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Echocardiographic assessment of regional ventricular function after device-based change of left ventricular shape
Echocardiographic Assessment of Regional Ventricular Function after Device-based Change of Left Ventricular Shape Zoran B. Popovic´, MD, Giuseppe Saracino, MS, Dimitri Deserranno, MS, Hua Yang, MD, Neil L. Greenberg, PhD, Masami Takagaki, MD, Kiyotaka Fukamachi, MD, Yoshie Ochiai, MD, Masahiro Inoue, MD, Soren Schenk, MD, Kazuyoshi Doi, MD, Jianxin Qin, MD, Patrick M. McCarthy, MD, Takahiro Shiota, MD, PhD, and James D. Thomas, MD, Cleveland, Ohio
We assessed the effects of implantation of Myosplint (Myocor, Maple Grove, Minn), a device that changes left ventricular (LV) cross-sectional shape from circular to bilobar, on regional LV function. A total of 10 open-chest dogs with tachycardia-induced cardiomyopathy were studied before and after Myosplint implantation. LV cross-sectional epicardial echocardiography at the papillary muscle level was performed along with acquisition of hemodynamic data. LV normalized thickening, fractional thickening, end-diastolic thickness, and end-diastolic curvatures were calculated for 10 LV segments. Myosplint implantation did not affect LV hemodynamics, but
In recent years, a concept of surgical remodeling of
the left ventricle (LV) has been introduced. It is on the basis of a proposition that heart failure is associated not only with LV chamber dilation, but also with a change of its shape.1 For this reason, several surgical procedures that aim to reshape the ventricle without changing myocardial contractility emerged.2-6 The rationale behind these procedures is that ventricular function is ineffective not only because of altered tissue characteristics, but also because LV shape decreases its efficiency.7 A potential alternative to more radical surgical remodeling procedures is implantation of the Myosplint device (Myocor, Maple Grove, Minn). Myosplint is a stringshaped structure with 2 pads in the end that is implanted through the LV in a short-axis direction on a beating heart.8,9 By reducing the distance between 2 pads, the device brings opposing walls closer and changes cross-sectional LV appearance From the Department of Cardiovascular Medicine, Cleveland Clinic Foundation. Supported in part by Myocor Inc (Maple Grove, Minnesota). Dr McCarthy is a consultant to Myocor Inc. Reprint requests: James D. Thomas, MD, Department of Cardiology, Desk F-15, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195 (E-mail: [email protected]). 0894-7317/$30.00 Copyright 2004 by the American Society of Echocardiography. doi:10.1016/j.echo.2004.01.015
decreased average end-diastolic curvature (P < .0001) and increased its segmental heterogeneity (P < .0001). There was no change in average fractional thickening, whereas normalized thickening increased (P ⴝ .05). In contrast, segmental heterogeneity of both normalized and fractional thickening increased (P ⴝ .02 and P ⴝ .01, respectively). Structural modeling confirmed that Myosplint implantation increases regional stress heterogeneity and curvature heterogeneity. LV cross-sectional shape markedly affects regional LV performance. (J Am Soc Echocardiogr 2004;17:411-7.)
from circular to bilobular. The implantation of the device dramatically decreases the LV size. Also, it has been proposed that Myosplint may reduce wall stress and possibly improve ventricular performance. However, implantation of Myosplint may restrict myocardial wall motion in proximal regions. The purpose of the study was to assess the effects of shape change induced by Myosplint implantation and tightening on regional LV function.
METHODS The study was approved by the Institutional Animal Care and Use Committee and is in compliance with the Guide for the Care and Use of Laboratory Animals published by the National Institutes of Health. Surgical Procedure We studied 10 initially healthy mongrel dogs with tachycardia-induced cardiomyopathy (body weight 27.1 ⫾ 1.5 kg) in which Myosplint implantation was performed as a part of a device-evaluation protocol. Dogs were paced for a period of 4 weeks to induce heart failure, as previously described.10 No medications for heart failure, including diuretics, were given during the heart failure induction phase. At the conclusion of the induction, transthoracic 2-dimensional (2D) echocardiograms were obtained during temporary resumption of normal in sinus rhythm to
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Figure 1 Illustration of effect of Myosplints on left ventricular cross-sectional and 3-dimensional shape. evaluate LV function, and the development of mitral and tricuspid regurgitation. At that time point, all dogs had an ejection fraction less than 0.35; 7 dogs had mitral regurgitation grade 2 or less, whereas 3 had mitral regurgitation grade 3 (0-4 grading scale). On the date of study, the pacemaker was programmed to a demand mode so that the animal would resume normal in sinus rhythm, and the animal was placed under general anesthesia as previously described.9 A pressure microtransducer-tipped catheter (SPC-562, Millar Instruments Inc, Houston, Tex) was placed by the carotid artery to record instantaneous LV pressures. A sternotomy incision was made and the chest and pericardium were opened. A transonic flow probe (Transonic Systems, Ithaca, NY) was positioned around the aorta. Myosplint implantation is performed on the beating heart in the following stages. First, LV diastolic epicardial diameter is determined by a special device. During implantation we used a device that enables avoidance of epicardial vessels, papillary muscles, and the mitral valve apparatus. Three Myosplints are implanted under echocardiographic guidance in septolateral direction, with the aim to bisect the LV cross-sectional shape in 2 halves (Figure 1). The Myosplints are distributed parallel to each other and within the same plane, over the length of the LV in 2-cm steps, with the first one implanted 1 cm below the
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Figure 2 End-diastolic frames before (A) and after (B) Myosplint (MS) implantation in representative animal, along with traced endocardial contours. Location of 100 data points and corresponding 10 ventricular segments before (C) and after (D) MS implantation (broken line). Arrows, Direction of tracing; arrowhead, MS tension member; dotted line, papillary muscles; hi, higher lobe; lo, lower lobe; RV, right ventricle.
