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Ann Thorac Surg 1999;68:894-902
© 1999 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Effects of mitral valve replacement on regional left ventricular systolic strain

^a Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, California, USA
^b Research Institute of the Palo Alto Medical Foundation, Palo Alto, California, USA

Address reprint requests to Dr Miller, Dept of Cardiovascular and Thoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247
e-mail: dcm{at}leland.stanford.edu

	Abstract

Top Abstract Introduction Material and methods Results Comment References

 
Background. Mitral valve replacement (MVR) with chordal excision impairs left ventricular (LV) systolic function, but the responsible mechanisms remain incompletely characterized. Loss of normal annular-papillary continuity also adversely affects LV torsional deformation, possibly due to changes in myocardial fiber contraction pattern.

Methods. Twenty-seven dogs underwent insertion of LV myocardial markers and a sham procedure (cardiopulmonary bypass, no MVR, n = 6), conventional MVR with chordae tendineae excision (n = 7), or chordal-sparing MVR with reattachment of the anterior leaflet chordae to the anterior annulus (n = 7) or to the posterior annulus (n = 7). In the anterior, lateral, posterior, and septal LV regions, linear chords were constructed from each region’s central marker to its surrounding markers. Percent systolic shortening (regional LV strain) was calculated for each chord, and the chords were assigned to one of four angular groups: I, left-handed oblique (subepicardial fiber direction); II, circumferential (midwall); III, right-handed oblique (subendocardial); or IV, longitudinal. Regional LV strain data were compared before and after MVR.

Results. Sham and anterior chordal-sparing MVR had minimal effects on regional LV strain. With posterior chordal-sparing MVR: anteriorly, left-oblique (I) strain fell (31%, p < 0.05), as did circumferential (II) and right-oblique (III) strains (by 49% and 51%, respectively; p < 0.01). Laterally, left-oblique (I) strain fell by 36% (p < 0.05), as did longitudinal (IV) strain (54% decline, p < 0.01). Conventional MVR with chordal excision disrupted regional fiber shortening diffusely, affecting oblique fibers (I and III) in the anterior and septal regions and impairing longitudinal (IV) strain in all regions (45% to 68% fall, p < 0.05).

Conclusions. Sham and anterior chordal-sparing MVR did not substantially alter regional LV strain; however, loss of normal anatomic valvular-ventricular integrity (conventional MVR) or posterior chordal-sparing MVR resulted in pronounced alterations in LV strain, most notably in the longitudinal and oblique fiber directions. These findings demonstrate that the deleterious effects of chordal excision are associated with perturbed internal myocardial systolic deformation, which suggests that chordal disruption distorts myofiber architecture or regional systolic loading.

	Introduction

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In 1956, Rushmer suggested that valvular-ventricular integrity was important for optimal left ventricular performance [1]. Nine years later, Lillehei and associates were the first to advocate the surgical application of this physiologic principle when they spared the chordae tendineae during mitral valve replacement (MVR) [2]. Since then, numerous experimental [3–9] and clinical [10–15] reports have demonstrated that chordal disruption impairs left ventricular (LV) systolic pump function postoperatively, but the mechanisms responsible for this deterioration remain uncharacterized. Although it was originally proposed that division of the subvalvular apparatus would chiefly affect the LV regions directly subtending the papillary muscles [5, 12, 13], it now appears that chordal disruption affects most areas of the ventricle to a substantial degree [4, 6, 11, 16]. Loss of normal annular-papillary continuity also impairs LV torsional deformation [17], possibly due to changes in myocardial fiber orientation and contraction pattern.

