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Right arrow Myocardial infarction

Ann Thorac Surg 2002;73:1507-1513
© 2002 The Society of Thoracic Surgeons

Original article: cardiovascular

Myocardial infarction scar plication in the rat: cardiac mechanics in an animal model for surgical procedures

Rosemeire M. Kanashiro, MSa, Emília Nozawa, MSa, Neif Murad, MD, PhDa, Luis R. Gerola, MD, PhDb, Valdir A. Moisés, MD, PhDc, Paulo J.F. Tucci, MD, PhD*a

a Department of Physiology, Universidade Federal de São Paulo, São Paulo, Brazil
b Department of Surgery, Universidade Federal de São Paulo, São Paulo, Brazil
c Department of Internal Medicine, Universidade Federal de São Paulo, São Paulo, Brazil

Accepted for publication October 17, 2001.

* Address reprint requests to Dr Tucci, Department of Physiology, Universidade Federal de São Paulo, Rua Estado de Israel, 181, 94, CEP: 04022-000, São Paulo, Brazil
e-mail: tucci{at}fcr.epm.br


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Backgund. The immediate effects of surgical reduction of left ventricle cavity on cardiac mechanics have not been well defined.

Methods. Cardiac mechanics were analyzed before and after myocardial infarction scar plication in 11 isolated infarcted rat hearts.

Results. Despite a decrease in myocardial stiffness, an increase in chamber stiffness was noted after myocardial infarction scar plication. Systolic function was favored in more than one way. For the same diastolic pressures, maximal developed pressures were higher after myocardial infarction scar plication, and the slope of the systolic pressure-volume relationship was steeper afterwards as compared with before; this means that Frank-Starling recruitment is accentuated in smaller cavities. In addition, the developed net forces needed to generate these pressures were clearly lower afterward than before, indicating reduced ventricular afterload.

Conclusions. The study results show that diastolic function is harmed and systolic function is favored by myocardial infarction scar plication. We suggest that preoperative evaluation of the degree of diastolic dysfunction and impairment of the Frank-Starling mechanism may help to identify patients who may have a poor postoperative outcome due to diastolic or systolic dysfunction.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 Acknowledgments
 References
 
To generte a certain level of ejection pressure, the force to be developed by myocardium will be higher as cavity radius increases, according to Laplace’s law (F = P x R/2h). Thus, dilated left ventricle (LV) hinders cardiac ejection. Accordingly, surgical LV volume reduction (LVVR) has been proposed as treatment for heart failure accompanying left ventricular cavity enlargement, as in cardiomyopaies and LV aneurysms.

In the clinical setting, it is difficult to make the necessary measurements and maneuvers required for a full understanding of the immediate impact of this procedure on cardiovascular function. Most data reported in the literature results from a longer or shorter postoperative period. Experimental models have been asked for a better understanding of the physiopathological basis of LVVR [1–4]. Some reports have emerged from experimental models relating to the immediate and short-term effects of LVVR on LV geometry as well as passive LV mechanics in the porcine heart [5], cardiac volume and pressure changes in sheep [6], and systolic and diastolic diameters in the rat heart [7]. Another work described the hemodynamic and molecular consequences in the rat heart 30 weeks after myocardial infarction scar plication (MISP) [8].

In this study we describe the immediate effects of MISP on cardiac mechanics in the isolated isovolumic rat heart as an experimental model of LVVR. The resulting data should potentially be helpful in making functional evaluations for selecting patients for LVVR.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 Acknowledgments
 References
 
The animals were cared for in compliance with the "Principles of Laboratory Animal Care" formulated by the National Institute of Health (National Institutes of Health publication no. 96-23, revised, 1996).

Myocardial infarction production and MISP
Myocardial infarction (MI) was induced in 25 female Wistar rats (200 to 250 g) according to a well-accepted technique. Briefly, after ether anesthesia, a left thoracotomy was performed. The heart was exteriorized and the left anterior descending coronary artery ligated using 6-0 polypropylene. The heart was quickly returned to its position and the thorax immediately closed.

Echocardiography was performed 5 weeks after MI using an Apogee Cx Ultrasound System (ATL Inc, Ambler, PA) with a 7.5-MHz transducer. Two-dimensional and M-mode images from the parasternal longitudinal and transverse views were obtained and recorded on a 0.5-inch videotape. Measurements of infarct size and cavity dimensions were performed off-line using the Image Vue System (Nova MicroSonics, Mahwah, NJ). Infarct size was estimated as the mean percentage of left ventricular cross-sectional perimeter of the basal, medial, and apical planes.