atrioventricular groove. The implantation plane is defined by the inferior edge of the anterolateral papillary muscle and the right ventricular (RV) side of the interventricular septum 3 cm away from the posterior descending artery (Figure 2, B and D). Although the aim is to evenly bisect LV shape, some degree of asymmetry of LV cross-sectional shape is usually observed at the papillary muscle level as Myosplint is positioned so as not to penetrate the body of the anterolateral papillary muscle. The devices are then tightened, using proprietary tables, to a level that decreases epicardial diameters of the newly formed bilobar LV shape to 20% of the initial epicardial diameter (Figure 1).9,11 In the tightening region, this resulted in epicardial diameter decrease of approximately 26%. Data Acquisition and Analysis Hemodynamic and echocardiographic data were acquired before Myosplint implantation, and after implantation and tightening. LV pressure curves were recorded at a steady state, with ventilation transiently stopped, at a sampling
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rate of 200 Hz using a commercially available data acquisition system (PowerLab, AD Instruments Inc, Mountain View, Calif) and digitally stored for subsequent analysis. From a pressure curve, we measured peak positive (dP/ dtmax) and negative (dP/dtmin) derivative of a pressure curve and a peak systolic and end-diastolic pressure, averaged from at least 10 beats, as indexes of ventricular performance. Stroke volume was obtained by integrating the signal from aortic flow probe. Cardiac output was calculated as a product of stroke volume and heart rate. Two-dimensional epicardial echocardiography was performed with an ultrasound machine (Sequoia, Siemens, Erlangen, Germany) using a 3.5-MHz transducer and digitally recorded at 30 frames/s resolution. Global and regional LV function. LV volumes before Myosplint implantation were calculated from apical 4- and 2-chamber views by Simpson’s biplane equation. LV crosssectional areas at the papillary muscle level (with the papillary muscles excluded from the LV tracing) were measured in end-diastole and end-systole both before and after Myosplint implantation. To analyze regional LV function we used the short-axis papillary muscle view. From each study representative end-diastolic frame (a frame immediately preceding peak of the R wave) and endsystolic frame (a frame with minimal systolic area) were selected and imported to software (Imagevue, Eastman Kodak, Rochester, NY). The x and y coordinates of LV endocardial and epicardial silhouettes were obtained by manual tracing in a clockwise direction, with papillary muscles excluded from the tracing (Figure 2, C and D). After initial tracing, the data were resampled to obtain 100 equidistant points. The manual tracing was repeated 3 times. The averaged data were used to calculate epicardial perimeter length and regional LV thickness in end-diastole and end-systole. From these data, we calculated regional normalized thickening (Thnorm) as:
Figure 3 Characteristic profiles of end-diastolic curvature before and after Myosplint (MS) implantation. Data are obtained from tracings of Figure 2, A and B. LV, Left ventricular.
Thnorm (%) ⫽ (thicknesss ⫺ thicknessd)/perimeterd ⫻ 100 Regional fractional thickening (FTh) was calculated as:
Figure 4 Initial 2-dimensional mash used for finite element analysis of cross-sectional ventricular shape before and after Myosplint implantation.
FTh (%) ⫽ (thicknesss ⫺ thicknessd)/thicknessd ⫻ 100 Where subscripts d and systole, respectfully.
s
signify end-diastole and end-
Regional curvature analysis. Regional curvature represents the rate of change of the direction of the curve and is equal to the inverse of local radius. To calculate local radii, we created software on the basis of reference12 using a C⫹⫹. First, endocardial xy coordinates of the LV in end-diastole were smoothed by Fast Fourier Transform (TableCurve 2D, Jandel Scientific, San Rafael, Calif) that eliminates harmonics higher than 10th.13 Smoothed data were than imported into our software, which as initial conditions used a pure algebraic approximation for the points and than obtained the final results implementing a conventional Levenberg-Marquardt method. Curvature was calculated as the inverse of radius. If curvature was
concave, data were assigned negative values. Figure 3 displays characteristic curvature profiles before and after Myosplint implantation obtained from tracings of Figure 2, A and B. Structural Modeling Because regional end-diastolic strains are difficult to quantify, we used structural model to illustrate the impact of Myosplint implantation on relative strain distribution. We constructed a 2D plane strain model consisting of 944 9-node quadrilateral elements (3391 nodes) using a finite element analysis package (Adina R and D Inc, Watertown, Mass) as illustrated in Figure 4. Because, at the equatorial level, the circumferential radii of the LV are 3 to 5 times smaller than meridional,14 unloaded LV cross-sectional
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shape was represented as a thick cylinder with a radius of 3.1 cm and wall thickness of 1 cm. Unloaded RV free wall was represented as a section of the cylinder with a wall thickness of 0.5 cm, a maximal distance between RV and LV walls of 1 cm, and anchoring points on LV wall that encompass one-third of the LV circumference. A large strain deformation analysis was performed in total Lagrangian formulation. The cardiac tissue was represented by a Mooney-Rivlin material as available in the analysis package. Material model parameters were determined by fitting the Mooney-Rivlin material to an existing model by Usyk et al.15 Stiffness values were adjusted to obtained prescribed end-diastolic and end-systolic volumes. Diastole parameters were determined by the value that enabled LV to increase its average radius so as to be equal to observed average end-diastolic radius before Myosplint implantation (ie, 5.13 cm) when subjected to internal pressure of 15 mm Hg (or 1.995 kPa). Systolic parameters were determined by the value that enabled LV to decrease its diameter to be equal to average end-systolic radius before Myosplint implantation (ie, 4.75 cm) while subjected to pressure of 100 mm Hg (or 13.3 kPa). The RV diastolic and systolic pressures were fixed to 5 and 15 mm Hg, respectively. This led to the following strain energy density functions for the Mooney-Rivlin material: Enddiastolic strain energy W ⫽ 1577共e I1⫺3 ⫺ 1兲
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Table Hemodynamic data before and after Myosplint implantation
HR (bpm) CO (L/min) LV PSP (mm Hg) LV EDP (mm Hg) dP/dtmax (mm Hg/s) dP/dtmin (mm Hg/s) LV cross-sectionsys (cm2) LV cross-sectiondia (cm2)
Before Myosplint
After Myosplint
94 ⫾ 17 2.0 ⫾ 0.5 77 ⫾ 6 14 ⫾ 6 704 ⫾ 90 ⫺701 ⫾ 155 21.2 ⫾ 2.3 18.1 ⫾ 2.3
93 ⫾ 17 1.8 ⫾ 0.4 76 ⫾ 10 15 ⫾ 6 719 ⫾ 146 ⫺708 ⫾ 206 15 ⫾ 2.9* 12.6 ⫾ 2.4*
CO, Cardiac output; dP/dtmax, maximum derivative of left ventricular pressure; dP/dtmin, minimum derivative of left ventricular pressure; HR, heart rate; LV cross-sectionsys/dia, left ventricular cross-sectional area at papillary muscle level in diastole/systole; LV EDP, left ventricular end-diastolic pressure; LV PSP, left ventricular peak systolic pressure. *P ⫽ .0001 vs before Myosplint.
ance (followed by Huynh-Feldt correction if needed) with time and segments as independent fixed factors was used to assess impact of Myosplint implantation on the same variables. Interaction between time and segments was taken to represent the change in segment heterogeneity after Myosplint implantation. A contrast analysis was used to compare individual segments before and after Myosplint implantation, if necessary. In all analyses, P ⱕ .05 was considered significant.