Streeter, Spotnitz, and others have shown that myocardial fiber orientation proceeds from a left-handed helix in the outer layers of the left ventricle to a right-handed helix in the inner layers [18–20]. This results in perpendicularly oriented oblique fibers in the subepicardial and subendocardial layers, whereas circumferentially oriented fibers predominate in the LV midwall (Fig 1). It has been suggested that the papillary muscles arise from epicardial fibers that originate from the aortic ring [21], and via their chordal attachments to the mitral annulus, a loop is completed that may help maintain global LV shape and regional LV contraction throughout the ventricle. Previous reports examining the effects of chordal division on LV geometry have convincingly shown that systolic bulging occurs in the vicinity of papillary muscle insertion and that the "untethered" ventricle assumes a more elliptical shape at both end-systole and end-diastole [3, 4, 8]. It remains unclear, however, as to whether or not loss of valvular-ventricular integrity after MVR impairs regional myocardial fiber geometry or contraction pattern and how changes in myocardial fiber architecture and load may effect systolic LV function. The purpose of the current investigation was to characterize the effects of MVR with and without chordal preservation on regional LV systolic strain in the longitudinal, circumferential, and oblique fiber directions.

View larger version (26K): [in this window] [in a new window]   Fig 1. Myocardial marker array inserted to measure left ventricular (LV) volume and regional LV strain. Subepicardial markers were inserted in the apical (below the level of papillary muscle insertion), equatorial, and bassal LV plances along eight meridians; anterior (from the origin of the left anterior descending coronary artery to the apex), anterolateral, lateral (obtuse margin), posterolateral, posterior (inferior wall along the posterior descending artery), posteroseptal, septal, and anteroseptal. One marker was also placed at the apex.

	Material and methods

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One to 3 weeks later, either MVR or a sham procedure was performed using cardiopulmonary bypass (CPB) with antegrade cold crystalloid cardioplegia and topical hypothermia. Animals were randomized into four groups: sham MVR (CPB with left atriotomy, but no MVR, n = 6); conventional MVR (excision of all chordae and leaflets, n = 7); or one of two chordal-sparing MVR techniques differing in their treatment of the anterior leaflet chordae with reattachment to either the anterior annulus ("quasianatomic" anterior chordal-sparing MVR, n = 7) [22], or transposition to the posterior annulus (posterior chordal-sparing MVR, n = 7) as described by Feikes and associates [23]. All chordae (anterior and posterior) were preserved in both chordal-sparing methods. Bioprosthetic valves (23 to 25 mm) were inserted, the pericardium was left open, and the chest was closed. Average aortic cross-clamp and CPB times were 39 ± 5 minutes and 78 ± 10 minutes, respectively. Epicardial echocardiography excluded significant mitral regurgitation and LV outflow tract obstruction in all animals. Three animals (one in each group except sham) required temporary inotropic drug support (dopamine, 5–10 µg/kg/min) during weaning from bypass, which was discontinued in all three animals greater than 30 minutes before data acquisition. After 1 to 2 hours of recovery from general anesthesia, the animals were restudied (post-MVR) in closed-chest, sedated conditions (intubated), with equivalent autonomic blockade. B-Euthanasia (0.2 mg/kg) was given at the completion of the study.

All animals received humane care in compliance with the Principles of Laboratory Animal Care formulated by the National Society for Medical Research and the Guide for Care and Use of Laboratory Animals prepared by the National Academy of Sciences and published by the National Institutes of Health (DHEW [NIH] Publication 85-23, revised 1985). The study was approved by the Stanford Medical Center Laboratory Research Animal Review Committee and conducted according to Stanford University Policy.

Data acquisition
Biplane videofluoroscopic imaging studies were performed as previously described recording 45-degree right and left anterior oblique images simultaneously at 60 frames/s, and the three-dimensional coordinates of each marker were determined throughout the cardiac cycle [9, 17]. Surface lead electrocardiogram, LV pressure, and systemic femoral arterial pressure (micromanometer-tipped catheters) were also recorded and merged with the 60-Hz marker data.

Data analysis
To minimize the effects of respiration on intrathoracic pressure, three end-expiratory beats were selected for analysis and averaged for each intervention. The maximum rate of LV pressure rise (dP/dt_max) and mean systemic arterial pressure (MAP) were calculated. Global LV volume was computed using a multiple tetrahedral model [9]. End-diastole (ED) was defined as the time of maximum LV volume (V_max), end-systole (ES) was defined arbitrarily as the time of minimum LV volume (V_min), and stroke volume was calculated (SV = V_max - V_min). The times of maximum and minimum volume were used to standardize measurement of chord shortening because: (1) they could be defined directly from the marker coordinate data; (2) they best approximate the times of maximum and minimum length for most chords; and (3) they avoid variations in excitation-contraction times and asynchrony of contraction [24].

