EJCTS Click here for details of sales representative
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Tom C. Nguyen
Neil B. Ingels, Jr.
David Craig Miller
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nguyen, T. C.
Right arrow Articles by Miller, D. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nguyen, T. C.
Right arrow Articles by Miller, D. C.
Related Collections
Right arrow Cardiac - physiology
Right arrow Cardiac - other
Right arrow Valve disease

Eur J Cardiothorac Surg 2007;31:423-429. doi:10.1016/j.ejcts.2006.12.019
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Septal-lateral annnular cinching perturbs basal left ventricular transmural strains

Tom C. Nguyena, Allen Chenga, Frederick A. Tibayana, David Liangb, George T. Daughtersa,c, Neil B. Ingels, Jr.a,c, David Craig Millera,*

a Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA, United States
b Division of Cardiovascular Medicine, Stanford, CA, United States
c Research Institute of the Palo Alto Medical Foundation, Palo Alto, CA, United States

Received 21 September 2006; received in revised form 4 December 2006; accepted 14 December 2006.

* Corresponding author. Address: Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247, United States. Tel.: +1 650 725 3826; fax: +1 650 725 3846. (Email: dcm{at}stanford.edu).


   Abstract
Top
 Abstract
1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
 5. Limitations
 References
 
Objective: Septal-lateral annular cinching (‘SLAC’) corrects both acute and chronic ischemic mitral regurgitation in animal experiments, which has led to the development of therapeutic surgical and interventional strategies incorporating this concept (e.g., Edwards GeoForm ring, Myocor Coapsys®, Ample Medical PS3). Changes in left ventricular (LV) transmural cardiac and fiber-sheet strains after SLAC, however, remain unknown. Methods: Eight normal sheep hearts had two triads of transmural radiopaque bead columns inserted adjacent to (anterobasal) and remote from (midlateral equatorial) the mitral annulus. Under acute, open chest conditions, 4D bead coordinates were obtained using videofluoroscopy before and after SLAC. Transmural systolic strains were calculated from bead displacements relative to local circumferential, longitudinal, and radial cardiac axes. Transmural cardiac strains were transformed into fiber-sheet coordinates (X f, X s, X n) oriented along the fiber (f), sheet (s), and sheet-normal (n) axes using fiber ({alpha}) and sheet (ß) angle measurements. Results: SLAC markedly reduced (~60%) septal-lateral annular diameter at both end-diastole (ED) (2.5 ± 0.3 to 1.0 ± 0.3 cm, p = 0.001) and end-systole (ES) (2.4 ± 0.4 to 1.0 ± 0.3 cm, p = 0.001). In the LV wall remote from the mitral annulus, transmural systolic strains did not change. In the anterobasal region adjacent to the mitral annulus, ED wall thickness increased (p = 0.01) and systolic wall thickening was less in the epicardial (0.28 ± 0.12 vs 0.20 ± 0.06, p = 0.05) and midwall (0.36 ± 0.24 vs 0.19 ± 0.11, p = 0.04) LV layers. This impaired wall thickening was due to decreased systolic sheet thickening (0.20 ± 0.8 to 0.12 ± 0.07, p = 0.01) and sheet shear (–0.15 ± 0.07 to –0.11 ± 0.04, p = 0.02) in the epicardium and sheet extension (0.21 ± 0.11 to 0.10 ± 0.04, p = 0.03) in the midwall. Transmural systolic and remodeling strains in the lateral midwall (remote from the annulus) were unaffected. Conclusions: Although SLAC is an alluring concept to correct ischemic mitral regurgitation, these data suggest that extreme SLAC adversely effects systolic wall thickening adjacent to the mitral annulus by inhibiting systolic sheet thickening, sheet shear, and sheet extension. Such alterations in LV strains could result in unanticipated deleterious remodeling and warrant further investigation.