For this study, only those animals with an infarct size greater than 40% were included. Myocardial infarction scar plication was performed on 11 isolated rat hearts, for a maximum of 10 minutes, 6 weeks after the induction of MI. Scar wedge was visually determined and the MI fibrous scar was plicated with a 6-0 polypropylene, double, continuous running suture at the internal border of the scar. Particular attention was paid to prevent plicated scar from invaginating into the ventricular cavity.

Isolated heart preparation
Cardiac mechanics was analyzed before and after MISP in the isovolumic isolated hearts. After heparinization (500 IU intraperitoneally), anesthesia (urethane 1.2 g/kg intraperitoneally), tracheotomy, and thoracotomy, the ascending aorta was cannulated. The heart was perfused at a perfusion pressure of 100 mm Hg using the Langendorff technique with Krebs-Henseleit bicarbonate buffer (pH 7.35 to 7.45) containing 10 IU insulin bubbled with 95% O2 and 5% CO2 (PO2 >480 mm Hg) and warmed to 36°C. The heart was quickly removed, the LV cavity vented by apical puncture, and a small latex balloon connected to a pressure transducer was placed inside the LV chamber. The right atrium, including the sinus node region, was removed and right ventricular pacing carried out using a bipolar pacemaker wire driven by a stimulator delivering 4-millisecond monophasic square waves of 5 V at a stimulation rate of 180 beats per minute. The LV volume was adjusted so that the diastolic pressure was zero (V0). After a-15 minute equilibration period, a pressure-volume relationship was determined by measuring LV peak systolic and diastolic pressures 30 seconds after 20-µL increments in the balloon volume until a maximal end-diastolic pressure of 40 mm Hg was obtained. The balloon was emptied and removed from the LV cavity. Myocardial infarction scar plication was carried out, the balloon placed back in the LV, and the liquid volume inside the balloon readjusted so that the diastolic pressure reached zero. After 10 minutes, a new pressure-volume relationship was determined for post-MISP status.

Calculations
Developed pressure (DP; systolic minus diastolic pressure) was used for contractile function evaluations. Net wall force was derived by the method described by Hefner and colleagues [9]. The net force generated by the ventricular wall in a direction perpendicular to any imaginary plane that transects the ventricle is equal to the product of intracavity pressure and the area of the cavity subtended by the plane (F = P x A). For a sphere this area is represented by {pi}Ri2, where Ri is derived from the ventricular volume (V) and the equation V = 4/3 {pi}Ri3. The chamber volume was the sum of the liquid volume inside the balloon plus the latex volume of the balloon (latex weight/0.936, the specific gravity of the latex balloon). Thus, Ri = [V/4/3{pi}]1/3. A linear fitting was done using the initial points of the ascending limb of the developed pressure-volume curve that complied with a linear distribution. Chamber stiffness and myocardial stiffness curves were constructed by fitting the resting pressure (Pr)/volume and resting force (Fr)/strain ({varepsilon} = V - V0/V0) data to a mono-exponential relation y = A (eKx - 1), where A and K are coefficients. Chamber stiffness (dPr/dV) and myocardial stiffness (dFr/d{varepsilon}) were computed at low (Pr = 5 mm Hg; Fr = 5 g) and high (Pr = 25 mm Hg; Fr = 25 g) values of pressure and force.

Data are presented as mean ± SEM. Physiologic variables determined before (B) and after (A) MISP were compared by a paired Student’s t test; p values less than 0.05 were considered to be significant.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 Acknowledgments
 References
 
The results observed in 11 preparations are shown in Figures 1 to 5. A marked reduction (B: 0.258 ± 0.013 mL; A: 0.107 ± 0.011 mL; p < 0.001) in ventricular volume was obtained after MISP. Figure 1 shows the general results for cardiac mechanics. A left and upward shift of the diastolic pressure-volume relationship was observed after MISP (Fig 2A) and the chamber stiffness increased at both low resting pressures (B: 0.05 ± 0.01 mm Hg/mL; A: 0.15 ± 0.02 mm Hg/mL; p < 0.001) and high resting pressures (B: 0.32 ± 0.02 mm Hg/mL; A: 0.83 ± 0.19 mm Hg/mL; p < 0.001). On the other hand, opposite results were obtained for myocardial stiffness: after MISP, resting force/strain curves were shifted to the right and down (Fig 2B), and myocardial stiffness decreased at low (B: 27 ± 3 g; A: 16 ± 2 g; p < 0.001) and high (B: 55 ± 3 g; A: 35 ± 4 g; p < 0.001) resting forces. These results show that, despite myocardial stiffness decrease, cavity volume reduction limits chamber filling capacity and LV filling occurs at higher resting pressure. Additionally, when diastolic force was projected as a function of resting pressure (Fig 2C) it was shown that, after MISP, higher diastolic pressures are needed to reach comparable values of stretching diastolic forces.