Regional LV systolic strain
Four regions were analyzed at the equatorial LV level (above the insertion of the papillary muscles), including the anterior, lateral, posterior, and septal walls. Each region was defined by a central reference marker, about which shortening was measured; chords were constructed from this central marker to its surrounding markers in all regions. The length of each chord (L) was calculated from the three-dimensional marker data, and percent systolic shortening was calculated for each chord: systolic strain = (L_ED - L_ES)/L_ED. Each chord was then assigned to one of four angular groups: I, left-handed oblique (subepicardial fiber direction); II, circumferential (midwall fiber direction); III, right-handed oblique (subendocardial fiber direction); IV, longitudinal. These groups correspond to those employed by Streeter in his study of transmural fiber angles (see Fig 2) [19].

View larger version (13K): [in this window] [in a new window]   Fig 2. Myocardial fiber orientation in the left ventricle proceeds from a left-handed helix in the subepicardium (group I) to a right-handed helix in the subendocardium (group III); midwall fibers are oriented circumferentially (group II). Although there are no longitudinal fibers per se (group IV), combined contraction of the oblique subepicardial and subendocardial fibers will decrease the base to apex dimension.

View larger version (17K): [in this window] [in a new window]   Fig 3. Determination of angular groups for the anterior region. (A) A reference system for each region (anterior region in this example) was defined. A reference long axis was defined by connecting the apex marker with the midpoint of the septal and lateral basal markers (midbase), and a reference plane was defined by these markers. (B) Chords were then constructed from the central reference marker (anterior equatorial marker in this example) to its surrounding markers (basal, equatorial, and apical markers in the septal, anteroseptal, anterior, anterolateral, and lateral walls in this example). Angles were measured relative to an imaginary line (through the central marker) perpendicular to the reference long axis (not pictured). The chords were then assigned to one of the four angular groups: group IV chords (longitudinal) were within 27.5° of the reference axis; group II chords (circumferential) were within 27.5° of a line perpendicular to the reference axis; and groups I and III chords were oriented obliquely between groups II and IV. Angular groups II and IV are shaded for clarity.

	Results

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Pre-MVR regional LV systolic strain
Baseline hemodynamic data in the pre-MVR condition for all 27 animals included LV V_max, 87 ± 23 mL; LV V_min, 66 ± 21 mL; LV SV, 21 ± 5 mL; MAP, 99 ± 13 mm Hg; and LV dP/dt_max, 1,475 ± 341 mm Hg/s. Table 1 summarizes average regional end-diastolic chord length for each region and angular group in all animals pre-MVR. Average chord length was greatest in the septal wall, lowest in the lateral wall, and intermediate in the anterior and posterior walls (p < 0.05, two-way ANOVA), probably due to variability in the location and depth of marker placement. Within each region, average chord lengths were not significantly different in the four angular groups (p > 0.81). Table 2 summarizes mean regional LV systolic chord shortening (strain) for each region and angular group in all 27 animals pre-MVR. Average LV strain was significantly greater in the posterior (7.3% ± 3.2%) and septal (7.3% ± 3.6%) walls than it was in the anterior (5.7% ± 2.6%) and lateral (6.1% ± 2.8%) walls (p < 0.05, two-way ANOVA). Regional LV strain between the four angular groups in each region were not significantly different in this study (p > 0.43).

Figure 4 illustrates the effects of each procedure on the various regional LV systolic strains. With sham operation and anterior chordal-sparing MVR, the changes in regional LV strain from pre-MVR to post-MVR were small (Figs 4A, 4B). In the posterior chordal-sparing group, however, LV strain was altered in a regionally heterogeneous manner (Fig 4C). In the conventional MVR group, deleterious changes in regional LV strain were most substantial in the longitudinal (IV) direction (Fig 4D).