End-systolic strain energy W ⫽ 20550共I 1 ⫺ 3兲 ⫹ 1577共e I1⫺3 ⫺ 1兲 With I1 the first invariant of the Cauchy-Green strain tensor. In both cases the material bulk modulus was set to 100 kPa. After initial simulation run, Myosplint implantation was modeled by restraining the movement of the node representing the RV-LV junction and the node on the outer (epicardial) side of the opposite wall in such a way that 2 arches demarcated by the nodes had a perimeter of 55% and 45% in respect to overall outer circumference. Statistical Methods Data are presented as mean ⫾ SD. To compare segmental LV end-diastolic thickness, normalized systolic thickening, fractional systolic thickening, and end-diastolic curvature before and after Myosplint implantation, individual points were averaged over 10 segments, beginning with the inferior border of the anterolateral papillary muscle (the implantation point of the Myosplint) and extending in the clockwise direction (Figure 2, C and D). In this way we obtained representative data of 10 LV segments. To evaluate the baseline heterogeneity of LV function and shape, segmental normalized thickening, fractional thickening, diastolic thickness, and diastolic curvature before Myosplint implantation were compared by 1-way repeated measures analysis of variance followed by Huynh-Feldt correction. A 2-way repeated measures analysis of vari-
RESULTS Before implantation, LV ejection fraction was 21.6 ⫾ 6.8%, with LV end-diastolic and end-systolic volumes being 91.3 ⫾ 14.4 and 72.0 ⫾ 15.2 mL, respectively. Average end-diastolic and end-systolic endocardial diameters at the papillary muscle level before Myosplint implantation were 5.1 ⫾ 0.3 cm and 4.8 ⫾ 0.3 cm, respectively. The Myosplint implantation was uneventful in all animals. The average distance between endocardial penetration points of Myosplint at the same level in end-diastole was 3.1 ⫾ 0.3 cm. In almost all animals, the asymmetric cross-sectional shape after Myosplint implantation was noted, with the lobe demarcated by anterior septum, anterior and lateral LV walls (“higher” lobe) having somewhat larger area than lobe demarcated by posterior wall and inferior septum (“lower” lobe). Global LV Function Myosplint implantation decreased LV end-diastolic and end-systolic cross-sectional area at the papillary muscle level. However, it did not produce any change in hemodynamic parameters (Table). Regional LV Function Before Myosplint implantation, we detected segmental heterogeneity in end-diastolic curvature (P ⬍
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Figure 5 Segmental fractional thickening (FTh) (A), normalized thickening (NTh) (B), end-diastolic curvatures (C), and thickness (D) before and after Myosplint (MS) implantation. *P ⬍ .05 for comparison with values before MS implantation. LV, Left ventricular.
.001), fractional thickening (P ⫽ .004), and normalized thickening (P ⫽ .009), whereas end-diastolic thickness was homogenous between segments. Myosplint implantation induced visible changes in regional myocardial function. Although there was no change in average fractional thickening after implantation (P ⫽ .14), interaction between segment and implantation was significant (P ⫽ .017), with contrast analysis showing improvement in segment 7 (free anterior wall) (P ⫽ .01) (Figure 5, A). Normalized thickening showed improvement after implantation (P ⬍ .05) with significant interaction between region and implantation (P ⫽ .01). Contrast analysis showed improved thickening at levels 7 to 9 (P ⬍ .03 for all) (Figure 5, B). As expected, average segmental end-diastolic curvature increased after Myosplint implantation (P ⬍ .001). Curvature increased significantly in segments 2 and 3 (P ⬍ .01 for both) and segments 7 to 9 (P ⬍ .03 for all) (Figure 5, C). Finally, there was no change in average LV end-diastolic thickness (P ⫽ .16), and no interaction between implantation and segment position (P ⫽ not significant) although somewhat higher values could be discerned in segments 1 to 3 and 8 to 10 (Figure 5, D). Structural Modeling Figure 6 presents structural modeling results. The diastolic and systolic areas predicted by the model before Myosplint implantation were 20.7 and 17.7 cm2, respectively, whereas they were 15.9 and 12.1 cm2, respectively, after Myosplint implantation, which was very similar to observed values. Finite
Figure 6 Color maps of stress distribution obtained by structural modeling of left ventricular (LV) cross-sectional shape. Before Myosplint (MS) implantation, different ventricular segments are subjected to similar stress levels. MS implantation resulted in overall decrease of myocardial stress but increase of heterogeneity of stress distribution both in diastole and systole. However, stress distribution was less heterogenous in systole, as a result of increased circularization of LV. Higher stresses occurred in higher lobe. Thin lines, Unstressed ventricular shape.
element analysis predicted that after Myosplint implantation LV cross section during diastole becomes
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Figure 7 Left ventricular (LV) diastolic segmental curvatures calculated from structural model results. Note similar distribution of modeled and observed segmental curvatures presented at Figure 4, D. MS, Myosplint.
asymmetrical, with the simulated shape resembling the observed one. Although average stresses decreased, stress distribution became very heterogenous. Maximum stress occurred around Myosplint implantation points but sharply decreased to its minimum, then gradually increasing with increasing distance from implantation point. Furthermore, higher stresses were observed in the higher lobe, in regions opposite the RV. Similar results were obtained in systole, except heterogeneity was less pronounced. Figure 7 shows that diastolic segmental curvatures of our structural LV model were similar to observed segmental curvatures (compare with Figure 5, C).
DISCUSSION Our data show that cross-sectional deformation of the LV increases regional function heterogeneity. This heterogeneity, which may be detected even before Myosplint implantation, seems to be related to diastolic LV curvature. Local changes of diastolic curvature induced by Myosplint implantation accentuate differences in regional function. Importantly, introduction of this heterogeneity led to improved echocardiographic measures of LV wall thickening.9 Regional LV Function in Dilated Cardiomyopathy and its Relation to LV Geometry Several studies have documented regional differences of LV function in dilated cardiomyopathy.16,17 Both heterogenous metabolism and stress distribution have been implicated, although with no firm cause and effect established.18,19 Our findings, that septal regions contribute the least and anterolateral regions the most to overall LV function, are in accordance to previous data.20
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A novel finding of this study is that regional performance heterogeneity parallels diastolic curvature heterogeneity. This implies the interdependence of regional shape and function. Indeed, a recent study relating LV shape to its performance showed that cross-sectional “elliptization” of the LV with the volume kept constant increases total ventricular output.21 Also, Moon et al22 have shown that LV unloading by assist device decreased septal curvature, and its contribution to LV output, even though the thickness of the septum increased. Conversely, Young et al23 reported that increased diastolic stretch of the septum induced by chronic mitral regurgitation was associated with larger septal contribution to cardiac output. It has been proposed that these findings may be explained by Frank-Starling mechanism, as changes in regional diastolic stretch (preload) may influence regional performance. Impact of Myosplint Implantation on LV Function In a similar vein, “pushing” of the myocardium by Myosplint pads toward LV center may decrease both regional curvature and diastolic stretch of the ventricular walls in their proximity. Although it also results in decrease of LV