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Ann Thorac Surg 1998;66:159-165
© 1998 The Society of Thoracic Surgeons

Original articles: cardiovascular

Acute functional consequences of left ventriculotomy

Louis R. DiBernardo, MDa, Paul M. Kirshbom, MDa, Lynne A. Skaryak, MDa, Renee L. Quarterman, MDa, Ronald L. Johnsona, Mark J. Davies, FRCSa, J. William Gaynor, MDa, Ross M. Ungerleider, MDa

a Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA

Address reprint requests to Dr Ungerleider, Duke University Medical Center, PO Box 3178, Durham, NC 27710

Presented at the Forty-second Annual Meeting of the Southern Thoracic Surgical Association, San Antonio, TX, Nov 9–11, 1995.


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Left ventriculotomies are sometimes used during intracardiac congenital defect repair. Acute changes in left ventricular function after longitudinal or apical ventriculotomy were assessed using dynamic pressure-dimensional data.

Methods. Ultrasonic dimension transducers along the major, minor, and septal free wall axes and micromanometers were placed in 24 piglets. Pressure-volume data were collected during caval occlusions at baseline and 60 minutes after warm cardiopulmonary bypass alone or with longitudinal ventriculotomy or apical left ventriculotomy. Hemodynamics, contractility, and contraction geometry were analyzed.

Results. Cardipulmonary bypass caused decreased compliance in all groups, with equally decreased preload and cardiac output. Heart rate increased, but ventriculotomy led to a significantly greater increase. Longitudinal ventriculotomy produced a greater loss of stroke volume and ejection fraction than apical ventriculotomy. Contractility assessed by the preload recruitable stroke work relationship showed no difference between groups; however, all groups showed a slight increase in unit myocardial power at 60 minutes. Axis fractional shortening revealed that the septal freewall is responsible for 50% of stroke volume and that this axis is significantly impaired after longitudinal ventriculotomy.

Conclusion. Apical left ventriculotomy impairs the less important major axis only and is predicted to be better tolerated.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
A left ventriculotomy is sometimes necessary to adequately visualize and repair congenital intracardiac defects such as apical ventricular septal defects. The consequences of such incisions on left ventricular function in the postoperative period are not known. Most previous investigations into left ventricular function in infants have focused on case reports of postoperative changes in hemodynamic parameters and not directly on left ventricular function itself.

The technique of sonomicrometry has proved to be a reliable means of gathering dynamic load-independent measurements of both ventricular and myocardial function [1]. The efficacy and validity of this technique has been proven under pathophysiologic states [2] and in the neonatal and pediatric age groups at other centers and in studies in our laboratory and operating rooms [3, 4]. Using a clinically relevant intact infant model, we assessed left ventricular function, including hemodynamics and also intrinsic contractility and contraction patterns, at baseline and after cardiopulmonary bypass alone or with a left ventriculotomy.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
Anesthesia and surgical procedures
Twenty-four DeKalb piglets (3 to 4 weeks old weighing 9 to 12 kg) were studied in 3 protocol groups. Animals used were treated with humane care as outlined in the "Guide for the Care and Use of Laboratory Animals" published by the National Institutes of Health (NIH publication 85-23, revised 1985) and with the approval of the institutional Animal Care and Use Committee. Basic operative anesthesia and surgical procedure (monitoring, cardiopulmonary bypass) were identical for each protocol group.

Anesthesia was induced using ketamine (20 mg/kg intramuscularly) and acepromazine (1 mg/kg intramuscularly). Piglets were rapidly intubated and placed on the ventilator (model IV-100B, Sechrist Infant Ventilator, Anaheim, CA) with a positive inspiratory pressure of 25 mm Hg and a positive end-expiratory pressure of 3 mm Hg. Respiratory rate and inspired oxygen fraction were titrated to maintain a partial pressure of carbon dioxide of 35 to 45 mm Hg and a partial pressure of oxygen of 150 to 250 mm Hg (oxygen saturation > 95%). Sodium bicarbonate (8.5%) was used to maintain a base excess between -3 and 3 mmol/L. Venous access was obtained via prominent ear veins, and all animals received methylprednisolone preoperatively (25 mg/kg intravenously).