View larger version (34K): [in this window] [in a new window]   Fig 4. Effects of: (A) sham mitral valve replacement (MVR) (n = 6); (B) anterior chordal-sparing MVR (n = 7); (C) posterior chordal-sparing MVR (n = 7); and (D) conventional MVR (n = 7) on regional left ventricular systolic chord shortening (strain). Data bars represent the difference in regional LV strain from pre-MVR to post-MVR for each angular group and region. Dark bars represent significant changes, whereas light bars represent insignificant changes (mean ± one standard error of the mean). +p < 0.05 pre-MVR versus post-MVR. Angular groups: I, left-handed oblique (subepicardial); II, circumferential; III, right-handed oblique (subendocardial); IV, longitudinal. A, anterior; L, lateral; P, posterior; S, septal.

	Comment

Top Abstract Introduction Material and methods Results Comment References

What is the mechanical basis for this heterogeneous pattern of regional LV contractile impairment after MVR with chordal disruption? Loss of normal papillary-annular continuity alters global LV geometry and impairs regional LV function throughout the ventricle [4–6, 12, 16]; however, the current experiment demonstrated that regional LV strain fell only in selected regions, possibly due to the unique architecture of the papillary muscles. Several functions have been ascribed to the papillary muscles and their chordal attachments [1, 25]. It has been suggested that basal epicardial fibers descend vertically toward the apex where they penetrate inward to form the fibers of the papillary muscles; the chordae tendineae then insert onto the fibrous endocardial skeleton through the mitral valve leaflets to complete the valvular-ventricular loop [21, 25]. Working through this loop, the subvalvular apparatus may influence regional LV systolic shortening by modulating regional LV afterload, global ventricular geometry, and the external work performed by the papillary muscles themselves. After transection of their chordal attachments, the papillary muscles retract; furthermore, disrupting their tethering effect hinders their ability to assist LV contraction near their insertion sites. Guccione and associates found that sarcomere shortening after chordal transection was similar in the anterior and posterior walls, despite the inherent mechanical differences between the two regions [26]. We have previously found that chordal transection impairs regional LV function and torsion throughout the ventricle, thus altering both anterior and posterior mechanics, albeit to a variable degree [16, 17]. Chordal disruption may change the preload, afterload, and orientation of the epicardial fibers that are linked to the papillary muscles, thereby, decreasing LV strain in the longitudinal direction via the Frank-Starling mechanism. In the posterior chordal-sparing group, right-oblique (subepicardial) strain fell in the anterior, lateral, and septal walls, consistent with previous findings of diminished LV torsion in these regions [17], but there was no significant change in the posterior wall. In the posterior wall, where oblique fibers are less abundant, disruption of the anterior chordal attachments may have had less of an impact than in the anterior or lateral walls where the oblique fibers predominate.

Takayama and colleagues examined the influence of the subvalvular apparatus on LV deformation at the site of anterior papillary muscle insertion and a more basal LV location, similar to the equatorial level examined in the current study [27]. After transection of only the anterior leaflet chordae, circumferential shortening at the papillary insertion site increased, but did not change significantly in the more basal location; longitudinal shortening did not change in either region. In their preparation, however, the anterior and posterior papillary muscles remained attached to the annulus via the posterior leaflet chordae, thereby, maintaining some degree of valvular-ventricular integrity. In the present study, we observed substantial changes in regional LV strain, measured at the equatorial level, with both posterior chordal transposition and complete transection of all chordae. When the anterior leaflet chordae were repositioned to the posterior annulus, longitudinal strain did not change in the anterior wall, but circumferential and oblique fiber shortening fell by one-third to one-half. With complete chordal division and disruption of all papillary-annular connections, circumferential contraction did not change in any region, but longitudinal strain was impaired throughout the ventricle. Global diminution of oblique fiber contraction may have occurred as a consequence of not only changes in fiber preload, but also the papillary contribution to regional LV function [1, 25], resulting in a substantial decline of shortening in the longitudinal direction.