systolic stress,9 the untoward effect is decreased contribution of these regions to systolic output. On the other hand, the parts of the ventricle remote to Myosplint insertion have the largest curvature, with the smallest obstruction to diastolic stretch and, thus, may be able to perform the most LV work. The RV-LV interaction, length of Myosplint tension members, and symmetry of its implantation may modify Myosplint impact. As an example, despite the increase of diastolic curvature in segments 2 and 3, there was no improvement in thickening in segments 1 to 4 that belonged to a lower lobe of LV cross-sectional shape. This phenomenon may be related to slightly asymmetric Myosplint insertion in a papillary muscle region that becomes pronounced during Myosplint tightening. Our structural modeling showed heterogenous stress distribution in diastole, with higher stresses (and consecutively higher stretch) in the higher lobe away from the RV, and lower stresses (and consecutively lower stretch) in the lower lobe. A complete tightening would exclude the function of this part of the ventricle (although it would have a high curvature), in a manner akin to surgical exclusion of this part. Although this stress heterogeneity exists also in systole, is it less pronounced as ventricle is becoming more evenly spherical. In contrast to regional function, in this study Myosplint implantation did not produce significant changes in hemodynamic indices (cardiac output, dP/dtmax, and dP/dtmin). In our previous report, we showed a decrease of LV volumes and systolic stress, with an improvement in LV ejection fraction from
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20% to 36% by real-time 3-dimensional echocardiography.9 Interestingly, similarly to this study, no change in hemodynamic indices was observed. Possibly this may reflect differences in assessing LV geometry as a 3-dimensional structure, as compared with a 2D cross-sectional assessment of LV. However, our aim was to assess not the global, but regional impact of Myosplint implantation. Clinical Implications and Limitations Our study indicates that acute cross-sectional manipulation of pathologic LV shape may have a profound effect on regional performance. Although no changes in cardiac output were observed, it was delivered under less overall stress. Our observations may be important for the decision-making process of matching the device position with pre-existing local regional function. However, our assumptions are on the basis of the correct identification of myocardial regions both before and after Myosplint implantation, which may be difficult when not performed by using myocardial markers.14 Finally, the chronic impact of passive constraint on LV function was not evaluated.24 This may emerge as a major indication of these types of procedures.25,26 In summary, the acute change of LV shape by Myosplint implantation induces changes in regional performance, which may be related to regional LV curvature. Probably, deformation of the LV in diastole induces the change in regional Frank-Starling mechanisms that drives the ventricle to resume a more spherical shape in systole, as seen by a greater thickening in more deformed regions. REFERENCES 1. Mann DL. Mechanisms and models in heart failure: a combinatorial approach. Circulation 1999;100:999-1008. 2. McCarthy PM, Starling RC, Wong J, Scalia GM, Buda T, Vargo RL, et al. Early results with partial left ventriculectomy. J Thorac Cardiovasc Surg 1997;114:755-65. 3. Popovic Z, Miric M, Gradinac S, Neskovic AN, Jovovic L, Vuk L, et al. Effects of partial left ventriculectomy on left ventricular performance in patients with nonischemic dilated cardiomyopathy. J Am Coll Cardiol 1998;32:1801-8. 4. Di Donato M, Sabatier M, Dor V, Toso A, Maioli M, Fantini F. Akinetic versus dyskinetic postinfarction scar: relation to surgical outcome in patients undergoing endoventricular circular patch plasty repair. J Am Coll Cardiol 1997;29:1569-75. 5. Kashem A, Santamore WP, Hassan S, Crabbe DL, Marculies KB, Melvin DB. CardioClasp: a new passive device to reshape cardiac enlargement. ASAIO J 2002;48:253-9. 6. Konertz WF, Shapland JE, Hotz H, Dushe S, Braun JP, Stantke K, et al. Passive containment and reverse remodeling by a novel textile cardiac support device. Circulation 2001;104:I270-5. 7. Douglas PS, Morrow R, Ioli A, Reichek N. Left ventricular shape, afterload and survival in idiopathic dilated cardiomyopathy. J Am Coll Cardiol 1989;13:311-5. 8. Burkhoff D. New heart failure therapy: the shape of things to come? J Thorac Cardiovasc Surg 2001;122:421-3.
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9. McCarthy PM, Takagaki M, Ochiai Y, Young JB, Tabata T, Shiota T, et al. Device-based change in left ventricular shape: a new concept for the treatment of dilated cardiomyopathy. J Thorac Cardiovasc Surg 2001;122:482-90. 10. Takagaki M, McCarthy PM, Ochiai Y, Dessoffy R, Doi K, Vidlund R, et al. Novel device to change left ventricular shape for heart failure treatment: device design and implantation procedure. ASAIO J 2001;47:244-8. 11. Schenk S, Reichenspurner H, Boehm DH, Groetzner J, Schirmer J, Detter C, et al. Myosplint implant and shapechange procedure: intra- and peri-operative safety and feasibility. J Heart Lung Transplant 2002;21:680-6. 12. Chernov N, Lesort C. Fitting circles and lines by least squares: theory and experiment. Available from: http://www.math. uab.edu/cl/cl1. Accessed October 28, 2002. 13. Kass DA, Traill TA, Keating M, Altieri PI, Maughan WL. Abnormalities of dynamic ventricular shape change in patients with aortic and mitral valvular regurgitation: assessment by Fourier shape analysis and global geometric indexes. Circ Res 1988;62:127-38. 14. DeAnda A Jr, Moon MR, Nikolic SD, Castro LJ, Fann JI, Daughters GT II, et al. A method to assess endocardial regional longitudinal curvature of the left ventricle. Am J Physiol 1995;268:H2553-60. 15. Usyk TP, Mazhari R, McCulloch AD. Effect of laminar orthotropic myofiber architecture on regional stress and strain in the canine left ventricle. J Elasticity 2000;61:143-64. 16. Franco-Cereceda A, McCarthy PM, Blackstone EH, Hoercher KJ, White JA, Young JB, et al. Partial left ventriculectomy for dilated cardiomyopathy: is this an alternative to transplantation? J Thorac Cardiovasc Surg 2001;121:879-93. 17. Young AA, Dokos S, Powell KA, Sturm B, McCulloch AD, Starling RC, et al. Regional heterogeneity of function in nonischemic dilated cardiomyopathy. Cardiovasc Res 2001;49:308-18. 18. Janz RF. Estimation of local myocardial stress. Am J Physiol 1982;242:H875-81. 19. Hayashida W, Kumada T, Nohara R, Tanio H, Kambayashi M, Ishikawa N, et al. Left ventricular regional wall stress in dilated cardiomyopathy. Circulation 1990;82:2075-83. 20. Bach DS, Beanlands RS, Schwaiger M, Armstrong WF. Heterogeneity of ventricular function and myocardial oxidative metabolism in nonischemic dilated cardiomyopathy. J Am Coll Cardiol 1995;25:1258-62. 21. Yamaguchi S, Tamada Y, Miyawaki H, Niida Y, Fukui A, Shirakabe M, et al. Resetting of regional preload due to ventricular shape change alters diastolic and systolic performance. Am J Physiol 1993;265:H1629-37. 22. Moon MR, Bolger AF, DeAnda A, Komeda M, Daughters GT II, Nikolic SD, et al. Septal function during left ventricular unloading. Circulation 1997;95:1320-7. 23. Young AA, Orr R, Smaill BH, Dell’Italia LJ. Three-dimensional changes in left and right ventricular geometry in chronic mitral regurgitation. Am J Physiol 1996;271:H2689-700. 24. Kass DA, Baughman KL, Pak PH, Cho PW, Levin HR, Gardner TJ, et al. Reverse remodeling from cardiomyoplasty in human heart failure: external constraint versus active assist. Circulation 1995;91:2314-8. 25. Sabbah HN, Kleber FX, Konertz W. Efficacy trends of the acorn cardiac support device in patients with heart failure: a one year follow-up. J Heart Lung Transplant 2001;20:217. 26. Chaudhry PA, Mishima T, Sharov VG, Hawkins J, Alferness C, Paone G, et al. Passive epicardial containment prevents ventricular remodeling in heart failure. Ann Thorac Surg 2000;70:1275-80.