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  		Fig 1. Mean values (symbols) ± SEM (vertical lines) of resting pressure (inverted triangles), resting force (squares), developed pressure (triangles), and developed force (circles) obtained in 11 infarcted hearts before (open symbols), and after (filled symbols) myocardial infarction scar plication.

 


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  		Fig 2. (A) Resting pressure-volume and (B) resting force-strain relationships before (open circles) and after (filled circles) myocardial infarction scar plication. (C) Resting force plotted as a function of resting pressure before (open circles) and after (filled circles) myocardial infarction scar plication.

 


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  		Fig 3. (A) Developed pressure plotted as a function of resting pressure before (open circles) and after (filled circles) myocardial infarction scar plication (MISP). Note that after MISP developed pressure increases for all values of resting pressure and the same level of developed pressure (broken line) is attained with lower values of resting pressures (broken arrows). (B) Individual values (symbols), mean values (horizontal solid line), and standard errors of means (horizontal dotted lines) for developed pressure achieved at zero resting pressure before (open circles) and after (filled circles) MISP. (C) Individual values (symbols), means (horizontal solid line), and standard error of means (horizontal dotted line) for maximal developed pressure before (open circles) and after (filled circles) MISP.

 


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  		Fig 4. (A) Individual values (symbols), mean values (horizontal solid line) and standard errors of means (horizontal dotted line) for maximal developed force before (open circles) and after (filled circles) myocardial infarction scar plication (MISP), showing reduction of force needed to generate pressure. (B) Developed pressure plotted as a function of developed force before (open circles) and after (filled circles) MISP. (C) Linear portions of developed pressure-volume relationship before (open circles) and after (filled circles) MISP showing that the Frank-Starling relationships turn steeper after cavity reduction.

 


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  		Fig 5. (A) Cardiac mechanics of a normal rat heart comparing the behavior of developed pressure (circles), developed net force (filled triangles), developed circumferential wall stress (filled inverted triangles), resting net force (open triangles) and resting circumferential wall stress (open inverted triangles). Note the similar behavior of circumferential wall stress and net force. Resting pressure-volume relationships were omitted for clarity. (B) Linear fitting of maximal developed pressures obtained before myocardial infarction scar plication plotted as a function of mass/volume ratios, showing that developed pressure increases proportionally to mass/volume ratio increase.

 
Systolic function was clearly favored by MISP. By projecting DP as a function of Pr we could see that cavity reduction allowed higher DP at all levels of Pr (Fig 3A), showing that after MISP systolic pressure is reached at lower diastolic pressure, thus allowing venous congestion attenuation. At zero Pr a significant difference was observed for DP (B: 41 ± 4 mm Hg; A: 58 ± 4 mm Hg; p < 0.001; Fig 3B). As Pr increased, the differences between developed pressures decreased. The maximal developed pressure (DPmax) levels reached after MISP (83 ± 3 mm Hg) were higher (Fig 3C) than those before surgery (75 ± 5 mm Hg), although the difference was not significant (p = 0.06). The DPmax levels were reached at significantly lower systolic forces after MISP (B: 56 ± 3 g; A: 35 ± 4 g; p < 0.001; Fig 4A), thus characterizing the left ventricular afterload reduction. Moreover, for comparable force values, developed pressures were always higher for reduced cavity scenarios (Fig 4B), indicating that the same pressure values are reached at lower developed forces. When the linear portions of DP/ventricular volumes were compared (Fig 4C), it was found that the slope of the straight line in A (373 ± 38 mm Hg/mL) was significantly higher (p = 0.0129) compared with B (211 ± 23 mm Hg/mL). Taken together, these data highlight the improved efficiency of transducing the variable that regulates muscular function (force) to the variable that regulates ejection function (chamber pressure) after volume reduction.