Study limitations
Measurement of regional LV strain is load dependent and, therefore, can be altered by changes in preload and afterload. We found that although global LV volume fell in the sham and chordal-sparing MVR groups, changes in end-diastolic chord length, which is more representative of regional fiber preload, were not substantial. In most regions, fiber preload was similar before and after MVR. In our preparation, we did not measure LV wall thickening (or radial strain), which probably accounts for most of the diminished global LV chamber volume in the sham and chordal-sparing groups. In the conventional group, global LV volume and regional LV preload was similar before and after MVR. A fall in regional LV wall stress (afterload), which is directly related to pressure and inversely related to wall thickness, would tend to increase LV strain, but we did not find this to be the case. Changes in MAP were inconsistent and reached statistical significance only in the posterior chordal-sparing group. A consistent fall in MAP would tend to decrease regional afterload and increase strain, but a simultaneous decrease in wall thickness may counteract these beneficial effects. We could not measure regional wall stress in the current preparation due to the absence of wall thickness markers. In a chronic preparation in which we measured regional wall stress, we found that MVR without chordal preservation was associated with increased regional wall stress throughout the ventricle when compared to MVR with chordal preservation [28]. Thus, diminished regional strain and increased regional stress may combine to impair global LV systolic function and output after MVR with chordal excision.

In the current investigation, deformation was measured at the equatorial level, midway between the apex and base. It is important to note that deformation and fiber geometry change as the longitudinal distance from the base increases. Streeter and associates observed a predominance of circumferential fibers at the base with progressively more oblique fibers towards the apex [18], whereas Takayama and associates demonstrated a substantially different response to chordal transection depending on the longitudinal distance at which the measurements were obtained [27]. Guccione and associates also noted substantial variation in fiber angle and wall stress along the length of the LV wall in dogs [29]. We selected to examine the equatorial level to minimize the unpredictable influence of contraction at the papillary insertion sites [30] and to avoid over-emphasis of either the circumferential (basal) or oblique (apical) fibers. Absolute measurements of LV strain are also dependent on the depth and location of each marker, as well as the size of the ventricle in question, making direct comparisons between individual subjects difficult. In the current study, however, although LV volume changed in some groups after MVR, each animal served as its own control, making direct comparison of pre-MVR and post-MVR data valid.

This study evaluated LV strain immediately after MVR (within 2 hours) in closed-chest dogs with presumably normal underlying cardiac function, a situation clearly not identical to the clinical scenario of most interest, ie, MVR in patients with chronically dilated hearts due to long-standing mitral regurgitation. Despite this, significant impairment of regional LV contractile function (chord shortening) was observed after disruption of normal valvular-ventricular continuity, consistent with the findings of previous acute and chronic animal preparations [3–6]. Our presumption is that in diseased hearts, such contractile dysfunction would be even more substantial; changes in discrete regional fiber shortening might be even greater (and more clinically important) in the setting of chronic mitral regurgitation with a very dilated ventricle, at which time cardiac reserve is limited. With respect to the duration of functional impairment, previous reports evaluating specific areas have convincingly shown that global and regional LV systolic dysfunction exist in patients after MVR with chordal excision [12, 13, 15].

	Acknowledgments

 
We appreciate the technical assistance provided by Terrence L. Tye, MS, Geraldine C. Derby, RN, Cynthia E. Handen, BA, Mary K. Zasio, BA, Carol W. Mead, BA, and Erin K. Schultz, BS. We gratefully acknowledge Yasuko Tomizawa, MD, PhD, and Conrad M. Vial, MD, for their assistance in this experiment. Finally, we would like to thank the Edwards CVS Division, Baxter Healthcare International, and the Heart Valve Division, Medtronic, Inc, for donating the bioprosthetic tissue valves used in this experiment.

Supported by Grants HL-29589 and HL-48837 from the National Heart, Lung, and Blood Institute (NHLBI) and the Veterans Administration Medical Research Service.

Drs Moon and DeAnda were supported by NHLBI Individual Research Service Awards HL-08532 and HL-08928, respectively; Drs Moon and DeAnda are Carl and Leah McConnell Cardiovascular Surgical Research Fellows.

	References

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