmetric annular dilatation and leaflet position and coaptation during ventricular systole [22, 23]. Patients do not have anatomically consistent coronary arterial anatomy, and usually do not have normal ventricles before infarction; therefore, after infarction, ventricular shape varies considerably between patients irrespective of the presence of MR. As a result, three-dimensional echocardiography may be a prerequisite for developing simple, individualized operations to restore mitral valve competence in patients who also must recover from the loss of a significant portion of pump function.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

 
Supported by grant HL 36308 from the National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

 
Presented at the Poster Session of the Thirty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Feb 3–5, 1997.

Address reprint requests to Dr Edmunds, Department of Surgery, 4 Silverstein, Hospital University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104.

^* Full tables with means and standard deviations at all four time points are available on request to the authors for Tables 1 to 3.

	References

Top Footnotes Abstract Introduction Material and Methods Results Changes in the Mitral... Movements of the Tips... Movements of the Bases... Comment Acknowledgments References

 

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