We assessed the effects of implantation of Myosplint (Myocor, Maple Grove, Minn), a device that changes left ventricular (LV) cross-sectional shape from circular to bilobar, on regional LV function. A total of 10 open-chest dogs with tachycardia-induced cardiomyopathy were studied before and after Myosplint implantation. LV cross-sectional epicardial echocardiography at the papillary muscle level was performed along with acquisition of hemodynamic data. LV normalized thickening, fractional thickening, end-diastolic thickness, and end-diastolic curvatures were calculated for 10 LV segments. Myosplint implantation did not affect LV hemodynamics, but
In recent years, a concept of surgical remodeling of
the left ventricle (LV) has been introduced. It is on the basis of a proposition that heart failure is associated not only with LV chamber dilation, but also with a change of its shape.1 For this reason, several surgical procedures that aim to reshape the ventricle without changing myocardial contractility emerged.2-6 The rationale behind these procedures is that ventricular function is ineffective not only because of altered tissue characteristics, but also because LV shape decreases its efficiency.7 A potential alternative to more radical surgical remodeling procedures is implantation of the Myosplint device (Myocor, Maple Grove, Minn). Myosplint is a stringshaped structure with 2 pads in the end that is implanted through the LV in a short-axis direction on a beating heart.8,9 By reducing the distance between 2 pads, the device brings opposing walls closer and changes cross-sectional LV appearance From the Department of Cardiovascular Medicine, Cleveland Clinic Foundation. Supported in part by Myocor Inc (Maple Grove, Minnesota). Dr McCarthy is a consultant to Myocor Inc. Reprint requests: James D. Thomas, MD, Department of Cardiology, Desk F-15, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195 (E-mail: [email protected]). 0894-7317/$30.00 Copyright 2004 by the American Society of Echocardiography. doi:10.1016/j.echo.2004.01.015
decreased average end-diastolic curvature (P < .0001) and increased its segmental heterogeneity (P < .0001). There was no change in average fractional thickening, whereas normalized thickening increased (P ⴝ .05). In contrast, segmental heterogeneity of both normalized and fractional thickening increased (P ⴝ .02 and P ⴝ .01, respectively). Structural modeling confirmed that Myosplint implantation increases regional stress heterogeneity and curvature heterogeneity. LV cross-sectional shape markedly affects regional LV performance. (J Am Soc Echocardiogr 2004;17:411-7.)
from circular to bilobular. The implantation of the device dramatically decreases the LV size. Also, it has been proposed that Myosplint may reduce wall stress and possibly improve ventricular performance. However, implantation of Myosplint may restrict myocardial wall motion in proximal regions. The purpose of the study was to assess the effects of shape change induced by Myosplint implantation and tightening on regional LV function.
METHODS The study was approved by the Institutional Animal Care and Use Committee and is in compliance with the Guide for the Care and Use of Laboratory Animals published by the National Institutes of Health. Surgical Procedure We studied 10 initially healthy mongrel dogs with tachycardia-induced cardiomyopathy (body weight 27.1 ⫾ 1.5 kg) in which Myosplint implantation was performed as a part of a device-evaluation protocol. Dogs were paced for a period of 4 weeks to induce heart failure, as previously described.10 No medications for heart failure, including diuretics, were given during the heart failure induction phase. At the conclusion of the induction, transthoracic 2-dimensional (2D) echocardiograms were obtained during temporary resumption of normal in sinus rhythm to
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Figure 1 Illustration of effect of Myosplints on left ventricular cross-sectional and 3-dimensional shape. evaluate LV function, and the development of mitral and tricuspid regurgitation. At that time point, all dogs had an ejection fraction less than 0.35; 7 dogs had mitral regurgitation grade 2 or less, whereas 3 had mitral regurgitation grade 3 (0-4 grading scale). On the date of study, the pacemaker was programmed to a demand mode so that the animal would resume normal in sinus rhythm, and the animal was placed under general anesthesia as previously described.9 A pressure microtransducer-tipped catheter (SPC-562, Millar Instruments Inc, Houston, Tex) was placed by the carotid artery to record instantaneous LV pressures. A sternotomy incision was made and the chest and pericardium were opened. A transonic flow probe (Transonic Systems, Ithaca, NY) was positioned around the aorta. Myosplint implantation is performed on the beating heart in the following stages. First, LV diastolic epicardial diameter is determined by a special device. During implantation we used a device that enables avoidance of epicardial vessels, papillary muscles, and the mitral valve apparatus. Three Myosplints are implanted under echocardiographic guidance in septolateral direction, with the aim to bisect the LV cross-sectional shape in 2 halves (Figure 1). The Myosplints are distributed parallel to each other and within the same plane, over the length of the LV in 2-cm steps, with the first one implanted 1 cm below the
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Figure 2 End-diastolic frames before (A) and after (B) Myosplint (MS) implantation in representative animal, along with traced endocardial contours. Location of 100 data points and corresponding 10 ventricular segments before (C) and after (D) MS implantation (broken line). Arrows, Direction of tracing; arrowhead, MS tension member; dotted line, papillary muscles; hi, higher lobe; lo, lower lobe; RV, right ventricle.
atrioventricular groove. The implantation plane is defined by the inferior edge of the anterolateral papillary muscle and the right ventricular (RV) side of the interventricular septum 3 cm away from the posterior descending artery (Figure 2, B and D). Although the aim is to evenly bisect LV shape, some degree of asymmetry of LV cross-sectional shape is usually observed at the papillary muscle level as Myosplint is positioned so as not to penetrate the body of the anterolateral papillary muscle. The devices are then tightened, using proprietary tables, to a level that decreases epicardial diameters of the newly formed bilobar LV shape to 20% of the initial epicardial diameter (Figure 1).9,11 In the tightening region, this resulted in epicardial diameter decrease of approximately 26%. Data Acquisition and Analysis Hemodynamic and echocardiographic data were acquired before Myosplint implantation, and after implantation and tightening. LV pressure curves were recorded at a steady state, with ventilation transiently stopped, at a sampling
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rate of 200 Hz using a commercially available data acquisition system (PowerLab, AD Instruments Inc, Mountain View, Calif) and digitally stored for subsequent analysis. From a pressure curve, we measured peak positive (dP/ dtmax) and negative (dP/dtmin) derivative of a pressure curve and a peak systolic and end-diastolic pressure, averaged from at least 10 beats, as indexes of ventricular performance. Stroke volume was obtained by integrating the signal from aortic flow probe. Cardiac output was calculated as a product of stroke volume and heart rate. Two-dimensional epicardial echocardiography was performed with an ultrasound machine (Sequoia, Siemens, Erlangen, Germany) using a 3.5-MHz transducer and digitally recorded at 30 frames/s resolution. Global and regional LV function. LV volumes before Myosplint implantation were calculated from apical 4- and 2-chamber views by Simpson’s biplane equation. LV crosssectional areas at the papillary muscle level (with the papillary muscles excluded from the LV tracing) were measured in end-diastole and end-systole both before and after Myosplint implantation. To analyze regional LV function we used the short-axis papillary muscle view. From each study representative end-diastolic frame (a frame immediately preceding peak of the R wave) and endsystolic frame (a frame with minimal systolic area) were selected and imported to software (Imagevue, Eastman Kodak, Rochester, NY). The x and y coordinates of LV endocardial and epicardial silhouettes were obtained by manual tracing in a clockwise direction, with papillary muscles excluded from the tracing (Figure 2, C and D). After initial tracing, the data were resampled to obtain 100 equidistant points. The manual tracing was repeated 3 times. The averaged data were used to calculate epicardial perimeter length and regional LV thickness in end-diastole and end-systole. From these data, we calculated regional normalized thickening (Thnorm) as:
Figure 3 Characteristic profiles of end-diastolic curvature before and after Myosplint (MS) implantation. Data are obtained from tracings of Figure 2, A and B. LV, Left ventricular.