Blood pressure monitoring and arterial blood gas sampling were achieved through a femoral arterial line. Body temperature was monitored with insertion of a nasopharyngeal probe (model YSI-400; Yellow Springs Instruments, Yellow Springs, OH). Anesthesia was maintained throughout the procedure with a pancuronium bolus (0.2 µg/kg) and continuous infusion of fentanyl (50 µg/kg/h). A median sternotomy was performed and the pericardium was incised. The heart was loosely suspended in a pericardial cradle. Umbilical tape was passed around the superior and inferior venae cavae. Purse string sutures were placed in the aortic root and right atrial appendage using 5-0 Prolene and 3-0 silk, respectively (Ethicon Inc, Somerville, NJ) for later placement of bypass cannulas. According to previously described methods, 2-mm ultrasonic dimension transducer crystals were sutured to the epicardium along three axes [1, 5, 6]. Major-axis crystals were placed at the left ventricular apex and at the base between the sinus of Valsalva and the left atrium. Minor-axis crystals were placed anteriorly approximately one third of the way along the left anterior descending coronary artery and directly across on the posterior wall, giving the maximum dimension. The third axis, the septal free wall, was measured by introducing a crystal into the interventricular septum in a track created by previous insertion of a 19.5-gauge needle. The placement was assessed by monitoring with a calibrated oscilloscope (model 2225, Tektronix, Beaverton, OR). Three-French micromanometers (model SPC-330; Millar Instruments, Houston, TX) were balanced and calibrated in a 38°C water bath and inserted into the pulmonary artery and left ventricle. An ultrasonic flow probe (model T-201; Transonic Systems Inc, Ithaca, NY) was placed on the aorta in pilot studies to verify cardiac output as measured by calculated dimensional changes. Blood gases were checked for stability after instruments were placed. In all protocol groups, baseline pressure and dimensional data were then collected under steady-state conditions and during a transient (10 to 20 seconds) vena caval occlusion. Dimension transducers were coupled to a sonomicrometer (Physiologic Monitoring Systems, Durham, NC). Data were filtered by a 50-Hz low-pass analog filter and digitalized in real time at an 8-channel sweep speed of 200 Hz by a digital-to-analog converter (Model 1012; ADAC, Woburn, MA) with storage on hard drive.

Animals were then placed on cardiopulmonary bypass. Animals were heparinized with 500 IU/kg and cannulated with a 10-F infant arterial cannula and a 24-F venous cannula (Electrocatheter Corp., Rahway, NJ). The circuit consisted of a Sarns roller pump (Model 7000MDX; Sarns/3M, Ann Arbor, MI), a Cobe membrane oxygenator (Cobe Laboratory, Lakewood, CO) and a Sarns water bath heater and cooler. The circuit was primed with a donor blood crystalloid mixture (hematocrit 20% to 25%) at 36°C to 37°C. Pump flow was set at 100 mL/kg per minute. Adequate ventricular emptying was assessed by visual inspection and by loss of pulmonary artery pressure. In all study groups hearts were maintained as empty beating throughout cardiopulmonary bypass. Circuit arterial blood gases were checked at 5-minute intervals to ensure continued maintenance of previously specified levels.

Control cardiopulmonary bypass only
Control animals (n = 8) were maintained on warm (36°C to 37°C) cardiopulmonary bypass for a time period approximating that necessary to create ventriculotomies and stabilize animals in pilot studies. Weaning from bypass was begun at 30 minutes of total cardiopulmonary bypass time. Respiratory rate, fraction of inspired oxygen, and sodium bicarbonate were used to maintain blood gases within the specified parameters. No inotropic agents were used to help remove animals from cardiopulmonary bypass or for postbypass hemodynamic support.

Longitudinal ventriculotomy
After verification of appropriate blood gas levels, those animals randomly assigned to undergo longitudinal ventriculotomy (n = 8) had a 3- to 3.5-cm incision made in the left ventricular freewall between the first and second circumflex marginal branches, parallel to the anterior descending artery. The interventricular septum was visualized through all ventriculotomies. The ventriculotomy was immediately closed with a continuous 3-0 Prolene suture. All ventriculotomies were completed within 20 minutes, and weaning from cardiopulmonary bypass was begun at 30 minutes as in the control group.

Apical ventriculotomy
Apical ventriculotomies (n = 8) were performed in a manner similar to the longitudinal ventriculotomies. Apical ventriculotomies (3 to 3.5 cm) were made parallel to the distal anterior descending artery, allowing visualization of the interventricular septum. Ventriculotomy closure was again achieved after 20 minutes and weaning initiated at 30 minutes.