Key Words: Mitral regurgitation • Ischemic mitral regurgitation • Mitral annuloplasty • Myocardial ischemia • Surgery • Myocardial strain


   1. Introduction
Top
 Abstract
 1. Introduction
2. Material and methods
 3. Results
 4. Discussion
 5. Limitations
 References
 
For over 30 years [1], annuloplasty rings have been widely employed for patients with functional (FMR) or ischemic mitral regurgitation (IMR) due to annular dilatation with normal (Carpentier type I) leaflet motion. Reduction in mitral annular area, particularly with recently popularized ‘undersized’ annuloplasty rings, however, might come with an unwanted price as Cheng et al. [2] from this laboratory recently demonstrated that undersized suture annuloplasty impairs systolic wall thickening adjacent to the mitral annulus. Annuloplasty rings also abolish normal annular dynamics [3] and restrict posterior leaflet excursion [4]. Isolated mitral annular reduction in the septal-lateral axis achieved with a simple suture across the valve (septal lateral annular cinching, or ‘SLAC’) is a novel surgical approach for acute and chronic IMR, and does not adversely influence annular shape, dynamics, or posterior leaflet motion [5,6]. Surgical and interventional strategies based on this concept have emerged, including the GeoForm and IMR ETlogix rings (Edwards Lifesciences, Irvine, CA), Rigid Saddle Ring (‘RSR’, St. Jude Medical, St. Paul, MN), Coapsys® transventricular chord device (Myocor, Maple Grove, MN), and the PS3 transatrial catheter deployed shortening device (Ample Medical, Foster City, CA). Understanding left ventricular (LV) mechanics in terms of myocardial strain patterns is important, but the effects of SLAC on regional transmural LV wall strain and fiber-sheet mechanics are not known. The objective of this study was to elucidate these relationships.


   2. Material and methods
Top
 Abstract
 1. Introduction
 2. Material and methods
3. Results
 4. Discussion
 5. Limitations
 References
 
2.1 Surgical preparation and marker and bead placement
The experimental preparation was similar to that described previously [2,7] and thus will only be outlined briefly. Eight sheep had radiopaque ventricular markers surgically implanted to silhouette the LV chamber along four equally spaced longitudinal meridians (Fig. 1a). Epicardial echocardiography was used to locate and measure the wall depth of a free segment of the midlateral equatorial LV wall between the papillary muscles and a site in the anterobasal LV wall cephalad to the anterior papillary muscle. To measure regional three-dimensional (3D) myocardial deformations, two triads consisting of three transmural columns of four beads were implanted into these two regions normal to the local epicardial tangent plane and evenly spaced from endocardium to epicardium using a depth adjustable insertion trocar. Eight radiopaque markers were implanted around the mitral annulus, and one marker was implanted at each of the mitral leaflet edges on cardiopulmonary bypass.


Figure 1
View larger version (29K):
[in this window]
[in a new window]

  		Fig. 1. (a) Locations of LV epicardial markers (shaded circles) surgically implanted to silhouette the LV chamber along four equally spaced longitudinal meridians. (b) Septal-lateral annular cinching (SLAC) showing a prolene suture anchored to the midseptal annulus and externalized to an epicardial tourniquet. ACOM: anterior commissure; PCOM: posterior commissure.

 
The SLAC suture was placed by anchoring a 2-0 polypropylene suture to the midseptal annulus (annular ‘saddle horn’) and externalizing it through the midlateral (or posterior in clinical terms) annulus in a tourniquet on the epicardial surface (Fig. 1b); this suture crossed the valve in the septal-lateral axis. The animal was weaned from CPB, and a micromanometer pressure transducer was placed in the ventricle through the apex. Immediately postoperatively, animals were taken to the cardiac catheterization laboratory and studied open-chest, intubated, mechanically ventilated, and anesthetized. With the heart in normal sinus rhythm and ventilation arrested at end-expiration, simultaneous biplane videofluoroscopy (60 Hz), ECG, and LV and aortic pressures were recorded during steady-state baseline conditions before (Control) and after tightening the SLAC suture (‘SLAC’) by 8–10 mm. Marker coordinates from the two radiographic views were subsequently digitized and merged to yield 3D spatial coordinates for each radiopaque marker every 16.7 ms. End-diastole (ED) was defined as the maximal second derivative of LV pressure corresponding with the frame immediately before the upstroke of LV pressure. End-systole (ES) was defined as the videofluoroscopic frame before the time of peak negative LV rate of pressure decrease (–dP/dtmax).

At the end of the study, 3.0 mm coronary perfusion balloon catheters (GUIDANT AgilTrac Dilation Catheter, Santa Clara, CA) were placed into the proximal circumflex and left anterior descending coronary arteries. The animal was euthanized with sodium pentothal administration followed by an intravenous bolus of potassium chloride to arrest the hearts in the depolarized state. After adjusting left ventricular pressure by blood withdrawal to match previous in vivo LV end-diastolic pressure, buffered glutaraldehyde (5%, 300 ml) was infused simultaneously into both coronary arteries to fix the hearts in situ. All hearts were then explanted and stored in 10% formalin for subsequent histological examination.

