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Giordano Tasca
Federico Brunelli
Marco Cirillo
Margherita Dalla Tomba
Zen Mhagna
Giovanni Troise
Eugenio Quaini
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Ann Thorac Surg 2005;79:1291-1296
© 2005 The Society of Thoracic Surgeons

Original articles: Cardiovascular

Impact of the Improvement of Valve Area Achieved With Aortic Valve Replacement on the Regression of Left Ventricular Hypertrophy in Patients With Pure Aortic Stenosis

Giordano Tasca, MD*, Federico Brunelli, MD, Marco Cirillo, MD, Margherita Dalla Tomba, MD, Zen Mhagna, MD, Giovanni Troise, MD, Eugenio Quaini, MD

Department of Cardiac Surgery, Poliambulanza Hospital, Brescia, Italy

Accepted for publication September 2, 2004.

* Address reprint requests to Dr Tasca, UF di Cardiochirurgia, Poliambulanza Hospital, Via L. Bissolati 57, 25125 Brescia, Italy (E-mail: cch-segreteria.poli{at}poliambulanza.it).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Previous studies have reported that patient-prosthesis mismatch may be associated with lesser regression of left ventricular hypertrophy. However, among the patients with mismatch, the extent of left ventricular mass regression varied markedly from one patient to another, and we hypothesized that it could be related to the magnitude of the increase in valve area achieved with aortic valve replacement. Our aim was to examine the relationship between the improvement in valve effective orifice area obtained with aortic valve replacement and the extent of postoperative left ventricular mass regression in patients with patient-prosthesis mismatch.

METHODS: Preoperative and postoperative measurements of valve effective orifice area, transvalvular pressure gradient, and left ventricular mass were obtained by Doppler echocardiography in 111 patients with pure aortic stenosis who were found to have patient-prosthesis mismatch based on an indexed effective orifice area of 0.8 cm2/m2 or less after operation.

RESULTS: On average, the valve effective orifice area increased by 0.45 ± 0.24 cm2/m2 with operation, and mean transvalvular pressure gradients decreased by –31.6 ± 13.5 mm Hg. The absolute and relative differences between preoperative and postoperative left ventricular mass were –28 ± 30 g and –17% ± 18%, respectively. In multivariate analysis, higher preoperative left ventricular mass (p < 0.0001) and larger increase in indexed valve effective orifice area with operation (p = 0.019) were independently associated with greater left ventricular mass regression.

CONCLUSIONS: This study shows that in patients with patient-prosthesis mismatch, the degree of left ventricular mass regression is influenced by the increase in valve effective orifice area achieved by aortic valve replacement.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
One of the main objectives of aortic valve replacement (AVR) is to relieve left ventricular (LV) burden and normalize LV mass (LVM). Patients undergoing AVR for pure aortic stenosis often receive a prosthesis that is too small in relation to body size, thus causing the persistence of abnormally high gradients after operation [1–4]. This problem, termed as patient-prosthesis mismatch (PPM), is considered to be present when the prosthetic effective orifice area (EOA) indexed for body surface area is less than 0.8 to 0.9 cm2/m2. Some previous studies have reported that PPM may be associated with lesser regression of LV hypertrophy after AVR [1, 5, 6]. Nonetheless, important variations were observed among patients with PPM with regard to the extent of LVM regression, and a significant proportion of these patients had substantial regression of LV hypertrophy.

Several studies have reported that there is a strong relationship between the transvalvular pressure gradi-ent and the indexed valve EOA [3, 4, 7]. However, it should also be emphasized that this relationship is curvilinear, and when the indexed EOA becomes less than 0.8 to 0.9 cm2/m2, the transvalvular gradient and thus the LV workload increase exponentially. Hence, even a relatively small increase in aortic valve EOA achieved by AVR may result in an important reduction of transvalvular pressure gradients and thus of LV hypertrophy in patients with severe aortic stenosis. To this effect, it should be mentioned that some patients with PPM may nonetheless have a significant improvement in EOA compared with their preoperative value, which, in turn, may result in a marked reduction of transvalvular gradients and LVM. This could explain why some patients with PPM may exhibit substantial regression of LVM despite the fact that their indexed EOA is not completely normalized.