Data collection and analysis
Animals that could not be weaned from bypass or that had blood gases that could not be corrected to within stated parameters, as well as animals that fibrillated and would have required electrical epicardial defibrillation, were excluded from the study. Caval occlusions producing a change in heart rate of greater than 10% of baseline were excluded. There was a 10% overall dropout and mortality rate evenly spread among the groups. One hour after successful weaning from cardiopulmonary bypass, physiologic data were collected at steady state during a transient vena caval occlusion. Animals were euthanized with potassium chloride. Hearts were excised and, after verification of proper septal crystal placement, the left ventricle was specifically excised and its wall volume (Vw) measured by saline displacement.

Data analysis was performed on a microprocessor with specifically developed programs (Microvax II/GPX Workstation; Digital Equipment Corp, Maynard, MA). The first time derivative of left ventricular pressure (dP/dt) was computed from the pressure waveform as a continuous 5-point polyorthagonal transformation. The cardiac cycle was defined automatically as described previously [5], with begin ejection 10 milliseconds after peak positive dP/dt and end ejection at peak negative dP/dt. Diastole began at the first zero crossing of dP/dt after peak negative dP/dt and ended 40 milliseconds before a positive dP/dt of 500 mm Hg/s. All beat-point assignments were checked by visual inspection.

Epicardial crystal volume modeling was verified in the piglet model in separate experiments in our laboratory. Established geometric and physiologic models of the left ventricle were used [6–8]. Left ventricular cavitary volume (V, in mL) was calculated by shell subtraction using a three-dimensional (major [a], minor [b], and septal freewall [c]) ellipsoid model: . Stroke volume (SV, in mL) was calculated from end diastolic (ed) and end ejection (ee) volumes: . Cardiac output (CO, in L/min) was calculated using heart rate (HR) as: , where heart rate is in beats/min. Global stroke work (SW) was calculated as the integral of ventricular pressure (P) and volume (V) over each cardiac cycle: . Normalized stroke work (SWn) was calculated using midwall latitudinal stress ({varepsilon}) and strain ({sigma}): . Ventricular performance was assessed by the preload recruitable stroke work relation between stroke work and left ventricular end-diastolic volume and expressed as the slope (Mw) and x-intercept (Lw) of the linear regression analysis as established by Glower and associates [6]. Variations in ventricular geometry and heart rate were controlled for by using the normalized stroke work, stress, and strain to determine the relationship between the myocardial power output (MPO) and end-diastolic circumferential strain to yield the slope (Mmp) as set forth by Glower and associates [6]: .

Statistical analysis
Analysis of variance corrected for repeated measures was used to compare data between groups for group and time differences. Unpaired two-tailed t tests were used to compare groups, and paired two-tailed t tests were used to compare variation within groups at different time points. A p value of less than 0.025 was considered significant. Analysis was performed on commercially available software (NCSS; J.L. Hintze, Hayesville, UT). All data are presented as the mean ± standard error of the mean.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
Animals
There were no significant differences in the animals that made up the study groups. All piglets weighed between 9.2 and 12.0 kg. (cardiopulmonary bypass, 10.5 ± 0.2 kg; longitudinal ventriculotomy, 11.0 ± 0.2 kg; apical ventriculotomy, 10.6 ± 0.4 kg; p > 0.05). Total bypass times for the 3 groups were not significantly different (cardiopulmonary bypass, 50.3 ± 0.8 minutes; longitudinal ventriculotomy, 51.9 ± 2.7 minutes; apical ventriculotomy, 52.9 ± 2.0 minutes; p > 0.05). Left ventricular wall volumes at the conclusion of the study were also not significantly different in the ventriculotomy groups versus the control group (cardiopulmonary bypass, 26.6 ± 0.6 mL; longitudinal ventriculotomy, 27.0 ± 0.6 mL; apical ventriculotomy, 27.0 ± 0.6 mL; p > 0.05).