2.2 Quantitative histology
The quantitative histological methods employed have been previously described in detail [7]. Briefly, a transmural rectangular block of myocardial tissue, directly contiguous and basal to the implanted marker columns, was removed from the LV wall in each region studied, with the edges of the block cut parallel to the local LV circumferential (X 1), longitudinal (X 2) and radial (X 3) axes, Fig. 2 . After recording the overall transmural thickness of the specimen, the tissue block was sliced into 1-mm thick sections parallel to the X 1–X 2 plane and digitized microphotographs of the X 1–X 2 face of each section were recorded. The fiber angle, alpha ({alpha}), between the local muscle fiber axis (X f), and the circumferential axis (X 1) was measured at five sites on each image using image-processing software (SPOT Advanced Version 4.0.1, Diagnostic Instruments Inc., Sterling Heights, MI) such that mean {alpha} characterized the fiber angle at each transmural depth. Two parallel cuts separated by approximately 1 mm were then made normal to the fiber axis in each of these transmural sections. The fiber-normal slices were placed in plastic molds (Tissue-Tek, Cryomold Intermediate, Miles Inc., Elkhart, IN), embedded in OCT compound (Tissue-Tek, Sakura Finetek USA Inc., Torrance, CA) and stored for 2–4 days in a –80° freezer. The myocardial slices were cut into 8–10 µm-thick sections using a cryostat (Jung Frigocut 2800 N, Leica Inc., Germany) and transferred to a glass slide where they were imaged immediately with a digital camera (RT Color, 1X HRD 100-NIK, Diagnostic Instruments Inc., Sterling Heights, MI) mounted on a light microscope (Leica Type 301-371.010, Leica Inc., Germany) at 25x magnification. Myolaminae coursing in the direction noted from the frozen specimen were observed and defined as sheets. Using image-processing software, five ß angles were measured between sheet orientations (X s) and X 3 normal to the endocardial face, over the length of the specimen, and average ß characterized the sheet angle at each transmural depth.


Figure 2
View larger version (23K):
[in this window]
[in a new window]

  		Fig. 2. A transmural tissue block excised from the anterobasal and lateral equatorial free wall of the left ventricle. Edges of the block are cut parallel to the local cardiac coordinates defined by circumferential (X 1), longitudinal (X 2), and radial (X 3) axes. A transmural fiber angle ({alpha}) was measured from serial sections cut parallel to the X 1–X 2 plane at varying transmural depths. Measured {alpha} and ß were then used to define a local ‘fiber-sheet’ coordinate system with basis vectors of fiber (X f) axis, sheet axis perpendicular to X f within sheet plane (X s), and axis normal to the sheet plane (X n). The black band illustrates sheet orientation. X f, X s, and X n represent a Cartesian coordinate system. X f lies in the X 1–X 2 plane; X s lies in the plane defined by X 3 and the axis normal to the fiber direction.

 
2.3 Cardiac finite strains
Cardiac normal and shear strains were calculated at 20, 50, and 80% depths from the epicardium, with end-diastole as the reference configuration and end-systole as the deformed configuration. Detailed strain analysis methodology has been described previously [8]. Briefly, a local LV long axis was defined by using the centroid of the three 1.7-mm epicardial surface beads atop the bead columns and the apical marker (Fig. 1), with local cardiac coordinates aligned with the circumferential, longitudinal, and radial axes of the LV lateral wall. Strains were interpolated along the centroid of the bead columns at 1% increments of wall depth from the epicardium at ED.

2.4 Sheet finite strains
As previously described [7], transmural cardiac strains were transformed into fiber-sheet coordinates (X f, X s, X n) oriented along the fiber (f), sheet (s), and sheet-normal (n) axes by application of the fiber ({alpha}) and sheet (ß) angle measurements (Fig. 2). The resulting fiber-sheet strains include stretch or shortening along the fiber (E ff), sheet (E ss), and sheet-normal (E nn) directions as calculated using the equation:


Formula

(1)

The sheet components of systolic wall thickening (E 33) in the anterobasal and lateral equatorial LV regions were calculated based the following equation:


Formula

(2)

2.5 End-diastolic and end-systolic sheet strains
End-diastolic cardiac and sheet strains were measured by comparing bead positions (in cardiac or sheet coordinates, respectively) at ED from the Control study (reference configuration, Control) with the bead positions at ED during SLAC (deformed configuration, SLAC). End-systolic cardiac and sheet strains were calculated by comparing bead positions at ES in cardiac or sheet coordinates from the Control study (reference configuration) with the bead positions at ES during SLAC (deformed configuration).