   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
Acknowledgments
 References
 
Customarily, circumferential wall stress is used for cardiac mechanics analyses using pressure, cavity volume, and myocardial mass values for calculations. The impossibility of setting up the value of myocardial mass to be considered after the scar is removed from the cavity makes stress calculation impossible. The net wall force calculated as the product of pressure and the cross-sectional area of the chamber included in the plane has been previously validated [9], and this method has permitted other investigators to obtain interesting and coherent information from studies of cardiac mechanics [10, 11]. This net force exists in the rim of myocardium determined by the imaginary plane, and its direction is perpendicular to the plane. Its magnitude is determined only by cavity pressure and cross-sectional area, and does not depend on the wall thickness, the shape or cross-sectional area of the rim, the size or shape of the remainder of the ventricle, the fiber orientation and the distribution of fiber-generated forces, or the presence of shearing forces [9]. Moreover, by comparing the values of circumferential wall stress as described by others [12] and the net force in normal rat heart, we have shown that the behaviors of these variables are very similar during the cardiac cycle (Fig 5A).

The data obtained here concerning the increase in chamber stiffness immediately after MISP are consistent with the theoretic premises of Dickstein and colleagues [1] and Ratcliffe and associates [13], as well as results reported by Gorcsan and colleagues [14] and Dowling and coworkers [15] for LVVR in human subjects and by Ratcliffe and coworkers [6] in sheep. On the other hand, we found downward and rightward deviations for the resting force-strain relationships, indicating that myocardial stiffness had been reduced. It may be argued that the reduction in myocardial stiffness obtained in the present study could be a characteristic strictly related to the removal of the large, rigid, fibrous scar. Nevertheless, lower myocardial stiffness after LVVR was also described in normal arrested porcine hearts [5] and in human cardiomyopathic hearts [16], meaning that reduction in myocardial stiffness may occur regardless of whether LVVR includes fibrous scar removal. In any case, we showed that, despite decrease in myocardial stiffness, LVVR caused chamber stiffness increase.

The LVVR has another relevant effect on diastolic function. The projection of Fr as a function of Pr showed that higher diastolic pressures are needed to reach a certain stretching force level when the cavity is smaller. Because resting force is the determining factor for diastolic myofibril stretching, it is foreseeable that the myocardial stretching required to adjust ventricular ejection by the Frank-Starling mechanism will occur at even higher filling pressures after LVVR.

These data lead to the conclusion that the LVVR influence on diastolic function predisposes to a tendency for the heart to work at high diastolic pressures, thus favoring venous congestion.

With respect to the effects of MISP on systolic function, it was clear that to develop the same pressure values, the force developed was always lower after fibrous scar removal (Fig 4B), leading to LV afterload reduction. This finding can be anticipated by Laplace’s law. By rearranging Laplace’s law we have P = 2F x h/R: that is, for the same developed force the pressure generated will increase with decreasing cavity radius (in other words, pressure development is facilitated in smaller cavities). Because pressure is the variable that regulates blood flow and therefore ventricular ejection, we can say that ventricular ejection is facilitated when chamber size is reduced. In our cases, the effects of chamber characteristics on pressure generation were characterized by a close association between DP and mass/volume ratio (r = 0.7425; p = 0.009; Fig 5B), thus showing that DP increases in proportion to the mass/volume ratio.

Other circumstances favor ventricular pressure generation after LVVR. Because a smaller cavity allows steeper DP/volume relations, Frank-Starling mechanism recruitment will be more effective after LVVR. This statement may contrast with the conclusion of Ratcliffe and colleagues [6], who considered that the Starling relationship is depressed, taking into account that stroke volume/end-diastolic pressure underwent a downward parallel shift with aneurysm plication. Certainly it seems valid to name the stroke volume/diastolic pressure as the Starling relationship within a historical context, as Ernest Henry Starling used these variables to determine that diastolic loading regulates systolic performance. However, the upper left shift of stroke work/ventricular volume and of systolic pressure-volume relationships reported by Ratcliffe and colleagues contradicts the conclusion that stroke volume/end-diastolic pressure downward shift implies depression of the Frank-Starling mechanism. In addition, the nonlinear characteristics of diastolic pressure-volume relationships could misrepresent the true diastolic filling/ventricular ejection relations. Furthermore, if we accept that stroke volume/diastolic pressure characterizes the Frank-Starling mechanism in the experiments conducted by Ratcliffe and colleagues, we are at a loss to explain how, in their results, postinfarction data showed an upper left shift of these relationships in relation to preinfarction data. Thus, these considerations, taken together with the present data, support the view that the Frank-Starling mechanism is accentuated after LVVR.

