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Ann Thorac Surg 1996;62:1084-1089
© 1996 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Left Ventricular Mass Regression Early After Aortic Valve Replacement

Divisions of Cardiovascular Surgery, Cardiology, and Anesthesia, Sunnybrook Health Science Centre, University of Toronto, Toronto, Ontario, Canada

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Appendix 1 Acknowledgments References

 
Background. Regression of left ventricular hypertrophy is an important and well-recognized salutary effect of aortic valve replacement. The earliest evidence of left ventricular mass regression after aortic valve replacement and the influence of prosthesis type are not well known, and were the focus of this study.

Methods. Transthoracic echocardiography was used to measure left ventricular mass index preoperatively and before discharge in 57 consecutive patients undergoing isolated aortic valve replacement (with or without coronary artery bypass grafting).

Results. Three patients were excluded from the study because of inability to obtain accurate M-mode echocardiographic images for left ventricular mass measurement preoperatively (1) or postoperatively (2). Of the remaining 54 patients, mechanical bileaflet valves were used in 19, stented tissue bioprostheses were implanted in 15, and a stentless porcine bioprosthesis was chosen for 20. Postoperative echocardiograms were obtained 4.9 ± 2.3 days after aortic valve replacement (range, 2 to 9 days). A two-way repeated-measures analysis of variance demonstrated a significant reduction of left ventricular mass index before discharge (preoperative 141.4 ± 45.2 g/m², postoperative 127.5 ± 32.8 g/m²; p = 0.0005) but no differences between prostheses.

Conclusions. Left ventricular mass regression begins early after aortic valve replacement, probably because of reduction of transvalvular gradients and left ventricular wall stress. At least in the very early postoperative period, the type of prosthesis does not influence the extent of mass regression.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Appendix 1 Acknowledgments References

 
Left ventricular hypertrophy produced by the pressure or volume overload of aortic valve disease is a beneficial adaptation that compensates for high intracavitary pressures [1]. Aortic valve replacement results in a significant reduction of transvalvular gradients [2, 3] and is accompanied by at least partial regression of left ventricular hypertrophy [4–6]. Regression of left ventricular mass after aortic valve replacement may reduce the long-term complications of sudden death and congestive heart failure associated with left ventricular hypertrophy [7–9]. The time course and earliest evidence of significant left ventricular mass regression after aortic valve replacement are controversial and range from 42 ± 7 days [10] to 1 year [11]. Differences in the rates of regression of left ventricular hypertrophy among various prostheses are unknown. This study was designed to assess the extent of left ventricular mass regression at the time of hospital discharge after aortic valve replacement and to evaluate the influence of various aortic valve prostheses on left ventricular hypertrophy.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Appendix 1 Acknowledgments References

 
Patient Population
Fifty-seven consecutive patients undergoing isolated aortic valve replacement (with or without coronary artery bypass grafting) at Sunnybrook Health Science Centre between August 1, 1994 and March 1, 1995 were evaluated prospectively. All clinical and echocardiographic data describing this population were prespecified and collected prospectively. Patients who had implantation of the investigational Toronto Stentless Porcine Valve (SPV) (St. Jude Medical, St. Paul, MN) signed a consent form approved by our Institutional Review Board. The choice of valve prosthesis was made preoperatively after consultations among the cardiac surgeon, cardiologist, and the patient. Clear M-mode imaging of the heart was not possible in 1 patient preoperatively and in 2 patients postoperatively. The remaining 54 patients, in whom measurements were possible, were included in the study.

Operative Technique
Cardiopulmonary bypass was instituted with ascending aortic and two-stage single atrial cannulation. Moderate hemodilution and mild systemic normothermia (>33°C) were used. A left ventricular vent was inserted through the right superior pulmonary vein. Myocardial protection was initiated with a single dose of high-potassium blood cardioplegia through the ascending aortic root to induce cardiac arrest. This was followed by continuous antegrade warm (n = 12) or cold (n = 35) oxygenated blood cardioplegia using direct cannulation of each coronary ostium, or continuous retrograde blood cardioplegia (n = 7).