Hemodynamics
Hemodynamic data before and after cardiopulmonary bypass in all groups is presented in Table 1. There were no significant differences in hemodynamic parameters between the study groups before cardiopulmonary bypass. Cardiopulmonary bypass alone was responsible for an increase in heart rate with decreased stroke volume and cardiac output (p < 0.025). Cardiac output was maintained at control postbypass levels in both ventriculotomy groups, but there were significant hemodynamic alterations. An increase in heart rate was more marked after ventriculotomy in either position (p < 0.001). Longitudinal ventriculotomy was responsible for a significant loss of stroke volume versus cardiopulmonary bypass alone (p < 0.025) and caused a significantly greater decrease in ejection fraction compared with apical ventriculotomy (p = 0.005) (Table 1). At 60 minutes after bypass the end-diastolic pressure was not significantly decreased in any group (cardiopulmonary bypass, 17.8 ± 1.2 mm Hg; longitudinal ventriculotomy, 20.1 ± 1.4 mm Hg; apical ventriculotomy, 19.0 ± 1.1 mm Hg; p > 0.05), yet all groups had a significant loss in end-diastolic volume (p < 0.025) at this pressure indicating a loss in ventricular compliance (Table 1).


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  		Table 1. Hemodynamic Variables Before and After Cardiopulmonary Bypass and Ventriculotomy

 
Contractility
The Frank-Starling relationship between stroke work (SW) and end-diastolic volume (Ved) was linear in all groups at all time points (Table 2a). A representative plot of the stroke work–end-diastolic volume relation is shown in Figure 1. The preload recruitable stroke work relationship as expressed by the slope of SW - Ved (Mw) was unchanged after bypass with or without ventriculotomy (Table 2). When changes in ventricular geometry and heart rate were controlled for by using Mmp, the slope of the relationship between normalized stroke work or myocardial power output and the end-diastolic circumferential strain, the result was also linear (Fig 2); however, all groups had a small but significant increase in Mmp versus baseline after cardiopulmonary bypass (Table 2). There were no significant differences in Mmp between groups at 60 minutes after bypass (p > 0.025).


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  		Table 2. Ventricular Contractility: Preload Recruitable Stroke Work and Myocardial Power Output in Relation to End-Diastolic Volume

 


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  		Fig 1. Preload recruitable stroke work (PRSW) is the global stroke work–end-diastolic volume relation. A representative linear relationship obtained during the course of a single vena caval occlusion is shown. The equation of the regression line is presented. (Lw = x-intercept; Mw = slope of the stroke work–end-diastolic volume relation; R2 = correlation coefficient of the line.)

 


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  		Fig 2. Intrinsic myocardial function relationship. A representative linear relationship between myocardial power output (a derivation of unit myocardial power based on stress-strain relations) and end-diastolic circumferential strain is shown. Data were obtained during a single vena caval occlusion. (Lmp = x-intercept; Mmp = slope of the relationship; MPO = myocardial power output; R2 = correlation coefficient of the line.)

 
Ventricular geometry
Changes in the pattern of ventricular contraction were assessed by examining the fractional shortening during ejection of each axis (Table 3). The importance of the septal freewall axis can be seen in its greater fractional shortening during contraction in all groups at baseline. During ejection the septal free wall axis experienced twice the shortening of either of the other axes and was the major component of volume ejection. After cardiopulmonary bypass, all axes experienced a loss of fractional shortening (p < 0.025) with the exception of the major axis in the longitudinal ventriculotomy group. The creation of a longitudinal ventriculotomy, however, significantly decreased the absolute and fractional shortening of the septal free wall axis beyond that occurring after cardiopulmonary bypass alone or after apical ventriculotomy (p < 0.025 and p < 0.001, respectively). Apical ventriculotomy caused a significant decrease in major axis shortening beyond that seen after cardiopulmonary bypass alone (p = 0.003), but not significantly greater than after longitudinal ventriculotomy (Table 3).


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  		Table 3. Alterations in Axis Shortening After Bypass With and Without Ventriculotomy

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
As early as the 1950s it was recognized that the benefits of a left ventriculotomy in the repair of certain ventricular septal defects could outweigh potential cardiac impairment. Specifically, in the case of low muscular and "Swiss cheese" ventricular septal defects, the atrial or right ventricular approach might be obstructed by the coarse trabeculations of the right ventricle. Warren and associates [9] showed, in dogs, as early as 1958 that left ventriculotomies could be tolerated without significant hemodynamic effects. Other studies followed and determined what type of ventriculotomy, a freewall longitudinal or an apical, would afford better postoperative function [10, 11]. The main factors affecting outcome were acknowledged to be (1) interruption of either the spiral muscle fibers or the concentric ventricular constrictor muscles of the left ventricle or (2) interruption of the coronary blood supply to the myocardium. Richard Lower in 1669 [12] initially described the left ventricular structure as being two layers of spiral-wrapping musclefibers and a central constrictor band. Studies by Rushmer and associates [13] and Grant [14] elicited the fact that in the left ventricle the constrictor musculature plays the dominant role in contraction. Waldhausen and associates [10], in 1964, demonstrated that an apical ventriculotomy interrupted the native coronary supply to the left ventricle less than a longitudinal incision.