Thnorm (%) ⫽ (thicknesss ⫺ thicknessd)/perimeterd ⫻ 100 Regional fractional thickening (FTh) was calculated as:
Figure 4 Initial 2-dimensional mash used for finite element analysis of cross-sectional ventricular shape before and after Myosplint implantation.
FTh (%) ⫽ (thicknesss ⫺ thicknessd)/thicknessd ⫻ 100 Where subscripts d and systole, respectfully.
s
signify end-diastole and end-
Regional curvature analysis. Regional curvature represents the rate of change of the direction of the curve and is equal to the inverse of local radius. To calculate local radii, we created software on the basis of reference12 using a C⫹⫹. First, endocardial xy coordinates of the LV in end-diastole were smoothed by Fast Fourier Transform (TableCurve 2D, Jandel Scientific, San Rafael, Calif) that eliminates harmonics higher than 10th.13 Smoothed data were than imported into our software, which as initial conditions used a pure algebraic approximation for the points and than obtained the final results implementing a conventional Levenberg-Marquardt method. Curvature was calculated as the inverse of radius. If curvature was
concave, data were assigned negative values. Figure 3 displays characteristic curvature profiles before and after Myosplint implantation obtained from tracings of Figure 2, A and B. Structural Modeling Because regional end-diastolic strains are difficult to quantify, we used structural model to illustrate the impact of Myosplint implantation on relative strain distribution. We constructed a 2D plane strain model consisting of 944 9-node quadrilateral elements (3391 nodes) using a finite element analysis package (Adina R and D Inc, Watertown, Mass) as illustrated in Figure 4. Because, at the equatorial level, the circumferential radii of the LV are 3 to 5 times smaller than meridional,14 unloaded LV cross-sectional
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shape was represented as a thick cylinder with a radius of 3.1 cm and wall thickness of 1 cm. Unloaded RV free wall was represented as a section of the cylinder with a wall thickness of 0.5 cm, a maximal distance between RV and LV walls of 1 cm, and anchoring points on LV wall that encompass one-third of the LV circumference. A large strain deformation analysis was performed in total Lagrangian formulation. The cardiac tissue was represented by a Mooney-Rivlin material as available in the analysis package. Material model parameters were determined by fitting the Mooney-Rivlin material to an existing model by Usyk et al.15 Stiffness values were adjusted to obtained prescribed end-diastolic and end-systolic volumes. Diastole parameters were determined by the value that enabled LV to increase its average radius so as to be equal to observed average end-diastolic radius before Myosplint implantation (ie, 5.13 cm) when subjected to internal pressure of 15 mm Hg (or 1.995 kPa). Systolic parameters were determined by the value that enabled LV to decrease its diameter to be equal to average end-systolic radius before Myosplint implantation (ie, 4.75 cm) while subjected to pressure of 100 mm Hg (or 13.3 kPa). The RV diastolic and systolic pressures were fixed to 5 and 15 mm Hg, respectively. This led to the following strain energy density functions for the Mooney-Rivlin material: Enddiastolic strain energy W ⫽ 1577共e I1⫺3 ⫺ 1兲
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Table Hemodynamic data before and after Myosplint implantation
HR (bpm) CO (L/min) LV PSP (mm Hg) LV EDP (mm Hg) dP/dtmax (mm Hg/s) dP/dtmin (mm Hg/s) LV cross-sectionsys (cm2) LV cross-sectiondia (cm2)
Before Myosplint
After Myosplint
94 ⫾ 17 2.0 ⫾ 0.5 77 ⫾ 6 14 ⫾ 6 704 ⫾ 90 ⫺701 ⫾ 155 21.2 ⫾ 2.3 18.1 ⫾ 2.3
93 ⫾ 17 1.8 ⫾ 0.4 76 ⫾ 10 15 ⫾ 6 719 ⫾ 146 ⫺708 ⫾ 206 15 ⫾ 2.9* 12.6 ⫾ 2.4*
CO, Cardiac output; dP/dtmax, maximum derivative of left ventricular pressure; dP/dtmin, minimum derivative of left ventricular pressure; HR, heart rate; LV cross-sectionsys/dia, left ventricular cross-sectional area at papillary muscle level in diastole/systole; LV EDP, left ventricular end-diastolic pressure; LV PSP, left ventricular peak systolic pressure. *P ⫽ .0001 vs before Myosplint.
ance (followed by Huynh-Feldt correction if needed) with time and segments as independent fixed factors was used to assess impact of Myosplint implantation on the same variables. Interaction between time and segments was taken to represent the change in segment heterogeneity after Myosplint implantation. A contrast analysis was used to compare individual segments before and after Myosplint implantation, if necessary. In all analyses, P ⱕ .05 was considered significant.