The objective of this study was therefore to determine whether the magnitude of valve EOA increase achieved with AVR may influence LVM regression in patients with pure aortic stenosis undergoing AVR and who were found to have PPM after AVR.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Acknowledgments
 References
 
Patient Population
The study population included 111 patients with pure aortic stenosis who underwent AVR between September 1997 and April 2003 and were found to have PPM based on an indexed EOA being 0.8 cm2/m2 or less after operation.

The exclusion criteria were more than mild aortic regurgitation, associated mitral valve surgery, previous heart surgery, myectomy-myotomy associated with AVR, previous myocardial infarction, and an ejection fraction of less than 0.50. We considered patients with hypertension those who had history of hypertension and were treated, at time of operation, with antihypertensive drugs.

The implanted prostheses were Carpentier-Edwards Perimount (78 cases), Mitroflow (7 cases), Carbomedics Standard (12 cases), Carbomedics Top-Hat (2 cases), Medtronic Free-style (3 cases), and Toronto SPV (9 cases). The prosthesis size was 19 mm in 42 patients (37.8%), 21 mm in 42 patients (37.8%), and 23 mm in 27 patients (24.4%). The patients had a Doppler echocardiographic examination 0 to 7 days before AVR and between 12 and 24 months postoperatively.

Doppler Echocardiographic Measurements
The preoperative and postoperative echocardiographic studies were performed by experienced echocardiographers using an Acuson 128 Computed Sonograph (Acuson, Mountain View, CA) equipped with 2.5- to 3.5-MHz transducers.

The peak and mean valve gradients were calculated using the modified Bernoulli equation with correction for subvalvular velocities. Valve EOA was calculated using the continuity equation and indexed for body surface area. The increase in valve EOA ({Delta}-EOA) achieved by AVR was calculated by subtracting the preoperative value of EOA from its postoperative value and then indexed to body surface area. The reduction of mean and peak transvalvular gradients obtained with AVR was calculated by subtracting the preoperative value from its respective postoperative value.

The dimensions of the LV were assessed using two-dimensionally guided M-mode tracings, with the measurements being made according to the recommendations of the American Society of Echocardiography [8]. If the M-mode recordings were technically inadequate, two-dimensional measurements were used. Left ventricular mass was calculated using the corrected American Society of Echocardiography formula as follows [9]:


{4018302.1291.si1}

where IVSd is the end-diastolic interventricular septum thickness, LVIDd is the LV end-diastolic internal diameter, and PWTd is the LV end-diastolic posterior wall thickness. Left ventricular hypertrophy was defined as an LVM index of greater than 131 g/m2 in men and greater than 100 g/m2 in women [10]. The relative wall thickness (RWT) was calculated using the following formula:


{4018302.1291.si2}

The LV systolic function was evaluated by means of the ejection fraction calculated using Simpson's rule.

Statistical Analysis
The data were statistically analyzed using SPSS 9.0 software (SPSS Inc, Chicago, IL). The continuous variables were expressed as mean ± standard deviation and compared using a two-tailed paired Student's t test. The normality of the distributions was tested by means of the Shapiro-Wilk test, and, when abnormal, the data were log transformed. The variables with a p value less than 0.10 at univariate analysis were entered in a multivariate multiple linear regression analysis to identify the independent predictors of LVM regression. The relationship between absolute LVM index regression and the indexed {Delta}-EOA was evaluated by means of simple linear regression analysis to calculate r (Pearson's correlation coefficient). A p value less than 0.05 was considered significant.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Acknowledgments
 References
 
Preoperative and Operative Data
The patients' preoperative and operative characteristics are shown in Table 1. Sixty-one percent (61%) of the patients were female, 37% had coronary artery disease, and 91% had preoperative LV hypertrophy before operation.


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  		Table 1. Preoperative and Operative Data
 
Aortic Valve Hemodynamics
The time interval between the preoperative and postoperative Doppler echocardiographic examinations was 1.5 ± 0.31 years. The postoperative indexed EOA was relatively small, which is not surprising given that, by definition, all patients included in this study had PPM (Table 2). Nonetheless, the postoperative indexed EOA was significantly (p < 0.0001) higher compared with the preoperative indexed EOA (Table 2). The {Delta}-EOA and indexed {Delta}-EOA were 0.45 ± 0.24 cm2 and 0.26 ± 0.12 cm2/m2, respectively. The postoperative mean and peak transvalvular gradients were 19 ± 6 mm Hg and 32 ± 11 mm Hg, respectively. The changes in mean gradient and in peak gradient were –32 ± 14 mm Hg and –53 ± 22 mm Hg, respectively.