In light of these studies, application of left ventriculotomies to the intracardiac repair of ventricular septal defects began with multiple case reports [15–19]. Although survival rates and hemodynamic patterns were generated, only McDaniel and associates [19] directly investigated any index of ventricular function, finding no change in the mean shortening fraction by echocardiography in 4 infants. These studies were limited by low numbers, the absence of specific control groups, and by indirect, low-precision means of evaluating ventricular function.

This study was designed to evaluate changes in the intrinsic function of the left ventricle as well as changes in the efficacy and pattern of contraction. Any assessment of postoperative functional changes must take into account those changes brought about by cardiopulmonary bypass alone. Therefore, a control group underwent cardiopulmonary bypass without ventriculotomy. After cardiopulmonary bypass all groups had a significant decrease in cardiac output. One potential cause this study revealed is that after bypass the left ventricle experiences a significant decrease in compliance as illustrated by decreased end-diastolic volumes producing prebypass end-diastolic pressures. The infant ventricle has been shown to have lower compliance in comparison with adults [20, 21]. Blatchford and associates [3] used uniaxial dimension transducers and showed that after bypass compliance decreases; however, they observed no change in end-diastolic dimension. Furthermore, the loss of compliance was not altered with hypothermia or cardioplegia. As a result of the loss of compliance the ventricles are unable to use increased filling pressures to generate higher preloading and maintain cardiac output in the face of increased afterloads. Blatchford and associates [3] termed this "pressure-recruitable preload". The recognized limitations of volume loading in children after repair of congenital defects is an outcome of this principle. Burrows and associates [22] studied volume-loading curves after congenital defect repairs and showed a downslope in cardiac function at increased filling volumes. However, they saw little change in function within the first 2 to 4 hours postoperatively. Observations in this study made at 1 hour postoperatively would not be invalidated but could be assessed as a best-case scenario with differences in function gaining even greater importance later in the postoperative course.

The animals in this study attempted to compensate for the loss of ventricular filling and stroke volume by increasing heart rate. Although all study groups had increased heart rates, the ventriculotomy groups had rates significantly higher than the control group. Hemodynamics after longitudinal ventriculotomy were further altered, with the longitudinal ventriculotomy group having significantly lower stroke volumes and cardiac outputs than the other groups. Ventriculotomy therefore produces functional losses beyond those attributable to cardiopulmonary bypass alone, with greater functional disturbances occurring after longitudinal ventriculotomy.

Ventricular performance and myocardial contractility changes are unlikely to be the cause of variable postoperative function in the study groups. The parameters describing the preload recruitable stroke work relationship, Mw and Lw, were unchanged after intervention. The relatively fixed preload demonstrated in these hearts limits stroke volume; therefore, stroke work necessary to overcome increased afterload may not be reached (impedance mismatching). As argued by Blatchford and associates [3], this feature of infant ventricles may nullify the inotropic effect one would expect to see after cardiopulmonary bypass. This study also looked at the unit function of the myocardium by using stress-strain relationships and the myocardial power output. A small but significant increase in contractility was demonstrated using this method of evaluation, which divests the influence of ventricular geometry from the calculation of work. The important differentiation in function between groups, therefore, is likely to lie in changes in the geometric patterns of contraction.

A key factor in ventricular function is the relative contributions of the different axes to stroke volume and cardiac output. This study showed that the dominant septal freewall axis is responsible for fully half of the cardiac output as its fractional shortening is twice that of the major or minor axes. Studies in our laboratory have verified this finding in neonatal animals as well. This finding corroborates the importance of the left ventricular constrictor muscles, as noted by Rushmer and associates [13] and Grant [14]. As expected with decreased compliance and ventricular filling, all axes had decreased fractional shortening after cardiopulmonary bypass. Ventriculotomy, however, significantly altered the pattern of change. Apical ventriculotomy produced an additional loss in shortening of the major axis. The functional fallout from this might not be expected to be great, because contraction along the major axis is derived from the less important left ventricular spiral musculature. The performance of a longitudinal ventriculotomy, however, produces additional impairment of fractional shortening of the septal freewall axis, significantly more so than in both the control group and the apical ventriculotomy group. Longitudinal ventriculotomy produces decreased constrictor muscle function and, as seen in the postoperative hemodynamics, additional losses in stroke volume and ejection fraction.