End-systolic strain energy W ⫽ 20550共I 1 ⫺ 3兲 ⫹ 1577共e I1⫺3 ⫺ 1兲 With I1 the first invariant of the Cauchy-Green strain tensor. In both cases the material bulk modulus was set to 100 kPa. After initial simulation run, Myosplint implantation was modeled by restraining the movement of the node representing the RV-LV junction and the node on the outer (epicardial) side of the opposite wall in such a way that 2 arches demarcated by the nodes had a perimeter of 55% and 45% in respect to overall outer circumference. Statistical Methods Data are presented as mean ⫾ SD. To compare segmental LV end-diastolic thickness, normalized systolic thickening, fractional systolic thickening, and end-diastolic curvature before and after Myosplint implantation, individual points were averaged over 10 segments, beginning with the inferior border of the anterolateral papillary muscle (the implantation point of the Myosplint) and extending in the clockwise direction (Figure 2, C and D). In this way we obtained representative data of 10 LV segments. To evaluate the baseline heterogeneity of LV function and shape, segmental normalized thickening, fractional thickening, diastolic thickness, and diastolic curvature before Myosplint implantation were compared by 1-way repeated measures analysis of variance followed by Huynh-Feldt correction. A 2-way repeated measures analysis of vari-
RESULTS Before implantation, LV ejection fraction was 21.6 ⫾ 6.8%, with LV end-diastolic and end-systolic volumes being 91.3 ⫾ 14.4 and 72.0 ⫾ 15.2 mL, respectively. Average end-diastolic and end-systolic endocardial diameters at the papillary muscle level before Myosplint implantation were 5.1 ⫾ 0.3 cm and 4.8 ⫾ 0.3 cm, respectively. The Myosplint implantation was uneventful in all animals. The average distance between endocardial penetration points of Myosplint at the same level in end-diastole was 3.1 ⫾ 0.3 cm. In almost all animals, the asymmetric cross-sectional shape after Myosplint implantation was noted, with the lobe demarcated by anterior septum, anterior and lateral LV walls (“higher” lobe) having somewhat larger area than lobe demarcated by posterior wall and inferior septum (“lower” lobe). Global LV Function Myosplint implantation decreased LV end-diastolic and end-systolic cross-sectional area at the papillary muscle level. However, it did not produce any change in hemodynamic parameters (Table). Regional LV Function Before Myosplint implantation, we detected segmental heterogeneity in end-diastolic curvature (P ⬍
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Figure 5 Segmental fractional thickening (FTh) (A), normalized thickening (NTh) (B), end-diastolic curvatures (C), and thickness (D) before and after Myosplint (MS) implantation. *P ⬍ .05 for comparison with values before MS implantation. LV, Left ventricular.
.001), fractional thickening (P ⫽ .004), and normalized thickening (P ⫽ .009), whereas end-diastolic thickness was homogenous between segments. Myosplint implantation induced visible changes in regional myocardial function. Although there was no change in average fractional thickening after implantation (P ⫽ .14), interaction between segment and implantation was significant (P ⫽ .017), with contrast analysis showing improvement in segment 7 (free anterior wall) (P ⫽ .01) (Figure 5, A). Normalized thickening showed improvement after implantation (P ⬍ .05) with significant interaction between region and implantation (P ⫽ .01). Contrast analysis showed improved thickening at levels 7 to 9 (P ⬍ .03 for all) (Figure 5, B). As expected, average segmental end-diastolic curvature increased after Myosplint implantation (P ⬍ .001). Curvature increased significantly in segments 2 and 3 (P ⬍ .01 for both) and segments 7 to 9 (P ⬍ .03 for all) (Figure 5, C). Finally, there was no change in average LV end-diastolic thickness (P ⫽ .16), and no interaction between implantation and segment position (P ⫽ not significant) although somewhat higher values could be discerned in segments 1 to 3 and 8 to 10 (Figure 5, D). Structural Modeling Figure 6 presents structural modeling results. The diastolic and systolic areas predicted by the model before Myosplint implantation were 20.7 and 17.7 cm2, respectively, whereas they were 15.9 and 12.1 cm2, respectively, after Myosplint implantation, which was very similar to observed values. Finite
Figure 6 Color maps of stress distribution obtained by structural modeling of left ventricular (LV) cross-sectional shape. Before Myosplint (MS) implantation, different ventricular segments are subjected to similar stress levels. MS implantation resulted in overall decrease of myocardial stress but increase of heterogeneity of stress distribution both in diastole and systole. However, stress distribution was less heterogenous in systole, as a result of increased circularization of LV. Higher stresses occurred in higher lobe. Thin lines, Unstressed ventricular shape.
element analysis predicted that after Myosplint implantation LV cross section during diastole becomes
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Figure 7 Left ventricular (LV) diastolic segmental curvatures calculated from structural model results. Note similar distribution of modeled and observed segmental curvatures presented at Figure 4, D. MS, Myosplint.
asymmetrical, with the simulated shape resembling the observed one. Although average stresses decreased, stress distribution became very heterogenous. Maximum stress occurred around Myosplint implantation points but sharply decreased to its minimum, then gradually increasing with increasing distance from implantation point. Furthermore, higher stresses were observed in the higher lobe, in regions opposite the RV. Similar results were obtained in systole, except heterogeneity was less pronounced. Figure 7 shows that diastolic segmental curvatures of our structural LV model were similar to observed segmental curvatures (compare with Figure 5, C).
DISCUSSION Our data show that cross-sectional deformation of the LV increases regional function heterogeneity. This heterogeneity, which may be detected even before Myosplint implantation, seems to be related to diastolic LV curvature. Local changes of diastolic curvature induced by Myosplint implantation accentuate differences in regional function. Importantly, introduction of this heterogeneity led to improved echocardiographic measures of LV wall thickening.9 Regional LV Function in Dilated Cardiomyopathy and its Relation to LV Geometry Several studies have documented regional differences of LV function in dilated cardiomyopathy.16,17 Both heterogenous metabolism and stress distribution have been implicated, although with no firm cause and effect established.18,19 Our findings, that septal regions contribute the least and anterolateral regions the most to overall LV function, are in accordance to previous data.20
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A novel finding of this study is that regional performance heterogeneity parallels diastolic curvature heterogeneity. This implies the interdependence of regional shape and function. Indeed, a recent study relating LV shape to its performance showed that cross-sectional “elliptization” of the LV with the volume kept constant increases total ventricular output.21 Also, Moon et al22 have shown that LV unloading by assist device decreased septal curvature, and its contribution to LV output, even though the thickness of the septum increased. Conversely, Young et al23 reported that increased diastolic stretch of the septum induced by chronic mitral regurgitation was associated with larger septal contribution to cardiac output. It has been proposed that these findings may be explained by Frank-Starling mechanism, as changes in regional diastolic stretch (preload) may influence regional performance. Impact of Myosplint Implantation on LV Function In a similar vein, “pushing” of the myocardium by Myosplint pads toward LV center may decrease both regional curvature and diastolic stretch of the ventricular walls in their proximity. Although it also results in decrease of LV