2.6 Mitral annular dimensions and dynamics
Septal-lateral annular diameter was calculated as the distance between the septal and mid-lateral annular marker in 3D space.

2.7 Statistical analysis
Data are reported as mean ± 1 SD. Cardiac and sheet strains were compared using two-way repeated measures ANOVA with Holm–Sidak pairwise multiple comparisons (Sigmastat 3.5, SPSS Inc., Chicago, IL). ED and ES strains were compared against zero using a one-sample t-test. Group mean annular dimensions and dynamics were compared between baseline and SLAC using two-tailed t-test for paired observation; p < 0.05 was considered statistically significant.

All animals received humane care in compliance with guidelines sets forth by the European Convention on Animal Care. This study was approved by the Stanford Medical Center Laboratory Research Animal Review Committee and conducted according to Stanford University policy.


   3. Results
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
4. Discussion
 5. Limitations
 References
 
The average weight of the animals was 61 ± 2 kg. Hemodynamic and annular geometric data before (Control) and during isolated septal-lateral reduction are shown in Table 1 . SLAC increased heart rate and decreased EDV, while dP/dtmax was unchanged. At end-diastole, SLAC decreased mitral septal-lateral diameter by 15 mm (approximately 60%). Mitral annular area (MAA) at ED and ES was slightly smaller after SLAC, but this finding was not statistically significant.


View this table:
[in this window]
[in a new window]

  		Table 1 Hemodynamics and mitral annular geometric data Control versus SLAC
 
Systolic cardiac strains in the anterobasal LV wall (ED reference configuration; ES deformed configuration) are summarized in Table 2 with data presented at 20% wall depth (subepicardium), 50% wall depth (midwall), and 80% wall depth (subendocardium). SLAC reduced systolic wall thickening in the subepicardium and midwall, with a trend toward a decrease in the subendocardium. SLAC also reduced longitudinal strain (E 22) in the subendocardium. In the midlateral wall, remote from the mitral annulus, SLAC had no effect of systolic cardiac normal or shear strains (Table 2).


View this table:
[in this window]
[in a new window]

  		Table 2 Transmural LV wall systolic cardiac strains
 
Transmural cardiac remodeling strains in the anterobasal region at ED and ES are summarized in Table 3 . Wall thickness at ED increased at all wall depths with SLAC, whereas ES wall thickness increased only in the midwall.


View this table:
[in this window]
[in a new window]

  		Table 3 Transmural anterobasal LV wall cardiac remodeling strains
 
Table 4 summarizes fiber-sheet systolic strains in the anterobasal LV wall at 20% wall depth (subepicardium), 50% wall depth (midwall), and 80% wall depth (subendocardium). Again, ED was the reference configuration, while ES represented the deformed configuration. SLAC reduced sheet thickening (E nn), sheet shear (E sn), and fiber-sheet shear (E fs) in the subepicardium. Sheet extension in the midwall was also reduced with SLAC. Remote from the mitral annulus in the lateral equatorial wall, SLAC had no effect on laminar sheet dynamics.


View this table:
[in this window]
[in a new window]

  		Table 4 Transmural LV wall systolic fiber-sheet strains
 
Transmural fiber-sheet remodeling strains in the anterobasal LV wall at ED and ES are summarized in Table 5 . SLAC decreased subendocardial fiber length at ED in the midwall and subendocardium. Other changes at ED with SLAC included an increase in E ss (midwall), E nn (subepicardium and subendocardium), and E sn (midwall). At ES, E ss increased in the midwall and E nn in the subepicardium with SLAC.


View this table:
[in this window]
[in a new window]

  		Table 5 Transmural anterobasal LV wall fiber-sheet remodeling strains
 
The three sheet components which cause systolic wall thickening are shown in Fig. 3 in the anterobasal wall comparing Control and SLAC. In the anterobasal LV wall, sheet shear (E sn) was an important component of systolic wall thickening at all transmural depths. With SLAC, however, E sn in the anterobasal region was reduced only in the subepicardium. Sheet thickening (E nn) was an important component of wall thickening in the subepicardium and subendocardium, while with SLAC, E sn decreased only in the subepicardium.