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  		Table 2. Preoperative and Postoperative Aortic Hemodynamic Data
 
Determinants of Left Ventricular Mass Regression
The preoperative and postoperative values of LV dimensions and function are shown in Table 3. Interventricular septum thickness, LV posterior wall thickness, LV internal dimension, LVM, and LVM index decreased significantly after AVR. Absolute LVM index regression was correlated to indexed {Delta}-EOA with r = –0.31, r2 = 10%, and p = 0.001 (Fig 1). In multivariate analysis, larger indexed {Delta}-EOA and higher preoperative LVM were the only factors associated with greater absolute regression of indexed LVM after AVR (Table 4).


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  		Table 3. Preoperative and Postoperative Left Ventricular Dimensions and Function
 


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  		Fig 1. Correlation between absolute left ventricular mass (LVM) index regression and increased indexed effective orifice area (r = –0.31; r2 = 10%; p = 0.001).

 

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  		Table 4. Factors Influencing Left Ventricular Mass Regression After Aortic Valve Replacementa
 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Acknowledgments
 References
 
A large amount of literature is available on the effect of AVR on LV hypertrophy regression. However, there are very few studies that directly address this issue in relation to PPM. In a study including 1103 patients with a porcine bioprosthetic valve, Del Rizzo and colleagues [5] found a strong and independent relationship between the indexed EOA and the extent of LVM regression after AVR. At 3 years after operation, there was a mean decrease in LVM of 23% in patients with an indexed EOA of greater than 0.8 cm2/m2 compared with only 4.5% in those with an indexed EOA of 0.8 cm2/m2 or less (p = 0.0001). In contrast to these results, Hanayama and associates [11] found no significant relationship between PPM and regression of LV hypertrophy. In a recent study, we reported that regression of LVM was significantly lower in patients with PPM (–48 ± 47 g; –17% ± 16%) compared with those with no PPM (–77 ± 49 g; –24% ± 14%) at 1.6 ± 0.3 months after operation [6]. Moreover in multivariate analysis, the indexed EOA, which reflects the degree of PPM, was an independent predictor of LVM regression. When analyzed collectively, these previous studies therefore suggest that PPM may reduce regression of LV hypertrophy after AVR. However, these studies also show that although patients with PPM have, on average, lesser regression of LV hypertrophy, the extent of LVM regression may vary markedly from one patient to another. Hence, some patients with PPM may indeed have substantial regression of LV hypertrophy despite the presence of a relatively high residual transvalvular gradient. The major finding of the present study is that in patients with PPM, regression of LVM is independently influenced by the increase in valve EOA achieved with AVR. In this context, it should be noted that the improvement in valve EOA that is obtained by implantation of a prosthetic valve may vary extensively among patients. The present study demonstrates that a part of the interindividual variability observed among patients with PPM with regard to LVM regression may be explained by the variability of valve EOA increase with AVR.

As previously emphasized the relationship between the indexed EOA and the transvalvular pressure gradients is curvilinear, and the turning point on this curve, ie, the point that separates the steep from the flat portion of the curve, is close to an indexed EOA of 0.8 to 0.9 cm2/m2 [1, 4, 12]. Below this threshold, the curve is steep, and, as a consequence, a small change in valve EOA will result in a major reduction of pressure gradient. Hence, if the indexed EOA is increased, for example, from 0.45 cm2/m2 before operation up to 0.75 cm2/m2 after operation, the gradient will be markedly reduced even if not completely normalized, and this will likely be associated with a significant regression of LVM. However, if the indexed EOA is increased from 0.60 to 0.75 cm2/m2 with AVR, there will be only a minimal change in gradient and thus in LVM. Hence, as suggested in this study, patients with PPM may have different outcomes in terms of normalization of gradient and LVM depending on the extent of EOA improvement that is achieved by AVR. On the other hand, when the postoperative indexed EOA is greater than 0.8 to 0.9 cm2/m2, the indexed EOA–gradient curve is relatively flat and the transvalvular gradients are low both at rest and during exercise regardless of the level of indexed EOA [1, 4, 12]. Hence, the reduction in gradient after AVR will likely be similar when the indexed EOA is increased from 0.6 to 0.9 cm2/m2 compared with the case in which it is increased from 0.6 to 1.5 cm2/m2. Consistent with this hypothesis, Del Rizzo and colleagues [5] found that patients with a postoperative indexed EOA of 0.8 cm2/m2 or less had markedly lower regression of LVM (–4.5%), but there was no difference between the patients with an indexed EOA between 0.8 and 1.0 cm2/m2 (–23%) and those with an indexed EOA greater than 1.0 cm2/m2 (–25%). The ideal objective is thus to obtain an indexed EOA greater than 0.8 to 0.9 cm2/m2 after operation. Even if this minimal objective cannot be reached, the present study suggests that the surgeon should attempt to approach this indexed EOA value to minimize the degree of PPM and promote LVM regression. Castro and coworkers [13] reported that with an appropriate strategy PPM might adequately be avoided. Hence an annulus enlargement or aortic root replacement in patients with severe hypertrophy could provide a valid option. Beyond 0.8 to 0.9 cm2/m2, there is probably not much benefit to be gained because the impact of a further increase in valve EOA will have a minimal effect on the gradient and thus on the LV workload.

