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Ann Thorac Surg 1996;62:756-761
© 1996 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Effects of Valve Replacement on Ventricular Mechanics in Mitral Regurgitation and Aortic Stenosis

David H. Harpole, Jr, MD, Stanley A. Gall, Jr, MD, Walter G. Wolfe, MD, J. Scott Rankin, MD, Robert H. Jones, MD

Division of Thoracic Surgery, Duke University Medical Center, Durham, North Carolina

Accepted for publication April 26, 1996.


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background. This study in humans assessed changes in left ventricular function early and late after correction of mitral regurgitation (MR) (n = 9) or aortic stenosis (AS) (n = 10).

Methods. Ventricular function was measured with radionuclide and micromanometer-derived pressure–volume loops during preload manipulation, thermodilution cardiac outputs, and echocardiograms. Late radionuclide and echocardiographic data were acquired at 24 hours and 20 months.

Results. Perioperative left ventricular performance (stroke work–end-diastolic volume relationship) did not change for patients with MR or AS. Significant changes in afterload occurred: ejection fraction (MR, 0.49 to 0.37; AS, 0.54 to 0.60; both, p= 0.013), mean left ventricular ejection pressure (MR, 73 to 91 mm Hg; AS, 138 to 93 mm Hg; both, p < 0.01), and end-systolic wall stress (MR, 26 to 42 x 103 dynes/cm2; AS, 37 to 22 x 103 dynes/cm2; both, p < 0.01). Ejection efficiency improved for MR patients (0.69 ± 0.26 to 1.0 ± 0.15; p < 0.05). The 20-month data showed improved New York Heart Association functional class, normal resting ejection fraction, and normal exercise response for both groups.

Conclusions.Early after operation, a significant change in left ventricular load was seen with correction of MR and AS. Data obtained late after operation showed improvement consistent with ventricular remodeling.


   Introduction
Top
 Footnotes
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Surgical correction of hemodynamically significant stenotic or regurgitant valvular lesions can be accompanied by changes in left ventricular function. Simple global measures of ventricular function such as ejection fraction, mean ejection pressure, and rate of rise of left ventricular pressure are confounded by the major loading alterations induced by cardiac valve replacement. Earlier work from our institution [1] described a method for load-independent evaluation of left ventricular function that used serially recorded pressure–volume loops before and immediately after cardiopulmonary bypass. However, effects on mechanical or pump efficiency and late follow-up data were not acquired. Therefore, the purpose of this project was to evaluate more completely changes in left ventricular loading that occur after correction of valvular lesions. The emphasis was on the effects of mechanical pump efficiency and myocardial remodeling on ventricular performance late after operation.


   Material and Methods
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
This study was approved by the institutional review board, and written informed consent was obtained from all participants.

Study Population
The study group consisted of 9 consecutive patients with 4+ degenerative mitral regurgitation (MR), and 10 consecutive patients with severe calcific aortic stenosis (AS) (mean aortic valve gradient, 55 ± 14 mm Hg; aortic valve area, 0.64 ± 0.12 cm2). There were 11 men and 8 women with a mean age of 65 ± 9 years. Fifteen patients had New York Heart Association functional class III or IV congestive heart failure. Seven of the AS patients were in Canadian Heart Association angina class III or IV. No patient had had a prior myocardial infarction or previous cardiac operation. All patients underwent coronary angiography and ventriculography. None of the MR patients had severe coronary artery disease. Four AS patients had coronary artery disease in one vessel without wall motion abnormalities. Minimal to moderate (1 to 2+) MR was seen in 4 patients with AS, whereas no patient had more than 1+ aortic insufficiency. All patients were in sinus rhythm.

Experimental Design
Anesthesia was induced with intravenous administration of fentanyl and midazolam hydrochloride. The cardiopulmonary bypass circuit consisted of bicaval venous return for mitral valve replacement and a single venous return cannula for aortic valve replacement. Standard aortic cannulation was used in all patients. A 3F high-fidelity micromanometer (Millar, Inc, Houston, TX) was electrically calibrated and inserted into the left ventricle using a transseptal approach. A Scinticor gamma camera (Scinticor, Inc, Milwaukee, WI) enclosed in a sterile sheath was positioned over the heart. The addition or withdrawal of blood through the aortic cannula achieved several steady-state levels of varied intravascular volume. An initial-transit radionuclide angiocardiogram was acquired during each steady-state period. During acquisition of radionuclide angiocardiographic (RNA) data, two-dimensional transesophageal echocardiograms (Hewlett-Packard, Inc, Sunnyvale, CA) in both the long-axis four-chamber and midpapillary short-axis views were also recorded, as were thermodilution cardiac outputs. Cardiopulmonary bypass was then initiated at a calculated flow rate of 2.0 L•min-1•m-2 and a temperature of 24° to 28°C. Topical cooling consisted of iced saline slush, and 700 to 1,200 mL of 4°C potassium crystalloid cardioplegia was infused after aortic cross-clamping to keep myocardial temperature lower than 15°C.