Figure 3
View larger version (21K):
[in this window]
[in a new window]

  		Fig. 3. Components of systolic wall thickening in the anterobasal left ventricular wall. Pairs of bar display data at the subepicardium, midwall, and subendocardium. The total height of each bar is transmural radial strain (E 33). * p < 0.05 from Student two-tailed paired t-test of Control compared with SLAC. Sheet shear (shaded), sheet thickening (not shaded), and sheet extension (hashed).

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
5. Limitations
 References
 
Ischemic mitral regurgitation continues to be a major clinical challenge with geometric distortions that include papillary muscle displacement laterally, posterior leaflet restriction apically, and annular dilatation [9]. Isolated septal-lateral reduction has emerged as a potential treatment strategy for acute and chronic IMR, particularly since annular shape, dynamics, and posterior leaflet motion are not adversely influenced [5,6].

In this acute study, we investigated the effects of a major degree (~60%) of SLAC-induced reduction of mitral septal-lateral dimension on regional transmural LV wall strains, fiber-sheet mechanics, and wall thickening mechanisms in eight normal (non-ischemic) ovine hearts. The following points highlight our results: (1) systolic wall thickening (radial strain, E 33) in the anterobasal LV region adjacent to the mitral annulus decreased in both the epicardium and midwall with SLAC, while end-diastolic wall thickness increased at all wall depths; (2) LV wall thickening in the anterobasal wall was impaired by SLAC due to decreased systolic sheet thickening [E nn] and sheet shear [E sn] in the epicardium and by reduced sheet extension [E ss] in the midwall; (3) Transmural systolic and remodeling strains in the lateral mid-wall (remote from the annulus) were unaffected by SLAC.

Perturbations in normal myocardial strain patterns may potentially be an important mediator of adverse LV remodeling [10,11] vis-à-vis myocyte apoptosis [12], activation of matrix metalloproteinases [13] and other proteinases, disruption of the extracellular matrix [14], and cell development, differentiation, and regeneration [15]. In a recent ovine study by Rodriguez et al. [10] from this laboratory alterations in transmural cardiac and fiber-sheet strains can occur within only 70 s of myocardial ischemia, and many of these strain abnormalities persist after 8 weeks of infarction [16]. Understanding alterations in myocardial strains is important as new therapeutic interventions for IMR emerge. Furthermore, elucidating laminar sheet dynamics which contribute substantially to overall LV systolic wall thickening can provide mechanistic insight into wall-thickening mechanisms and the deleterious LV remodeling cascade. Systolic LV wall thickening is primarily due to the following previously described independent sheet mechanisms [17]: (1) sheet shear (E sn); (2) sheet extension (E ss); and (3) sheet thickening (E nn).

The undersized mitral ring annuloplasty principle has been recently popularized as an effective surgical treatment for patients with IMR [18]. By reducing annular area, ‘undersized’ annuloplasty not only improves leaflet coaptation, but because of the geometric interdependence of the valvular–ventricular complex, can also normalize subvalvular geometry to some extent [19], thereby reshaping the ventricle and reducing LV wall stress [18,20]. In a similar experiment, Cheng et al. [2] recently examined the effects of simulated undersized suture annuloplasty on regional transmural LV wall strains. In an acute ovine model, undersized suture annuloplasty decreased systolic wall thickening near the mitral annulus at all wall depths, but did not influence wall thickening in a remote (mid-equatorial) region. Impairment of systolic wall thickening in Cheng's study was found to be due to the following mechanisms: (1) reduced systolic fiber shortening in the subendocardium; (2) transmural decrease in systolic sheet shear (E sn), reduced sheet extension (E ss) in the midwall, and decreased sheet thickening (E nn) in the subepicardium and subendocardium.