A transverse aortotomy was performed approximately 5 cm above the aortic annulus. The native aortic valve was excised completely, and the annulus, aorta, and anterior leaflet of the mitral valve were extensively debrided of calcium when it was present. Annular and sinotubular junction sizing of the SPV and conventional valves has been documented previously [12]. All mechanical and stented tissue valves were implanted using interrupted mattress and pledgeted 2-0 Ticron sutures (Davis & Geck, Danbury, CT). All pledgets were placed in the subannular position. In the noncoronary cusp, sutures were placed from outside the aorta to accommodate a larger prosthesis. The insertion technique for the SPV has been reported by our group [12]. The base of the SPV was sutured in the annular position using interrupted single 4-0 Ticron sutures circumferentially. The commissure and sinuses of the SPV were sutured to the aorta using three continuous running 4-0 Prolene sutures (Ethicon, Somerville, NJ). Mechanical valves consisted of CarboMedics (Austin, TX) (n = 16) and St. Jude Medical (St. Paul, MN) (n = 3) valves. Stented tissue bioprostheses consisted of the Hancock II standard (Medtronic Inc, Minneapolis, MN) (n = 9) and the Carpentier-Edwards pericardial (Baxter Healthcare Corp, Irvine, CA) (n = 6) valves.

Measurements
All patients underwent transthoracic echocardiography within 1 week before operation and 1 or 2 days before discharge after aortic valve replacement. Effective orifice area, peak and mean pressure gradients, and left ventricular mass index were measured preoperatively (Appendix 1). Only left ventricular mass index was measured in the early postoperative period. All patients had complete preoperative and postoperative measurements of left ventricular mass, thus allowing paired analysis of the results.

Echocardiographic Studies
A Hewlett-Packard Sonos 1000E (Hewlett-Packard Inc, Palo Alto, CA) with a 2.5-MHz transducer was used for echocardiographic assessment. The examination included 2-dimensional, 2-dimensional derived M-mode, continuous wave and pulsed Doppler, and color Doppler studies. Standard left parasternal, apical, right parasternal, subcostal, and suprasternal views were obtained in a step-by-step successive pattern of interrogation. Left ventricular mass was calculated from 2-dimensional derived M-mode measurements taken according to the American Society of Echocardiography recommendations. Each measurement was averaged from three cardiac cycles in sinus rhythm and six cardiac cycles in atrial fibrillation. The postoperative measurements were made without knowledge of the preoperative values. Only two experienced sonographers with interobserver variability documented at less than 5% were employed for this study.

Statistical Analysis
Postoperative left ventricular mass regression was prespecified as the primary outcome in this study. Two-way repeated-measures analysis of variance was used to assess the influence of time and prosthesis type on left ventricular mass index and left ventricular dimensions. Perioperative demographic characteristics of each prosthesis group were compared using ² test for categoric variables and analysis of variance for continuous variables. Continuous data in the text and tables are presented as mean ± standard deviation; standard error bars are used in the figure.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Appendix 1 Acknowledgments References

 
There were no postoperative deaths. One patient who received an SPV and 2 patients who received a stented tissue valve required an intraaortic balloon pump postoperatively. One patient with an SPV had a transient reversible neurologic deficit postoperatively.

Perioperative clinical variables describing the patient population are given in Table 1. Patients receiving stented tissue valves were older than the other valve groups and tended to have a higher prevalence of coronary artery disease and diabetes preoperatively. Patients who received the SPV had a higher percentage of large valve sizes implanted. The average valve size inserted was 26.6 ± 2.0 mm for the SPV, compared with 24.3 ± 3.1 mm for the stented tissue valves and 23.7 ± 2.1 mm for the mechanical valves (p < 0.05). Effective orifice area, peak pressure gradient, and mean pressure gradient measured preoperatively are shown in Table 2.

View larger version (42K): [in this window] [in a new window]   Fig 1. . Preoperative (preop) and postoperative (postop) left ventricular (LV) mass index for the entire patient population and for each prosthesis group. There was no significant difference among valve prostheses for left ventricular mass index at baseline or at postoperative follow-up. A two-way repeated-measures analysis of variance demonstrated a significant reduction in left ventricular mass index from the preoperative to postoperative periods (p = 0.0005) but no difference among prosthesis groups (p = 0.43). (Echo = echocardiography; SPV = Stentless Porcine Valve.)