Any use of cardiopulmonary bypass can be expected to have adverse consequences on left ventricular function. When a left ventriculotomy is to be used, additional impairment of ventricular performance in the initial postoperative period is best minimized by using an apical incision.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Rushmer R.F., Franklin D.L., Ellis R.M. Left ventricular dimensions recorded by sonocardiometry. Circ Res 1956;4:684-688.[Abstract/Free Full Text]
  2. Bavaria J.E., Ratcliffe M.B., Gupta K.B., Wenger R.K., Bogen D.K., Edmunds L.H. Changes in left ventricular wall stress during biventricular circulatory assistance. Ann Thorac Surg 1988;45:526-532.[Abstract]
  3. Blatchford J.W., Barragry T.P., Lillehei T.J., Ring W.S. Effects of cardioplegic arrest on left ventricular systolic and diastolic function of the intact neonatal heart. J Thorac Cardiovasc Surg 1994;107:527-535.[Abstract/Free Full Text]
  4. Heinle J., Lodge A., Mault J., Whitaker E., Ungerleider R.M. Geometric modeling of the neonatal left ventricle [Abstract]. J Am Coll Cardiol 1993;21:475A.
  5. Rankin J.S., McHale P.A., Arentzen C.E., Ling D., Greenfield J.C., Anderson R.W. The three-dimensional dynamic geometry of the left ventricle in the conscious dog. Circ Res 1976;39:304-313.[Abstract/Free Full Text]
  6. Glower D.D., Spratt J.A., Snow N.S., et al. Linearity of the Frank-Starling relationship in the intact heart: the concept of preload recruitable stroke work. Circulation 1985;71:994-1009.[Abstract/Free Full Text]
  7. Mirsky I. Review of various theories for the evaluation of left ventricular wall stresses. In: Mirsky I., Ghista D.N., Sandler H., eds. Cardiac mechanics. New York: Wiley, 1974:381-410.
  8. Streeter D.D., Hanna W.T. Engineering mechanics for successive states in canine left ventricular myocardium. Circ Res 1973;33:639-664.[Abstract/Free Full Text]
  9. Warren W.D., Muller W.H., East M., Sosa M. Experimental study of the anatomic and physiologic effects of incisions into the left ventricle. Surg Forum 1958;9:257-261.[Medline]
  10. Waldhausen J.A., Herendeen T., Taybi H. Left ventriculotomy: effects on ventricular function and coronary vessels. Surgery 1964;56:868-873.[Medline]
  11. Replogle R.L., Kundler H., Gross R.E. Left ventricular performance following apical ventriculotomy. Arch Surg 1967;95:892-897.[Abstract/Free Full Text]
  12. Lower R. Tractatus de corde. London, 1669.
  13. Rushmer R.F., Crystal D.K., Wagner C. The functional anatomy of ventricular contraction. Circ Res 1953;1:162-170.[Abstract/Free Full Text]
  14. Grant R.P. Notes on the muscular architecture of the left ventricle. Circulation 1965;32:301-308.[Free Full Text]
  15. Aaron B.L., Lower R.R. Muscular ventricular septal defect repair made easy. Ann Thorac Surg 1975;19:568-570.[Abstract]
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  18. Griffiths S.P., Turi G.K., Ellis K., et al. Muscular ventricular septal defects repaired with left ventriculotomy. Am J Cardiol 1981;48:877-886.[Medline]
  19. McDaniel N., Gutgesell H., Nolan S.P., Kron I.L. Repair of large muscular ventricular septal defects in infants employing left ventriculotomy. Ann Thorac Surg 1989;47:593-594.[Abstract]
  20. Lee J.S., Downing S.E. Left ventricular distensibility in newborn piglets, adult swine, young kittens, and adult cats. Am J Physiol 1974;226:1484-1489.[Free Full Text]
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  22. Burrows F.A., Williams W.G., Teoh K.H., et al. Myocardial performance after repair of congenital cardiac defects in infants and children: response to volume loading. J Thorac Cardiovasc Surg 1988;96:548-556.[Abstract]



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