Although undersized annuloplasty and SLAC appear to cause similar strain perturbations in the myocardium in the anterobasal region near the mitral valve in that both interventions decreased systolic wall thickening, several important differences are noteworthy. While SLAC had no effect on systolic fiber shortening (E ff), annuloplasty reduced E ff in the endocardium. Similarly, SLAC reduced sheet shear (E sn) only in the epicardial layer, but simulated undersized annuloplasty decreased E sn in all wall depths (Table 4). In the subepicardial and subendocardial layers, sheet thickening (E nn) was reduced after simulated annuloplasty, while after SLAC E nn was reduced in only the subepicardium. Indeed, although both suture annuloplasty and SLAC decreased systolic wall thickening near the mitral annulus, the magnitude, location, and mechanisms of this decrease appear to differ. The significance of these differences is unclear, and further studies are clearly needed, but our results suggest that SLAC perturbs strain mechanics less than does annuloplasty. SLAC provides several other theoretical advantages over mitral annuloplasty. SLAC maintains annular saddle shape geometry [6], which is important for proper leaflet stress distribution [21], and preserves normal anterior and posterior leaflet motion [22]. Ring annuloplasty, on the other hand, abolishes annular dynamics [3,23] and effectively freezes posterior leaflet motion [4].

As new therapeutic strategies emerge for the treatment of IMR, understanding transmural cardiac and fiber-sheet strains will become increasingly important. Interventions for IMR include disease-specific rings (Edwards GeoForm and IMR ETlogix rings, St. Jude Medical RSR ring) that disproportionately reduce the mitral septal-lateral annular dimension, and more recently percutaneous septal-lateral reduction using a transatrial approach (Ample Medical, PS3 System) [24]. A transventricular approach to septal-lateral reduction has also been developed and is undergoing clinical testing (Myocor Coapsys® device) with promising short-term results [25]. In our acute open-chest animal studies, both annuloplasty and isolated septal-lateral reduction decrease systolic wall thickening in the anterobasal LV wall region near the mitral annulus. SLAC, however, had less of an effect on systolic wall thickening than annuloplasty and the mechanisms of systolic wall thickening are different. Future studies are needed to measure the significance of these changes, and we encourage further explorations in evaluating SLAC as a therapeutic strategy for IMR.


   5. Limitations
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
 5. Limitations
References
 
It is important to mention inherent limitations of this acute, open-chest study in normal sheep hearts. Direct extrapolation of strain perturbations in sheep hearts to the clinical scenario of long-standing IMR or FMR in human patients must be done cautiously. Furthermore, this study was conducted in healthy sheep hearts without myocardial ischemia or infarction. Future studies examining the effect of SLAC and strain perturbations in a chronic infarction model are being considered by our research group. Lastly, an extreme amount of septal-lateral annular reduction was obtained with SLAC in this study, on the order of 60%, or approximately 15 mm, reduction in the mitral septal-lateral dimension. It is possible that an extreme degree of SLAC might cause functional mitral stenosis given the decrease in EDV and increase in heart rate after SLAC. MAA was slightly smaller at ED and ES after SLAC (Table 1), but this was not statistically significant. We did not have left atrial catheter, so could not measure left atrial pressure and instantaneous mitral pressure gradients. While we did not look specifically at pulse wave or continuous wave Doppler tracings across the mitral valve before, during, or after SLAC, we did examine the aliasing bands (Nyquist frequency) in the mitral inflow color Doppler signals during diastole on the TEE tapes. The absence of diastolic aliasing at the Nyquist limits (0.4–0.6 m/s) at the depths imaged excludes the possibility of any important degree of mitral stenosis during SLAC. The mitral inflow color signal never wrapped before, during, or after SLAC, suggesting that the peak mitral inflow velocity never exceeded 1.2 m/s. Perhaps, this is not surprising since an important degree of functional mitral stenosis does not occur clinically after a Bolling radically undersized mitral annuloplasty, in part because the leaflets are morphologically normal. In previous studies by Timek et al. [22], in an acute IMR preparation, SLAC reduced septal-lateral dimensions by only 6.0 ± 2.6 (22% reduction) mm. In the chronic IMR experiments by Tibayan et al. [6] where the annulus was dilated, SLAC reduced mitral septal-lateral annular diameter by 10–11 mm to approximately 6 mm less than baseline (26% reduction). Finally, although we describe decreased systolic wall thickening with SLAC, the effects of SLAC on LV strains are probably different in various LV regions as SLAC is expected to produce different geometric changes in different regions of the heart. In this study, we only looked at strain alterations in the anterobasal and midlateral equatorial LV regions.


   Acknowledgments
 
This work was supported by Grants HL-29589 and HL-67025 from the National Heart, Lung and Blood Institute. Drs Nguyen and Cheng were Leah McConnell Cardiovascular Surgical Research Fellows. Dr Nguyen was a recipient of the Thoracic Society Foundation Research Fellowship Award. We deeply appreciate the technical expertise provided by Mary K. Zasio, B.A., Maggie Brophy, A.S., and Katha Gazda, B.A. We also thank Drs Akinobu Itoh and Robert A. Oakes for their generous help and advice.