systolic stress,9 the untoward effect is decreased contribution of these regions to systolic output. On the other hand, the parts of the ventricle remote to Myosplint insertion have the largest curvature, with the smallest obstruction to diastolic stretch and, thus, may be able to perform the most LV work. The RV-LV interaction, length of Myosplint tension members, and symmetry of its implantation may modify Myosplint impact. As an example, despite the increase of diastolic curvature in segments 2 and 3, there was no improvement in thickening in segments 1 to 4 that belonged to a lower lobe of LV cross-sectional shape. This phenomenon may be related to slightly asymmetric Myosplint insertion in a papillary muscle region that becomes pronounced during Myosplint tightening. Our structural modeling showed heterogenous stress distribution in diastole, with higher stresses (and consecutively higher stretch) in the higher lobe away from the RV, and lower stresses (and consecutively lower stretch) in the lower lobe. A complete tightening would exclude the function of this part of the ventricle (although it would have a high curvature), in a manner akin to surgical exclusion of this part. Although this stress heterogeneity exists also in systole, is it less pronounced as ventricle is becoming more evenly spherical. In contrast to regional function, in this study Myosplint implantation did not produce significant changes in hemodynamic indices (cardiac output, dP/dtmax, and dP/dtmin). In our previous report, we showed a decrease of LV volumes and systolic stress, with an improvement in LV ejection fraction from
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20% to 36% by real-time 3-dimensional echocardiography.9 Interestingly, similarly to this study, no change in hemodynamic indices was observed. Possibly this may reflect differences in assessing LV geometry as a 3-dimensional structure, as compared with a 2D cross-sectional assessment of LV. However, our aim was to assess not the global, but regional impact of Myosplint implantation. Clinical Implications and Limitations Our study indicates that acute cross-sectional manipulation of pathologic LV shape may have a profound effect on regional performance. Although no changes in cardiac output were observed, it was delivered under less overall stress. Our observations may be important for the decision-making process of matching the device position with pre-existing local regional function. However, our assumptions are on the basis of the correct identification of myocardial regions both before and after Myosplint implantation, which may be difficult when not performed by using myocardial markers.14 Finally, the chronic impact of passive constraint on LV function was not evaluated.24 This may emerge as a major indication of these types of procedures.25,26 In summary, the acute change of LV shape by Myosplint implantation induces changes in regional performance, which may be related to regional LV curvature. Probably, deformation of the LV in diastole induces the change in regional Frank-Starling mechanisms that drives the ventricle to resume a more spherical shape in systole, as seen by a greater thickening in more deformed regions. REFERENCES 1. Mann DL. Mechanisms and models in heart failure: a combinatorial approach. Circulation 1999;100:999-1008. 2. McCarthy PM, Starling RC, Wong J, Scalia GM, Buda T, Vargo RL, et al. Early results with partial left ventriculectomy. J Thorac Cardiovasc Surg 1997;114:755-65. 3. Popovic Z, Miric M, Gradinac S, Neskovic AN, Jovovic L, Vuk L, et al. Effects of partial left ventriculectomy on left ventricular performance in patients with nonischemic dilated cardiomyopathy. J Am Coll Cardiol 1998;32:1801-8. 4. Di Donato M, Sabatier M, Dor V, Toso A, Maioli M, Fantini F. Akinetic versus dyskinetic postinfarction scar: relation to surgical outcome in patients undergoing endoventricular circular patch plasty repair. J Am Coll Cardiol 1997;29:1569-75. 5. Kashem A, Santamore WP, Hassan S, Crabbe DL, Marculies KB, Melvin DB. CardioClasp: a new passive device to reshape cardiac enlargement. ASAIO J 2002;48:253-9. 6. Konertz WF, Shapland JE, Hotz H, Dushe S, Braun JP, Stantke K, et al. Passive containment and reverse remodeling by a novel textile cardiac support device. Circulation 2001;104:I270-5. 7. Douglas PS, Morrow R, Ioli A, Reichek N. Left ventricular shape, afterload and survival in idiopathic dilated cardiomyopathy. J Am Coll Cardiol 1989;13:311-5. 8. Burkhoff D. New heart failure therapy: the shape of things to come? J Thorac Cardiovasc Surg 2001;122:421-3.
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9. McCarthy PM, Takagaki M, Ochiai Y, Young JB, Tabata T, Shiota T, et al. Device-based change in left ventricular shape: a new concept for the treatment of dilated cardiomyopathy. J Thorac Cardiovasc Surg 2001;122:482-90. 10. Takagaki M, McCarthy PM, Ochiai Y, Dessoffy R, Doi K, Vidlund R, et al. Novel device to change left ventricular shape for heart failure treatment: device design and implantation procedure. ASAIO J 2001;47:244-8. 11. Schenk S, Reichenspurner H, Boehm DH, Groetzner J, Schirmer J, Detter C, et al. Myosplint implant and shapechange procedure: intra- and peri-operative safety and feasibility. J Heart Lung Transplant 2002;21:680-6. 12. Chernov N, Lesort C. Fitting circles and lines by least squares: theory and experiment. Available from: http://www.math. uab.edu/cl/cl1. Accessed October 28, 2002. 13. Kass DA, Traill TA, Keating M, Altieri PI, Maughan WL. Abnormalities of dynamic ventricular shape change in patients with aortic and mitral valvular regurgitation: assessment by Fourier shape analysis and global geometric indexes. Circ Res 1988;62:127-38. 14. DeAnda A Jr, Moon MR, Nikolic SD, Castro LJ, Fann JI, Daughters GT II, et al. A method to assess endocardial regional longitudinal curvature of the left ventricle. Am J Physiol 1995;268:H2553-60. 15. Usyk TP, Mazhari R, McCulloch AD. Effect of laminar orthotropic myofiber architecture on regional stress and strain in the canine left ventricle. J Elasticity 2000;61:143-64. 16. Franco-Cereceda A, McCarthy PM, Blackstone EH, Hoercher KJ, White JA, Young JB, et al. Partial left ventriculectomy for dilated cardiomyopathy: is this an alternative to transplantation? J Thorac Cardiovasc Surg 2001;121:879-93. 17. Young AA, Dokos S, Powell KA, Sturm B, McCulloch AD, Starling RC, et al. Regional heterogeneity of function in nonischemic dilated cardiomyopathy. Cardiovasc Res 2001;49:308-18. 18. Janz RF. Estimation of local myocardial stress. Am J Physiol 1982;242:H875-81. 19. Hayashida W, Kumada T, Nohara R, Tanio H, Kambayashi M, Ishikawa N, et al. Left ventricular regional wall stress in dilated cardiomyopathy. Circulation 1990;82:2075-83. 20. Bach DS, Beanlands RS, Schwaiger M, Armstrong WF. Heterogeneity of ventricular function and myocardial oxidative metabolism in nonischemic dilated cardiomyopathy. J Am Coll Cardiol 1995;25:1258-62. 21. Yamaguchi S, Tamada Y, Miyawaki H, Niida Y, Fukui A, Shirakabe M, et al. Resetting of regional preload due to ventricular shape change alters diastolic and systolic performance. Am J Physiol 1993;265:H1629-37. 22. Moon MR, Bolger AF, DeAnda A, Komeda M, Daughters GT II, Nikolic SD, et al. Septal function during left ventricular unloading. Circulation 1997;95:1320-7. 23. Young AA, Orr R, Smaill BH, Dell’Italia LJ. Three-dimensional changes in left and right ventricular geometry in chronic mitral regurgitation. Am J Physiol 1996;271:H2689-700. 24. Kass DA, Baughman KL, Pak PH, Cho PW, Levin HR, Gardner TJ, et al. Reverse remodeling from cardiomyoplasty in human heart failure: external constraint versus active assist. Circulation 1995;91:2314-8. 25. Sabbah HN, Kleber FX, Konertz W. Efficacy trends of the acorn cardiac support device in patients with heart failure: a one year follow-up. J Heart Lung Transplant 2001;20:217. 26. Chaudhry PA, Mishima T, Sharov VG, Hawkins J, Alferness C, Paone G, et al. Passive epicardial containment prevents ventricular remodeling in heart failure. Ann Thorac Surg 2000;70:1275-80.