None of the MR patients were considered candidates for valve repair because of the severe degeneration present. Mitral valve replacement consisted of complete excision of the anterior mitral leaflet and preservation of the posterior leaflet [2]. Aortic valve replacement was undertaken with instillation of cardioplegia directly into the coronary ostia, and concurrent aortocoronary bypass grafting was done in 4 patients. The heart was electrically defibrillated if a spontaneous rhythm did not occur after adequate rewarming. Epicardial atrial and ventricular pacing electrodes were placed. Pacing was begun when needed to obtain heart rates equivalent to those seen before bypass. Cardiopulmonary bypass was stopped when a rectal temperature of 36°C was achieved, usually 10 minutes after removal of the aortic cross-clamp. The echocardiographic and RNA studies at varied intravascular volumes were then repeated. Twenty-four hours postoperatively, each patient had a single repeat RNA study in the intensive care unit after endotracheal extubation and discontinuation of intravenous medications.

From 18 to 24 months (mean time, 20 months) after operation, follow-up data comprising echocardiography and Bruce protocol treadmill test with rest and exercise initial-transit radionuclide angiocardiography were acquired.

Radionuclide Angiocardiography
Initial-transit radionuclide angiocardiograms were acquired at 20-millisecond intervals using the Scinticor multicrystal gamma camera. Ten millicuries of technetium 99m–labeled diethylenetriamine pentaacetic acid was injected as a single bolus through an internal jugular vein Teflon catheter with a data acquisition time of 15 to 20 seconds for each study. Scinticor software calculated heart rate, cardiac output, left ventricular ejection fraction, left ventricular end-diastolic volume, and end-systolic volume. The accuracy and reproducibility of these measurements have been previously reported [3]. High-fidelity left ventricular pressure data were digitized and recorded with each 20-millisecond radionuclide image. From these data, pressure–volume loops representing an average cardiac cycle were constructed [3].

Two-Dimensional Echocardiography
Two-dimensional echocardiograms were obtained early and late after operation using a 5-mHz transesophageal Hewlett-Packard echocardiographic probe intraoperatively and a transthoracic 5-mHz short-focus probe postoperatively. Echocardiographic images recorded on videotape included left ventricular long-axis and left ventricular midpapillary muscle short-axis views. Epicardial and endocardial short-axis cross-sectional areas were measured along with the long-axis dimensions at end-diastole and end-systole. The average of systolic and diastolic wall volumes as determined by the following equation was taken as the left ventricular wall volume [4]: wall volume = (EpiSAA x EpiLA) - (EndoSAA x EndoLA), where EpiSAA = left ventricular epicardial short-axis area, EpiLA = left ventricular epicardial long-axis dimension, EndoSAA = left ventricular endocardial short-axis area, and EndoLA = left ventricular endocardial long-axis dimension. Left ventricular end-systolic meridional wall stress (103 dynes/cm2) was estimated for each patient before and after the valve operation with this equation [5, 6]: wall stress = [(0.334 x LVESD) x LVEDP]/[h x (1 + h/LVESD)], where LVESD = left ventricular end-systolic dimension, LVEDP = left ventricular end-diastolic pressure, and h = end-systolic wall thickness.

Left Ventricular Performance
To evaluate ventricular performance, serial pressure–volume loops obtained before and after each valve replacement were analyzed for left ventricular end-diastolic volume and stroke work (SW): SW = P x dV, where P = left ventricular pressure, and dV = the derivative of RNA left ventricular volume.

The preload-recruitable SW relationship coordinates for each pressure–volume loop were plotted before and after the procedure and the data fit to the following equation: SW = Mw (V0 - Vedv) where V0 = x-intercept, Vedv = left ventricular end-diastolic volume for each pressure–volume loop, and MW = slope of linear regression of discrete pressure-volume measurements [7–9].