   Footnotes
 
\#9734; Presented at the joint 20th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 14th Annual Meeting of the European Society of Thoracic Surgeons, Stockholm, Sweden, September 10–13, 2006.


   References
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
 5. Limitations
 References
 

  1. Carpentier A, Deloche A, Dauptain J, Soyer R, Blondeau P, Piwnica A, Dubost C, McGoon DC. A new reconstructive operation for correction of mitral and tricuspid insufficiency. J Thorac Cardiovasc Surg 1971;61(1):1-13.[Medline]
  2. Cheng A, Nguyen TC, Malinowski M, Liang D, Daughters GT, Ingels Jr. NB, Miller DC. Effects of undersized mitral annuloplasty on regional transmural left ventricular wall strains and wall thickening mechanisms. Circulation 2006;114(Suppl. 1):I600-I609.[CrossRef][Medline]
  3. Glasson JR, Green GR, Nistal JF, Dagum P, Komeda M, Daughters GT, Bolger AF, Foppiano LE, Ingels Jr. NB, Miller DC. Mitral annular size and shape in sheep with annuloplasty rings. J Thorac Cardiovasc Surg 1999;117(2):302-309.[Abstract/Free Full Text]
  4. Green GR, Dagum P, Glasson JR, Nistal JF, Daughters 2nd GT, Ingels Jr. NB, Miller DC. Restricted posterior leaflet motion after mitral ring annuloplasty. Ann Thorac Surg 1999;68(6):2100-2106.[Abstract/Free Full Text]
  5. Timek TA, Lai DT, Tibayan FA, Daughters GT, Liang D, Dagum P, Ingels Jr. NB, Miller DC. Septal-lateral annular cinching (SLAC) reduces mitral annular size without perturbing normal annular dynamics. J Heart Valve Dis 2002;11(1):2-9discussion 10.[Medline]
  6. Tibayan FA, Rodriguez F, Langer F, Zasio MK, Bailey L, Liang D, Daughters GT, Ingels Jr. NB, Miller DC. Does septal-lateral annular cinching work for chronic ischemic mitral regurgitation?. J Thorac Cardiovasc Surg 2004;127(3):654-663.[Abstract/Free Full Text]
  7. Cheng A, Langer F, Rodriguez F, Criscione JC, Daughters GT, Miller DC, Ingels Jr. NB. Transmural sheet strains in the lateral wall of the ovine left ventricle. Am J Physiol Heart Circ Physiol 2005;289(3):H1234-H1241.[Abstract/Free Full Text]
  8. Cheng A, Langer F, Rodriguez F, Criscione JC, Daughters GT, Miller DC, Ingels Jr. NB. Transmural cardiac strains in the lateral wall of the ovine left ventricle. Am J Physiol Heart Circ Physiol 2005;288(4):H1546-H1556.[Abstract/Free Full Text]
  9. Tibayan FA, Rodriguez F, Zasio MK, Bailey L, Liang D, Daughters GT, Langer F, Ingels Jr. NB, Miller DC. Geometric distortions of the mitral valvular-ventricular complex in chronic ischemic mitral regurgitation. Circulation 2003;108(Suppl. 1):II116-II121.[Medline]
  10. Rodriguez F, Langer F, Harrington KB, Cheng A, Daughters GT, Criscione JC, Ingels NB, Miller DC. Alterations in transmural strains adjacent to ischemic myocardium during acute midcircumflex occlusion. J Thorac Cardiovasc Surg 2005;129(4):791-803.[Abstract/Free Full Text]
  11. Jackson BM, Gorman JH, Moainie SL, Guy TS, Narula N, Narula J, John-Sutton MG, Edmunds Jr. LH, Gorman RC. Extension of borderzone myocardium in postinfarction dilated cardiomyopathy. J Am Coll Cardiol 2002;40(6):1160-1167discussion 1168–71.[Abstract/Free Full Text]
  12. Olivetti G, Abbi R, Quaini F, Kajstura J, Cheng W, Nitahara JA, Quaini E, Di Loreto C, Beltrami CA, Krajewski S, Reed JC, Anversa P. Apoptosis in the failing human heart. N Engl J Med 1997;336(16):1131-1141.[Abstract/Free Full Text]
  13. Mukherjee R, Brinsa TA, Dowdy KB, Scott AA, Baskin JM, Deschamps AM, Lowry AS, Escobar GP, Lucas DG, Yarbrough WM, Zile MR, Spinale FG. Myocardial infarct expansion and matrix metalloproteinase inhibition. Circulation 2003;107(4):618-625.[Abstract/Free Full Text]