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Appendix 1 Acknowledgments References

Importance of Left Ventricular Hypertrophy
The myocardial response to pressure or volume overload imposed by aortic valve disease is left ventricular hypertrophy. Hypertrophy is characterized by a concentric increase in muscle mass to preserve a normal relation between systolic wall stress and ejection fraction [1]. Regression of left ventricular hypertrophy after aortic valve replacement is an important end point. All prosthetic valves are relatively stenotic because the valve sewing ring and stents reduce the effective orifice area. After aortic valve replacement, transvalvular gradients often remain elevated, and left ventricular hypertrophy does not resolve completely [13]. Evidence from the hypertension literature indicates a strong correlation between left ventricular hypertrophy and sudden death, congestive heart failure, myocardial infarction, and cardiovascular mortality [14, 15]. Ghali and associates [16] demonstrated that patients with even moderate left ventricular hypertrophy had a greater risk of death from any cause (even after adjustment for age, sex, coronary artery disease, and hypertension). Concerns about the long-term effects of residual hypertrophy after aortic valve replacement have been raised by various investigators [7–9]. Late deaths after aortic valve replacement are often caused by sudden cardiac arrest, arrhythmias, and congestive heart failure [7–9]. These late events may be caused by or influenced by left ventricular hypertrophy. Left ventricular mass regression after aortic valve replacement may be an important and underestimated determinant of long-term outcome.

Left Ventricular Mass Regression
Echocardiographic mass measurements are noninvasive and reproducible estimates of the extent of left ventricular hypertrophy. M-mode echocardiography has been shown to correlate well with contrast left ventriculography for left ventricular mass measurement. Devereux and Reichek [17] estimated antemortem human left ventricular mass with M-mode echocardiography and compared their values with postmortem mass. They found a good correlation (r = 0.98) between estimated and actual left ventricular mass. Left ventricular mass measurements have been used to demonstrate regression of hypertrophy in experimental [18] and clinical studies [19] of the treatment of hypertension.

Left ventricular mass reflects the severity of aortic stenosis, is positively correlated with peak aortic valve gradients [20], and has been used to confirm at least partial regression of hypertrophy after aortic valve replacement [13]. The extent and time course of left ventricular mass regression after valve replacement remain controversial. Kennedy and colleagues [21] and others [13] used catheterization techniques to assess 11 to 24 patients with preoperative aortic stenosis and reported left ventricular mass regression after aortic valve replacement ranging between 28% and 38% at mean follow-up times ranging from 18 ± 6 to 22 ± 8 months. At later mean follow-up times ranging from 56 ± 23 to 96 ± 31 months, they reported left ventricular mass regression ranging from 47% to 60%. Kurnik and colleagues [4], using ultrafast computed tomography, reported 27% regression of left ventricular mass at 4 months after aortic valve replacement and a total of 36% regression at 8 months. Panidis and associates [11], using echocardiography, demonstrated a nonsignificant 10% regression at less than 6 months and a significant 34% regression at greater than 6 months. However, Henry and associates [6] demonstrated a 16% mass reduction at 6 months after aortic valve replacement for aortic stenosis, with no further changes at 1 year. They observed that most of the regression occurred within the first month after operation. St. John Sutton and associates [10] examined 16 patients by echocardiography and documented a 30% regression of left ventricular mass in 42 ± 7 days, thus confirming that the majority of mass regression occurs early after aortic valve replacement. We have concluded in this study that there is significant left ventricular mass regression of 10% within 4.9 ± 2.4 days of operation. The amount of mass regression actually may have been underestimated. In the early period after aortic valve replacement, there may be substantial edema in the tissues, especially myocardial tissue, and this may artificially increase left ventricular dimensions.