Our results are also consistent with the results obtained by Rajappan and colleagues [14] in 22 patients with pure aortic stenosis and normal coronary angiograms evaluated by positron emission tomography before and 1 year after operation. They found that the improvement of myocardial blood flow and coronary vasodilatory reserve after AVR is directly dependent on the improvement of valve EOA that is achieved with AVR. Hence, when implanting a prosthesis the surgeon should attempt to provide the largest possible valve EOA in a given patient because the larger the postoperative EOA, the lower the residual pressure overload imposed on the LV, and the better will be the regression of LVM and the recovery of LV function.

Several studies have reported that significant regression of LVM occurs in patients receiving a small prosthesis [7, 15–17]. This observation should not necessarily be considered as an argument to conclude that PPM has no or little influence on the regression of LVM. First, most of these studies did not directly address the issue of PPM based on the indexed EOA. And to this effect, a small prosthesis may provide an adequate PPM in a small patient, whereas the same prosthesis may be inadequate for a larger patient with higher cardiac output requirement. Second, the fact that there is substantial regression of LVM in patients with a small prosthesis or with PPM does not necessarily mean that the regression is optimal and complete. It is indeed difficult to ascertain what would have been the extent of LVM regression and the recovery of LV function if the patient had received a larger valve EOA and had thus been left with no or minimal residual pressure gradient. Third, the present study demonstrates that the magnitude of valve EOA increase obtained with AVR may independently influence the extent of LVM regression. In this context, it should be considered that a significant proportion of patients with a small prosthesis or with PPM may still have a substantial improvement in valve EOA with AVR and may thus have some benefit in terms of recovery of LVM and function. Our study takes into consideration the improvement in valve EOA achieved by AVR in the analysis of the determinants of LVM regression.

Limitations of the Study
The multivariate model obtained in this study only explains 42% of the variance of LVM regression (Table 4). This suggests that other factors may also influence the regression of LV hypertrophy. The regression of LVM is indeed a complex phenomenon that is influenced by several patient-related and prosthesis-related factors. Incomplete regression of LV hypertrophy after relief of LV pressure overload may be explained by potentially irreversible changes in the hypertrophied myocytes and interstitium owing to longstanding disease [18–20].

In the present study, the time course of the disease before operation was not taken into account in the statistical analysis, but we excluded patients with moderate or severe LV systolic dysfunction in an attempt to attenuate the effect of the irreversible component of LV hypertrophy [21]. Furthermore, nonhemodynamic factors, such as genetic [22, 23], insulin-like growth factor-1 [24], and environmental factors may also be involved in the process of LVM regression [23]. These factors were not measured in this study.

Left ventricular hypertrophy regression largely occurs within the first 2 postoperative years, but could continue more slowly for several years thereafter [25–27]. A longer follow-up of our patients is therefore necessary to determine what is the effect of the improvement in valve EOA with AVR on the long-term changes in LVM.

Most our patients had a history of hypertension without specific information about its degree. Although in multivariate analysis the p value was not significant, hypertension could have had a significant influence on the degree of LVM regression.

Conclusion
This study shows that in patients with PPM, the extent of LVM regression is independently influenced by the increase in valve EOA achieved by AVR. These findings further underline the importance of implanting a prosthesis with the largest possible EOA in a given patient.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
References
 
We are grateful to Prof Philippe Pibarot for his contribution in the preparation of the manuscript.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

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