The DP/Pr relationship (Fig 3A), as shown by our data, may also contribute to better heart pump function. After LVVR, under the same Pr levels, higher DP values are reached. Because systolic pressures are reached at lower Pr, it is fair to say that this sort of change in the filling-systolic pressure interplay may attenuate the tendency toward an increase in filling pressure.

It is fair to assume that all of these favorable influences of LVVR on systolic function may lead to a postsurgical reduction in ventricular filling pressure. These could be the reasons explaining the intriguing report on maintained or enhanced post-LVVR human cardiac ejection associated with diastolic ventricular pressure equal to or lower than preoperative levels [15, 17–21].

Briefly, our data clearly showed that the effects of LVVR on cardiac mechanics tend to harm diastolic function and to facilitate systolic function. It has been further shown that, besides LV afterload reduction, LVVR can favor ventricular ejection by magnifying Frank-Starling mechanism mobilization. These seem to be relevant points that are not considered in the clinical setting. To date, the only functional criterion for patient selection when LVVR is considered for treatment of heart failure has been the presence of marked contraction depression. Our data indicate that it would be interesting to include the degree of diastolic dysfunction and Frank-Starling mechanism impairment among the predictors of postoperative outcome. It is possible that the existence of high levels of presurgical diastolic dysfunction may contribute to later impaired evolution, as has been already described for aneurysmectomy [22]. The ability to respond to the Frank-Starling mechanism can also be of interest. We have shown that LVVR makes length-tension relationships steeper, so that Frank-Starling mechanism recruitment should be favored. For this very reason, one may admit that postsurgical ventricular ejection adjustments depend on the greater or lesser ability of the myocardium to intensify contraction when muscle stretching occurs. In our cases, contractile ability was intensified by myocardial stretching in all experiments. However, there are doubts about the integrity of the Frank-Starling mechanism in the end-stage, failing human myocardium. Schwinger and colleagues [23] reported that stretching myocardial samples of failing human hearts did not intensify myofilament calcium responsiveness, a predominant factor in determining the Frank-Starling mechanism [24–26]. Conversely, Holusbarsch and coworkers [27] have identified myocardial myofilament responsiveness when submitting the failing human myocardium to stretching. Vahl and associates [28] concluded that in failing human hearts length-dependent developed force increase is flatter than in normal hearts. Because our results pointed out that in the presence of myocardial responsiveness to stretching, the surgical procedure favors the Frank-Starling mechanism, it seems important to recognize each patient’s ventricular ejection response to diastolic volume variations. Those patients who show systolic volume variations according to Frank-Starling mechanism integrity will have more favorable postsurgical adjustments.

Myocardial infarction scar plication in rats includes favorable and unfavorable elements as a model of LVVR. Small cardiac structures present inevitable constraints and, thus, structural details are jeopardized in the model. The animal used and how easily infarction can be produced and fibrous scar removed are favorable aspects. It should be anticipated that such method is already in use in our laboratory in hearts in situ, and initial experiments indicate this method is successfully applicable for further monitoring of the animals. In addition, Schwarz and colleagues [7] have proved that rats subjected to MISP can be followed-up postoperatively for weeks. The perspective for in vivo studies stands as an interesting alternative to short- and long-term monitoring of the LVVR influence on myocardial remodeling, as well as heart failure associated with advanced ventricular dysfunction. The long-term monitoring of animals subjected to surgery and of infarcted rats that have not undergone operation will allow the evaluation of LVVR benefits on a long-term basis. Confirmation through an experimental model that MISP has the ability to provide improved survival may help in the evaluation as to whether MISP can act as a therapeutic alternative to be put into practice at earlier stages for large myocardium infarction in human subjects, with the purpose of avoiding the inexorable development of ventricular hypertrophy to the final failing state. Recent works recommending earlier surgical procedures for ventricular aneurysm [2, 3, 29, 30] encourage the use of experimental models for the investigation of earlier removal of onerous, large fibrous scars in infarction in human patients.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
References
 
This work was carried out during the tenure of grants in aid from the National Research Council [CNPq, processo 300.692/80–3(NV)] and from Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP, processo 99/0045–3). The authors appreciate the skillful technical assistance in surgical preparation by Airton Andrade Santos. Special acknowledgment is given to Clovis de Araujo Peres, PhD, for advice in the statistical analyses, and to Regina H. E. Alfarano, PhD, for assistance with language correction and style.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 

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