We examined the influence of prosthesis type on the regression of left ventricular hypertrophy after operation. Although patient selection and different valve sizes prevented direct comparisons of the valves in this study, we documented a consistent and similar regression for all three valve types. The reduction in afterload early after aortic valve replacement was more significant than the relatively smaller residual gradient differences among valves, which may account for the similar extent of early left ventricular mass regression. To study differences among valves, mass measurements must be examined at later times. As well, valves should be compared by annulus size, valve type, and aortic lesion. It would be expected that incomplete left ventricular mass regression would be especially evident in small aortic roots. However, evidence of incomplete regression exists even with appropriately large valves. Monrad and associates [13] assessed 11 patients after aortic valve replacement for aortic stenosis and demonstrated that left ventricular mass regressed from 158 ± 33 g/m² preoperatively to 114 ± 27 g/m² at 18 ± 6 months postoperatively, compared with 85 ± 9 g/m² for control patients. The prostheses used in the study by Monrad and associates [13] included two 27-mm tissue valves and nine Bjork-Shiley valves with an average size of 24 ± 4 mm. Pantely and colleagues [5] assessed 10 patients with aortic stenosis who had the relatively obstructive Starr-Edwards mechanical valve implanted, and measured a left ventricular mass index of 123 ± 10 g/m² at 20 months' mean follow-up. However, mass regression after aortic valve replacement is dependent on a host of factors. Persistence of myocardial collagen fibrosis may account for some of the incomplete regression. Age, sex, hypertension, coronary artery disease, left ventricular function, and diabetes also may be determinants of left ventricular mass.

In this study, we have demonstrated that left ventricular mass regression begins early after aortic valve replacement. We have shown that at least in the very early postoperative period, the type of prosthesis does not influence the extent of left ventricular mass regression. The conclusions from this study, however, are restricted by potential limitations of the study design. There was an absence of other hemodynamic correlates such as gradients, valve areas, and left ventricular function. Furthermore, we studied a mix of patients with aortic stenosis and regurgitation as well as various different types and sizes of prostheses. Finally, patient selection was used; this was not a randomized trial. Further studies are necessary to identify the time course and determinants of left ventricular mass regression after aortic valve replacement.

	Appendix 1

Top Footnotes Abstract Introduction Material and Methods Results Comment Appendix 1 Acknowledgments References

 
Calculations
1. EFFECTIVE ORIFICE AREA.
Effective orifice area was calculated by reconfiguration of the continuity equation:

where EOA = effective orifice area in cm²; CSA_LVOT = cross-sectional area of the left ventricular outflow tract in cm² obtained using 2-dimensional measurement of the left ventricular outflow tract diameter; TVI_LVOT = velocity time integral of forward blood flow in cm, derived from the pulsed-wave Doppler study obtained in the left ventricular outflow tract; and TVI_AO = velocity time integral of forward blood flow in cm, derived from the software integration of transvalvular continuous-wave Doppler.

2. PEAK PRESSURE GRADIENT.
Peak velocities, obtained from pulsed-wave and continuous-wave Doppler, were converted to peak pressure gradient using Bernoulli's equation:

where P_PEAK = peak systolic aortic pressure gradient in mm Hg; V₂ = prosthetic peak velocity in m/s, measured with continuous-wave Doppler; and V₁ = peak velocity proximal to valve in m/s, measured with pulsed-wave Doppler.

3. MEAN PRESSURE GRADIENT.
Mean transvalvular pressure gradient was calculated by subtraction of the mean pressure proximal to the valve from the mean distal pressure:

(3)

where P_MEAN = mean transvalvular pressure gradient in mm Hg; P₂ = prosthetic mean pressure measured with continuous-wave Doppler; and P₁ = proximal mean pressure measured with pulsed-wave Doppler in the left ventricular outflow tract.

4. LEFT VENTRICULAR MASS INDEX.
Left ventricular mass was calculated by the ASE cube method:

where LVM = left ventricular mass in g; LVED = left ventricular end-diastolic dimension in cm; IVS = interventricular septal wall thickness in cm; and LVP_WALL = thickness of the left ventricular posterior wall in cm.

Left ventricular mass was indexed by body surface area:

where BSA = body surface area in m².

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Appendix 1 Acknowledgments References

 
This study was supported by grant B2317 from the Heart and Stroke Foundation of Ontario.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Appendix 1 Acknowledgments References

 
Presented at the Poster Session of the Thirty-second Annual Meeting of The Society of Thoracic Surgeons, Orlando, FL, Jan 29–31, 1996.

Address reprint requests to Dr Christakis, Division of Cardiovascular Surgery, Sunnybrook Health Science Centre, 2075 Bayview Ave, H406, Toronto, Ont, Canada M4N 3M5.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Appendix 1 Acknowledgments References

 

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