Mechanical Efficiency
Mechanical efficiency was estimated for MR and AS patients using the relationship of forward SW (thermodilution stroke volume times mean left ventricular ejection pressure) and RNA left ventricular volumetric SW before and after valve replacement. For both MR and AS patients after operation, the forward and volumetric SW measurements would be similar (efficiency = 1.0). Therefore, linear regression analysis was used to define a constant for each patient that correlated the postoperative values to normalize values from two different techniques. This constant was used to compare the measurements before valve replacement for inefficiency [10].

Statistical Analysis
Significance of change was estimated for each variable measured before and after the valve procedure using Student's paired t test and analysis of variance with the level of significance at 0.05. All data are presented as the mean ± the standard deviation. Perioperative preload-dependent variables were compared at matched end-diastolic volumes.


   Results
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
All patients tolerated the surgical procedure well, and no major perioperative complications occurred. No patient had perioperative myocardial ischemia measured by electrocardiogram, cardiac isoenzymes, or RNA wall motion changes. One AS patient who had concomitant cerebrovascular disease died 7 days after operation of a cerebral infarction, for a 30-day mortality rate of 5%.

Total cardiopulmonary bypass and aortic cross-clamp times were not significantly different for the two groups of patients (Table 1Go). The mean preload range obtained from the four to five RNA studies before and after the valve procedure was 11 to 23 mm Hg for left ventricular end-diastolic pressure and 137 to 190 mL for end-diastolic volume (see Table 1Go). Heart rhythm was normal sinus for all patients before the procedure, and no patient was on a regimen of digoxin. Other oral agents that might have interfered with results (eg, ß antagonists) were discontinued 1 week prior to operation. Care was taken to match hemodynamic data (heart rate, blood pressure, preload range) obtained before and after bypass. An atrially conducted rhythm was present in 16 of the 19 patients for the 10-minute postbypass studies, and the remaining 3 patients required A/V sequential pacing for atrioventricular synchrony. Average heart rate increased insignificantly from 78 beats/min before bypass to 88 beats/min after the procedure. No patient required therapeutic inotropic support, defined as more than 3 µg•kg-1•min-1 of dopamine hydrochloride (renal dose dopamine), and cardiac depressants such as inhaled anesthetic agents and ß blockers were specifically avoided during the study period.


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  		Table 1. . Cardiopulmonary Bypass Time and Preload Range for Intraoperative Studies Variable
 
Data obtained early after operation revealed no significant change in left ventricular wall volume index (MR, 152 ± 41 to 161 ± 47 mL/m2; AS, 156 ± 38 to 160 ± 33 mL/m2). Afterload changes were measured for both MR and AS patients. Mean left ventricular ejection fraction decreased from 0.44 ± 0.12 to 0.34 ± 0.09 for the MR group (p < 0.01) and increased from 0.51 ± 0.13 to 0.56 ± 0.11 (p < 0.01) for the AS group. Left ventricular end-systolic meridional wall stress changed in both groups (MR, 26 ± 13 to 42 ± 21 103 dynes/cm2, AS, 37 ± 15 to 22 ± 7 103 dynes/cm2; both, p < 0.01). Mean left ventricular ejection pressure increased in MR patients (72.7 ± 9 to 91 ± 21 mm Hg; p < 0.001), and a significant decrease was observed in AS patients (131 ± 39 to 91 ± 23 mm Hg; p < 0.001). These results are demonstrated in Figure 1Go.



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  		Fig 1. . (A) Mean ejection pressure demonstrated a significant increase in left ventricular (LV) afterload 10 minutes after mitral valve replacement in patients with mitral regurgitation (MR), whereas total ejection fraction was diminished. (B) Mean ejection pressure demonstrated a significant decrease in afterload after aortic valve replacement in patients with aortic stenosis (AS). Left ventricular ejection fraction improved after valve replacement.

 
Performance Data
The SW–end diastolic volume relationship for each patient before and after operation was highly linear (mean r = 0.98). No significant perioperative change occurred in the preload-recruitable SW relationship for patients with MR (slope, 8.4 ± 2.3 x 104 to 7.8 ± 3.3 x 104 ergs/mL; x-intercept, 84 ± 19 to 64 ± 31 mL) or AS (slope, 18.5 ± 8.1 x 104 to 14.0 ± 5.7 x 104 ergs/mL; x-intercept, 67 ± 32 to 63 ± 14 mL). There were also no differences in the SW–end diastolic volume relationship comparing patients with and without concomitant aortocoronary bypass grafting or patients separated by cardiac rhythm after bypass.

Mechanical Efficiency
Data from MR patients revealed a decrease in the volumetric cardiac output (7.3 ± 2.1 to 5.4 ± 1.5 L/min; p < 0.05) and an increase in the thermodilution cardiac output (3.4 ± 1.3 to 4.5 ± 1.2 L/min; p < 0.05). Patients with AS increased both volumetric (6.0 ± 1.3 to 6.9 ± 1.3 L/min; p = 0.1) and thermodilution (4.6 ± 1.0 to 5.9 ± 1.3 L/min; p < 0.05) outputs. Mechanical efficiency, or the ratio of forward SW to total SW, was significantly increased after valve replacement for MR patients (0.69 ± 0.26 to 1.01 ± 0.15; p < 0.05). Mechanical efficiency did not change for AS patients (0.93 ± 0.20 to 1.05 ± 0.12) (Fig 2Go).



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  		Fig 2. . (A) Total cardiac output (CO), forward CO, and mechanical pump efficiency were all significantly affected by mitral valve replacement for mitral regurgitation (MR). (B) After aortic valve replacement for aortic stenosis (AS), mechanical pump efficiency was not affected because there was a proportional increase in both forward and total COs. (NS = not significant.)

 
Follow-up Data
Early follow-up data obtained after endotracheal extubation and discontinuation of intravenous medications 24 hours after operation revealed no change in mean heart rate compared with data obtained 10 minutes after bypass. Left ventricular ejection fraction measured immediately after the valve procedure was maintained for both MR and AS patients (Table 2Go). All patients were in sinus rhythm at hospital discharge.


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  		Table 2. . Follow-up Data
 
A mean of 20 months after operation (range, 18 to 24 months), there were four deaths evenly distributed between the AS and MR groups. In the MR group, 1 patient had development of a dilated cardiomyopathy 8 months after mitral valve replacement, and 1 patient died of septicemia 5 months after hospital discharge. One patient with AS died 7 days postoperatively and a second patient with AS died 4 months after operation of an aspiration pneumonia without evidence of congestive heart failure. At a mean of 20 months after operation, the remaining 15 patients were evaluated by physical examination, transthoracic echocardiography, and rest and exercise radionuclide angiocardiography (n = 14). All surviving patients were found to have a significantly improved New York Heart Association functional class (Fig 3Go). All 15 patients were in sinus rhythm, and no patient was on a regimen of digoxin or ß antagonists.



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  		Fig 3. . (A) New York Heart Association (NYHA) functional class before and 20 months after operation demonstrated significant improvement for the surviving patients in the mitral regurgitation (MR) group. There was an increase in left ventricular ejection fraction (LVEF) at follow-up and a normal exercise response. (B) New York Heart Association functional class before and 20 months after operation demonstrated significant improvement for the surviving patients in the aortic stenosis (AS) group. There was maintenance of a normal LVEF at follow-up and a nearly normal exercise response. (NS = not significant.)

 
Follow-up RNA data demonstrated an improved left ventricular ejection fraction (from 0.41 24 hours after operation to 0.54; p < 0.05) and a decreased end-diastolic volume (from 166 to 125 mL; p < 0.01) for the MR patients (see Table 2Go). A normal rest to exercise response was observed in this group. The AS patients maintained a normal resting ejection fraction with a decrease in heart rate (from 95 to 72 bpm; p < 0.01) and no change in end-diastolic volume (see Fig 3Go). Exercise data for AS patients were also normal (see Table 2Go). The Bruce protocol exercise treadmill data revealed an adequate heart rate increase (76 to 130; p < 0.001), with no evidence of myocardial ischemia on 12-lead electrocardiograms in any surviving patient. Fatigue was the reason for ending exercise testing in all patients.

When data were regrouped for the entire study and reanalyzed for living patients only, no difference in results was obtained for patients with MR or AS. Estimated echocardiographic ventricular performance was normal or nearly normal in all instances, and no significant (>2+) mitral or aortic regurgitation was seen. Of note, no significant wall motion abnormalities were observed using radionuclide angiocardiography (n = 14) and echocardiography (n = 15), but long-axis and short-axis echocardiographic images were inadequate for accurate analysis of wall volume.


   Comment
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
This project was designed to measure left ventricular performance early and late after significant load alterations induced by mitral or aortic valve replacement in humans. Volume overload (MR) and pressure overload (AS) were chosen. Initial-transit radionuclide angiocardiograms were recorded simultaneously with micromanometer-derived left ventricular pressure, two-dimensional echocardiograms, and thermodilution cardiac outputs to quantify left ventricular performance and mechanical efficiency. All cardiodepressant or therapeutic inotropic medications were avoided during the study to allow longitudinal analysis.

It is the practice at our institution to repair all mitral valves if anatomically possible. However, these patients had severe MR as a result of substantial long-term degeneration of the valvular apparatus, and they were not candidates for a valve repair procedure. The posterior mitral apparatus was left intact in all patients to preserve a more normal ventricular systolic geometry [11–13]. The AS patients had calcific degeneration requiring valve replacement. Four of them underwent concomitant aortocoronary bypass grafting of a single vessel. This added procedure did not have a major impact on short-term or long-term results.

No intraoperative deaths occurred, and there was one 30-day death (mortality rate, 5%) from known cerebrovascular disease. A total of 4 patients died in the follow-up period, for an overall 2-year survival rate of 74%. These results are comparable with those published in the literature [14, 15]. Late after valve operation, echocardiograms and Bruce protocol treadmill testing with rest and exercise RNA data were acquired to measure changes in function secondary to ventricular remodeling. Transesophageal echocardiographic left ventricular wall thickness and wall mass measurements were significantly elevated for both groups of patients, findings consistent with advanced eccentric hypertrophy caused by volume overload in MR and concentric hypertrophy caused by pressure overload in AS. The 20-month echocardiographic images were obtained in an attempt to measure any regression of hypertrophy. However, these images were acquired using a transthoracic technique and were not of sufficient quality for an accurate assessment of ventricular wall volume.

Spratt and colleagues [10] created a left ventricular–left atrial shunt in conscious dogs to simulate chronic MR with a regurgitant fraction of 0.20 to 0.40. Animals were studied after creation of congestive heart failure with data acquired before and after shunt closure, mimicking a valve replacement. Left ventricular afterload significantly increased, resulting in a significant decrease in total SW after shunt closure. However, mechanical efficiency increased from 0.62 to 1.0 (p < 0.01). Our data in humans recorded angiocardiographic pressure–volume loops with simultaneous two-dimensional echocardiograms and thermodilution cardiac outputs before and after valve replacement for MR. A change in mechanical efficiency similar to that seen by Spratt and colleagues was observed with correction of MR, whereas no change in AS patients verified an absence of major aortic insufficiency.

The 10 patients with pressure-overloaded left ventricles (AS) had a significant decrease in left ventricular load after valve replacement without a significant change in ventricular performance. There was a slight decrease in the slope of the SW–end-diastolic volume relationship for several patients with a large measured ventricular mass, possibly signifying reversible ischemia of the subendocardium caused by inadequate myocardial protection. Newer methods of blood cardioplegia with antegrade and retrograde delivery may correct these changes. However, the absence of a shift in the volume intercept of the SW–end-diastolic volume relationship tends to exclude severe ischemic injury as the underlying mechanism.

Longitudinal alterations in ventricular function were assessed by RNA and echocardiographic data recorded both at 24 hours and 20 months after operation. Compared with data obtained 10 minutes after operation, data acquired 1 day after operation and endotracheal extubation demonstrated no significant change in afterload or performance. This suggests that a new baseline of function had been reached early after valve replacement. Both patient groups had improved New York Heart Association functional class and exercise tolerance 20 months after operation. Interestingly, the 4 patients who died late after operation had an initial resting ejection fraction lower than 0.40 and substantial congestive heart failure (New York Heart Association functional class IV).

Although the MR group tolerated valve replacement well, the immediate postbypass increase in afterload may predispose to diminished ventricular function if overdistention occurs in an already dilated, eccentrically hypertrophied ventricle. Spinale and co-workers [16] measured increased cardiac myocyte size, decreased fibril content, and decreased myocyte length in dogs after 3 months of chronic MR. Three months after mitral valve replacement, normal fibril content and length were observed, whereas myocyte size remained significantly larger than control measurements. Barbosa and Barbosa [17] noted a significant decrease in the cardiothoracic ratio and in the epicardial end-diastolic dimensions measured 3.6 years after valve replacement for MR in 74 patients, which suggested late regression of hypertrophy. These two studies define anatomic and ultrastructural changes in the ventricle that explain the improved function we observed late after operation for MR.

After correction of the pressure-overload lesion (AS) with valve replacement, performance was maintained in the normal range. Krayenbuehl and colleagues [18] restudied 49 patients with AS 22 months after valve replacement and observed no change in measured myocardial fibrosis and a significant decrease in myocardial biopsy–measured myofiber diameter and angiographically measured ventricular muscle mass, supporting regression of hypertrophy. Kurnik and co-workers [19] measured left ventricular mass before and 8 months after valve replacement for AS in 17 patients using ultrafast computed tomography. They observed a significant decrease in ventricular mass and an improved New York Heart Association functional class in these patients. These data suggest that the measured normal rest and exercise function observed at 20 months in our patients with AS may have been due to regression of hypertrophy and normalization of ventricular geometry.


   Acknowledgments
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
This work was supported in part by grants HL17670, HL09315, and HL29436 from The National Institutes of Health.

We thank Katherine Kisslo, RMDS, from the Department of Medicine for acquiring the echocardiographic data and L. Richard Smith, PhD, from the Division of Biometry and Medical Informatics for the statistical analyses. We also thank Mary Sullivan Visciano for editorial assistance.


   Footnotes
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 Footnotes
Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Address reprint requests to Dr Harpole, Division of Thoracic Surgery, Duke University Medical Center, DUMC-3617, Durham, NC 27710.


   References
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Harpole DH, Rankin JS, Wolfe WG, et al. Efficacy of crystalloid cardioplegia in preserving left ventricular function during cardiac valvular operations. Circulation 1989;80(Suppl 3):1–9.[Abstract/Free Full Text]
  2. Lillehei CW, Levy MJ, Bonnabeau RC. Mitral valve replacement with preservation of papillary muscles and chordae tendineae. J Thorac Cardiovasc Surg 1964;47:532–43.[Medline]
  3. Harpole DH, Skelton TN, Davidson CJ, Jones RH, Bashore TM. Validation of pressure volume data in patients using first-pass radionuclide angiocardiography. Am Heart J 1989;118:983–9.[Medline]
  4. Feneley MP, Gaynor JW, Maier GW, et al. In vivo estimation of left ventricular wall volume in volume-overloaded canine hearts. Am J Physiol 1988;255:1399–1404.
  5. Grossman W, Jones D, McLaurin LP. Wall stress and patterns of hypertrophy in the human ventricle. J Clin Invest 1975;56:56–61.[Medline]
  6. DePace NL, Ren JG, Iskandrian AS, et al. Correlation of echocardiographic wall stress and left ventricular pressure and function in aortic stenosis. Circulation 1983;67:854–9.[Abstract/Free Full Text]
  7. Sagawa K, Suga H, Shoukas AA, Bakalar KM. End-systolic pressure/volume ratio: a new index of ventricular contractility. Am J Cardiol 1977;40:748–55.[Medline]
  8. Spratt JA, Tyson GS, Glower DD, et al. The end-systolic pressure-volume relationship in conscious dogs. Circulation 1987;75:1295–304.[Abstract/Free Full Text]
  9. Glower DD, Spratt JA, Snow ND, 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]
  10. Spratt JA, Olsen CO, Tyson GS, et al. Experimental mitral regurgitation. J Thorac Cardiovasc Surg 1983;86:479–89.[Abstract]
  11. Ghosh PK, Shah S, Das A, et al. Early evidence of beneficial effects of chordal preservation in mitral valve replacement on left ventricular dimensions. Eur J Cardio-thorac Surg 1992;6:655–9.[Abstract/Free Full Text]
  12. Ishihara K, Zile MR, Kanazawa S. Left ventricular mechanics and myocyte function after correction of experimental chronic mitral regurgitation by combined mitral valve replacement and preservation of the native mitral apparatus. Circulation 1992;86(Suppl 2):16–25.
  13. Okita Y, Miki S, Ueda Y, et al. Comparative evaluation of left ventricular performance after mitral valve repair or replacement with or without chordal preservation. J Heart Valve Dis 1993;2:159–66.[Medline]
  14. Morris JJ, Schaff HV, Mullany CJ, et al. Determinants of survival and recovery of left ventricular function after aortic valve replacement. Ann Thorac Surg 1993;56:22–30.[Abstract/Free Full Text]
  15. Delahaye JP, de Gevigney G, Gare JP. Results of surgery in mitral valve insufficiency with impaired left ventricular function. Arch Mal Coeur Vaiss 1991;84:19–24.[Medline]
  16. Spinale FG, Ishihara K, Zile M, et al. Structural basis for changes in left ventricular function and geometry because of chronic mitral regurgitation and after correction of volume overload. J Thorac Cardiovasc Surg 1993;106:1147–57.[Abstract]
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