  14. Prabhu SD. Post-infarction ventricular remodeling: an array of molecular events. J Mol Cell Cardiol 2005;38(4):547-550.[CrossRef][Medline]
  15. Discher DE, Janmey P, Wang YL. Tissue cells feel and respond to the stiffness of their substrate. Science 2005;310(5751):1139-1143.[Abstract/Free Full Text]
  16. Cheng A, Langer F, Nguyen TC, Malinowski M, Ennis DB, Daughters GT, Ingels Jr. NB, Miller DC. Transmural left ventricular shear strain alterations adjacent to and remote from infarcted myocardium. J Heart Valve Dis 2006;15(2):209-218discussion 218.[Medline]
  17. Costa KD, Takayama Y, McCulloch AD, Covell JW. Laminar fiber architecture and three-dimensional systolic mechanics in canine ventricular myocardium. Am J Physiol 1999;276(2 Pt. 2):H595-H607.[Medline]
  18. Bach DS, Bolling SF. Improvement following correction of secondary mitral regurgitation in end-stage cardiomyopathy with mitral annuloplasty. Am J Cardiol 1996;78(8):966-969.[CrossRef][Medline]
  19. Tibayan FA, Rodriguez F, Langer F, Liang D, Daughters GT, Ingels NB, Miller DC. Mitral suture annuloplasty corrects both annular and subvalvular geometry in acute ischemic mitral regurgitation. J Heart Valve Dis 2004;13(3):414-420.[Medline]
  20. Bolling SF, Pagani FD, Deeb GM, Bach DS. Intermediate-term outcome of mitral reconstruction in cardiomyopathy. J Thorac Cardiovasc Surg 1998;115(2):381-386discussion 387–8.[Abstract/Free Full Text]
  21. Salgo IS, Gorman 3rd JH, Gorman RC, Jackson BM, Bowen FW, Plappert T, St John Sutton MG, Edmunds Jr. LH. Effect of annular shape on leaflet curvature in reducing mitral leaflet stress. Circulation 2002;106(6):711-717.[Abstract/Free Full Text]
  22. Timek TA, Lai DT, Tibayan F, Liang D, Daughters GT, Dagum P, Ingels Jr. NB, Miller DC. Septal-lateral annular cinching abolishes acute ischemic mitral regurgitation. J Thorac Cardiovasc Surg 2002;123(5):881-888.[Abstract/Free Full Text]
  23. Dagum P, Timek T, Green GR, Daughters GT, Liang D, Ingels Jr. NB, Miller DC. Three-dimensional geometric comparison of partial and complete flexible mitral annuloplasty rings. J Thorac Cardiovasc Surg 2001;122(4):665-673.[Abstract/Free Full Text]
  24. Rogers JH, Macoviak JA, Rahdert DA, Takeda PA, Palacios IF, Low RI. Percutaneous septal sinus shortening: a novel procedure for the treatment of functional mitral regurgitation. Circulation 2006;113(19):2329-2334.[Abstract/Free Full Text]
  25. Grossi EA, Saunders PC, Woo YJ, Gangahar DM, Laschinger JC, Kress DC, Caskey MP, Schwartz CF, Wudel J. Intraoperative effects of the coapsys annuloplasty system in a randomized evaluation (RESTOR-MV) of functional ischemic mitral regurgitation. Ann Thorac Surg 2005;80(5):1706-1711.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Eur. J. Cardiothorac. Surg.Home page
T. A. Timek, D. Liang, G. T. Daughters, N. B. Ingels Jr., and D. C. Miller
Effect of local annular interventions on annular and left ventricular geometry
Eur. J. Cardiothorac. Surg., June 1, 2008; 33(6): 1049 - 1054.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Tom C. Nguyen
Neil B. Ingels, Jr.
David Craig Miller
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nguyen, T. C.
Right arrow Articles by Miller, D. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nguyen, T. C.
Right arrow Articles by Miller, D. C.
Related Collections
Right arrow Cardiac - physiology
Right arrow Cardiac - other
Right arrow Valve disease

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS