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Eur J Cardiothorac Surg 2005;27:441-449
© 2005 Elsevier Science NL
Universitary General Hospital of Valencia, Av. Tres Cruces s/n, C/ Artes Gráficas n°4, esc. izq. pta. 3, 46014 Valencia, Spain
Received 11 September 2004; received in revised form 3 November 2004; accepted 22 November 2004.
* Corresponding author. Tel.: +34 96 3622216; fax: +34 96 197 2163. (E-mail: rgfuster{at}terra.com).
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Abstract |
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 Top Abstract 1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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0.85cm2/m2). The influence of high degrees of preoperative left ventricular mass on in-hospital mortality has also been evaluated. Left ventricular mass index was considered increased if the calculated value was over the superior quartile of the frequency distribution of all the values observed in both sexes. Results: Mismatch was found in 38% of the patients. In the absence of mismatch, the absolute mass regression was proportional to the preoperative left ventricular mass. This regression was higher in patients with increased left ventricular mass indexed (vs not increased): –38.0±7.8 vs –8.8±4.7g/m2, p<0.01 (1st month) and –67.7±16.9vs –23.5±6.7g/m2, p<0.05 (1st year). Mass regression was impaired in the presence of mismatch, particularly, in patients with previously increased left ventricular mass: –8.2±11.6 vs –5.6±6.3g/m2 (p=0.83) and –24.6±12.6 vs –11.7±10.5g/m2 (p=0.54). This worse regression was reflected on a 100% incidence of residual hypertrophy at follow-up (1st month-1st year). In the presence of mismatch, increased ventricular mass was associated with higher mortality: 14.7% vs 2.1% (p<0.01). In the absence of mismatch, ventricular mass was not associated with mortality: 4.1 vs 2.5% (p=0.55). Conclusions: In patients with severe ventricular hypertrophy it may be important to elude patient-prosthesis mismatch to avoid a significant increase in mortality and improve ventricular mass regression. Mismatch may be tolerable in those patients with lesser degree of hypertrophy.
Key Words: Aortic stenosis • Aortic valve replacement • In-hospital mortality
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1. Introduction |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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The degree of preoperative left ventricular hypertrophy may also play an important role on this mortality. Several studies have reported the early and late prognostic importance of preoperatively increased left ventricular mass index (LVMI) in aortic valve surgery [6,7]. As PPM is also a predictor of mortality and it can be responsible for postoperative high transvalvular pressure gradients and impairment of left ventricular mass regression, the influence of severe preoperative left ventricular hypertrophy on patients with PPM may be of relevance in aortic valve replacement. Unlike left ventricular dysfunction, preoperative ventricular hypertrophy has seldom been addressed as a prognostic factor in relation to PPM. So, the aim of our study was to determine whether PPM is always tolerable in our current practice and the potential influence of a previous increased LVMI on aortic valve replacement outcomes in the presence of PPM.
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2. Materials and methods |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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2.2. Echocardiography
Preoperative 2D and Doppler echocardiographic assessment was performed in all patients. Postoperative evaluation was obtained in 312 patients at 1st month and in 190 patients at least one echocardiogram was performed between 6 months and one year postoperatively (median: 10 months, interquartile range: 7–11 months). Most of echocardiographic data were collected from the Section of Echocardiography database in our hospital.
Diastolic measurements of left ventricular internal diameter (LVID), interventricular septal thickness (IVST) and posterior wall thickness (PWT) (in millimeters) were used to calculate LVMI by means of the formula described by Devereux and colleagues [8,9]:
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These measurements were calculated by M-mode guided by 2D echocardiography. According to this author, LVMI was considered as increased if greater than 134g/m2 in men and greater than 110g/m2 in women.
Postoperative residual left ventricular hypertrophy was also defined as a LVMI higher than 134g/m2 in males and higher than 110g/m2 in females. But for the purpose of our study, we have evaluated the influence of higher degrees of preoperative LVMI on in-hospital mortality and a higher cut-off point of LVMI values was considered, dividing the global group of patients into two subgroups: with and without significant increased LVMI. This cut-off point was established at the first value of the superior quartile of the frequency distribution of LVMI values in both sexes. Thus, according to this value, preoperative increased LVMI was present when LVMI was >226g/m2 in males and >216g/m2 in females.
Combined wall thickness was considered as the sum of IVST and PWT and relative wall thickness as the ratio of Combined Wall Thickness to LVID.
Left ventricular ejection fraction (LVEF) was calculated by 2D echocardiography with Simpson's method. Aortic valve hemodynamics were assessed by Doppler echocardiographic examination. The left ventricular outflow tract area was calculated from the diameter of the outflow tract measured from a two-dimensional image in early systole. Flow velocities in the outflow tract (2.5-MHz pulsed Doppler) were recorded from an apical long-axis view, and the maximal instantaneous aortic valve gradient was calculated from the peak aortic Doppler velocity by the modified Bernoulli equation. Mean aortic pressure gradient and time velocity integral of the aortic and left ventricular outflow tract flow velocities were measured. The velocity-time integral of blood flow in the left ventricular outflow tract was determined to give stroke distance. Left ventricular stroke volume was thus calculated from the product of stroke distance with outflow tract cross-sectional area. Thereafter, aortic valve area was calculated with the continuity equation (stroke volume divided by valve flow velocity–time integral as determined by continuous-wave Doppler). The postoperative effective orifice area (EOA) of the aortic prosthesis was calculated by the continuity equation and then indexed to body surface area to assess the presence of PPM.
Of the 339 patients, 222 (65.5%) had preoperative coronary angiography. All angiographies revealed absence of significant coronary artery disease.
2.3. Operative technique
All surgical records were reviewed to determine the type and size of aortic valve prosthesis, the surgical procedure performed, the cardioplegic technique employed and cross-clamp and cardiopulmonary bypass (CPB) times. Operations were performed by seven surgeons during this 8-year period and the prostheses to implant were used to the discretion of the operating surgeon. 98 bioprostheses and 241 mechanical prostheses were implanted. Prostheses used included: Carpentier–Edwards Perimount (82 patients) (Baxter Healthcare Corp, Edwards Division, Santa Ana, Calif), Carbomedics Top-Hat Supra-annular (63 patients) and Carbomedics standard aortic valves (48 patients) (CarboMedics, Inc, Austin, TX), Omnicarbon heart valve (46 patients) (Medical CV, Inc, Inver Grove Heights, Minn), St Jude Medical HP and Regent Mechanical Valves (45 patients) (St Jude Medical, Inc, St Paul, Minn), Bicarbon Standard and Slimline Valves (26 patients) (Sorin Biomedica Cardio, S.p.A., Saluggia, Via Crescentino, Italy), ATS Standard Aortic Valve (13 patients) (ATS Medical, Inc, Minneapolis, Minn), St Jude Medical Biocor Valve (11 patients) and St Jude Medical Toronto SPV (5 patients) (St Jude Medical, Inc, St Paul, Minn). Manufacturer-derived in vitro valve areas were available in all the patients included in this study (Table 1).
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2.4. Estimation of PPM
Estimation from manufacturer-derived in vitro valve areas: PPM was assessed by calculating the two variables proposed for this purpose, i.e. the indexed EOA derived from the published normal value of EOA for the type and size of the implanted prosthesis divided by the patient's body surface area. Manufacturer-derived in vitro EOA were available in all the patients included in this study allowing classification into two subgroups, with and without mismatch. This method can be used routinely in the operating room as a preventive strategy to avoid PPM. It was used in this study in order to assess the impact of PPM in in-hospital mortality.
On one hand, PPM was considered as not clinically significant (i.e. mild or no PPM) if the indexed EOA was >0.85cm2/m2. On the other hand, significant PPM was defined by indexed EOA of 0.85cm2/m2, or less. Severe mismatch was considered if indexed EOA was 0.65cm2/m2 or less and moderate if it was >0.65cm2/m2 and 0.85cm2/m2.
Estimation from postoperative echocardiography: a postoperative indexed EOA of 0.85cm2/m2 or less was considered evidence of mismatch on the basis of previous studies. This parameter was calculated in 220 patients at first month and in 110 patients at first year.
2.5. Definitions
Chronic renal insufficiency was defined as a serum creatinine 
2mg/dl. Previous stroke was defined as history of a central neurologic deficit persisting for more than 72h. Diabetes was defined as a history of diabetes mellitus regardless of its duration or need for oral or insulin treatment. Chronic Obstructive Pulmonary Disease (COPD) was defined as the need for pharmacologic therapy for chronic pulmonary compromise or as a preoperative espirometry with the diagnosis of moderate or severe obstructive pulmonary disease. Urgent operation was considered when the surgical procedure was performed during the hospital stay of an acute clinical episode. Postoperative renal failure was defined as the increase in baseline creatinine value of greater than 2mg/dl in the absence of end-stage renal failure on dialysis. Respiratory failure was considered as the need for respiratory support for more than 48h. Low cardiac output syndrome was considered in the analysis when postoperative inotropic support was used for more than 24h. Finally, in-hospital mortality was defined as death at any time before discharge from the hospital.
2.6. Statistics
Statistical analysis was carried out with SPSS 10.0 for Windows. Continuous data are presented as mean ± SD if normally distributed or as median and inter-quartile ranges if skewed distributed. Nominal data are presented as frequencies and percentages. Associations among nominal variables were compared by Pearson's 
2 test, continuity correction or 2-sided Fisher exact test as appropriate. Continuous variables were compared by unpaired t-test. Mann–Whitney test was used to compare not normally distributed data. Several preoperative and intraoperative variables were investigated for association with hospital death at univariate analysis using these statistical tests. All variables with a p value of less than 0.10 at univariate analysis were entered in the subsequent multivariate analysis. Stepwise logistic-regression models were used to determine independent predictors of in-hospital mortality with a selection cut-off set at 0.05. Models fit was evaluated using the Hosmer and Lemeshow goodness-of-fit statistic and residual analysis. Odds ratios, 95% confidence intervals and p values were reported. Area under the receiver-operating characteristic curve (or c-statistic) was calculated as a measure of predictive power. Linear correlations were computed using Pearson's coefficient. A p value less than 0.05 was considered statistically significant.
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3. Results |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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21mm). On the contrary, the bioprosthesis St Jude Medical Biocor had the lowest index EOA mean value (0.76±0.05cm2/m2) (Fig. 1).
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3.2. Morbidity and hospital stay
Univariate comparisons of postoperative morbidity in both groups of patients are presented in Table 3. There were no significant differences between groups with respect to most of the common postoperative complications, although low cardiac output syndrome incidence was clearly higher in patients with significant PPM (p<0.01).
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3.3. Clinical and echocardiographic follow-up: LVMI regression
Clinical and echocardiographic evaluation was obtained in 190 patients at a median of 10 months at follow-up. Patients from non-significant PPM group were more frequently asymptomatic or slightly symptomatic (NYHA functional class I-II) than those with PPM: 110/118 (93.2%) versus 62/72 (86.1%) patients in the respective groups (p=0.10). Preoperative and postoperative echocardiographic data obtained at first month and at first year phases are presented in Table 4. Significant differences in LVMI with respect to preoperative values were observed in non-significant PPM group at short term follow-up (first month and first year). Absolute LVMI regression was higher in these patients: –22.2±4.6g/m2 vs –6.4±5.6g/m2 (p<0.05) at 1st month and –41.7±8.6g/m2 vs –14.6±8.5g/m2 (p<0.05) at 1st year (non-significant PPM versus significant PPM). The absolute LVMI regression at follow up was proportional to the preoperative LVMI level in patients without mismatch; i.e. higher regression in patients with higher preoperative LVMI: –38.0±7.8g/m2 vs –8.8±4.7g/m2 (p<0.01) at 1st month and –67.7±16.9g/m2 vs –23.5±6.7g/m2 (p<0.05) at 1st year in patients with and without increased LVMI, respectively. On the contrary, in patients with significant PPM, a lower absolute regression was observed in both LVMI groups but, particularly, in those patients with elevated LVMI: –8.2±11.6g/m2 vs –5.6±6.3g/m2 (p=0.83) at 1st month and –24.6±12.6g/m2 vs –11.7±10.5g/m2 (p=0.54) at 1st year, respectively (Fig. 2a). Moreover, a significant correlation between preoperative LVMI and absolute postoperative LVMI regression was observed in the global group and, especially, in patients without mismatch. In the presence of PPM this significant correlation was lost (Fig. 2b). The direct consequence of this impaired LVMI regression in patients with PPM and increased LVMI was a higher postoperative residual left ventricular hypertrophy. In the less favourable setting (i.e. significant PPM and increased LVMI) all patients had residual hypertrophy at follow up. On the contrary, patients with non-significant mismatch and not increased LVMI had a residual hypertrophy incidence of 75 and 65% at first month and at first year, respectively.
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50%) had a higher mortality in the global group: 10% (6/60) vs 2.5 (7/279) (p<0.05, LVEF50% with respect to patients with LVEF>50%). These patients also had a higher mortality in the presence of PPM (but statistically not significant). Moreover, the double association of increased LVMI and low LVEF was shown to be particularly delitereous on in-hospital mortality (Fig. 3).
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2=1.94, df=2, p=0.37) with a good predictive power (area under the ROC curve: 0.77).
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4. Discussion |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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In the present study, indexed EOA has been employed to estimate PPM. Nowadays, the indexed EOA is the only parameter yet demonstrated as being valid to identify PPM [11]. This mismatch is considered as not clinically significant (i.e. mild or no PPM) if the indexed EOA is >0.85cm2/m2, as moderate if it is >0.65cm2/m2 and 0.85cm2/m2, and as severe if it is 0.65cm2/m2 [5]. On the contrary, several previous studies have defined PPM on the basis of the indexed internal geometric area calculated from the anatomically measured internal diameter of the prosthesis divided by the patient's body surface area [2,12]. However, other important reports have shown that this parameter overestimates EOA in varying proportions depending on prosthesis type and geometry [11].
In our current practice, we have a high proportion of patients with aortic stenosis and small aortic annulus. We have described a series of 339 patients from a geographically well defined area who underwent consecutively aortic valve replacement during an 8 year period (Mar-94 to Nov-01). Elderly Spanish patients have a particular demographic characteristic: a very low body surface area and a high prevalence of small aortic annulus. The insertion of a small prosthesis into these aged patients is usually a challenging operation. The higher incidence of PPM and the more complex surgical alternatives to small valve implantation (ie, stentless, homografts or aortic root enlargement) are factors of increasing operative risk in these difficult patient population.
We have been restrictive with the patient selection criteria considered in this study. It is very important to obtain a homogeneous group of patients and to avoid confounding factors in order to address the impact of PPM on in-hospital mortality. Unfortunately, previous studies have been based on inhomogeneous groups of patients [5]. Significant aortic valve regurgitation, coronary artery bypass grafting, infectious endocarditis, emergent or redo operations have not been considered as exclusion criteria by most of these reports. Several of these factors have been previously found as independent predictors of short-term mortality related to aortic valve replacement: emergent operation, infectious endocarditis, associated coronary artery disease, recent myocardial infarction and other factors as age, female gender, poor left ventricular ejection fraction, diabetes, hypertension, left ventricular hypertrophy or small prosthetic valves [6,13–15]. Therefore, we have selected patients who underwent isolated aortic valve replacement because of pure or predominant aortic valve stenosis and several exclusion criteria have been considered: aortic regurgitation, emergent operation, infectious endocarditis, coronary artery disease and concomitant surgical procedures other than aortic valve replacement.
The real impact of PPM on survival remains controversial, particularly the relation between PPM and short-term mortality [5]. Many previous reports have considered PPM as negligible because this is an unfrequent phenomenon [16] and/or because its presence do not affect negatively clinical outcomes [1,2,15]. On the contrary, Blais et al. [5] reported a dramatic increase in mortality risk due to the combination of poor left ventricular function and moderate–severe PPM. This result is indirectly consistent with the study by Connolly et al. [14], that reported a markedly higher mortality (47 vs 15%; p=0.03) in patients with aortic stenosis and severely depressed myocardial contractility (LVEF 35%) receiving a small prosthesis (21mm) as compared with a larger prosthesis. In the former study the authors suggested that the greatest impact of PPM with regards to survival was in the early postoperative period when the left ventricle is most vulnerable [5]. A natural selection process at that time of operation during which many patients at risk do not survive beyond the early postoperative period could explain the relatively better prognosis of moderate–severe PPM beyond that critical period. These findings are really important given that moderate–severe PPM is not unfrequent with a prevalence between 19 and 70% being reported in the literature [17,18] (38% in our patients).
Other factors as high degree of left ventricular hypertrophy could be important in this early operative phase given that the left ventricle is more vulnerable and sensitive to the increased hemodynamic exigence imposed by PPM. Moreover, as this mismatch has been shown to seriously hamper left ventricular mass regression after aortic valve replacement [19], it would be of great interest to determine if PPM is not only important in patients with left ventricular dysfunction but also in those with higher degrees of left ventricular hypertrophy. Therefore, in the present study we have evaluated not only the influence of PPM on in-hospital mortality, but its impact on left ventricular mass regression in patients with preoperatively increased LVMI. Most patients had a preoperative echocardiogram performed at our institution and LVMI values were available in all of them. Previous studies have reported the prognostic importance of increased LVMI early and late after aortic valve replacement [6,7]. Indeed, we have evidenced a significant increased in in-hospital mortality in patients with high LVMI in the presence of PPM. Without mismatch, increased LVMI was not associated to a significant higher mortality. Moreover, PPM was not found as an independent predictor of mortality by itself, but it has been a promoter factor of LVMI impact on mortality. Thus, in the subgroup of patients with mismatch, increased LVMI was the strongest predictor of mortality. On the contrary, Blais et al. [5] found that PPM was an independent risk factor directly associated to short-term mortality. In our experience, the negative influence of PPM on short-term mortality in patients with left ventricular dysfunction was not as evident as the impact observed in patients with increased LVMI. But the triple association of PPM, increased LVMI and low LVEF may be particularly deletereous on in-hospital mortality. In our study, in-hospital mortality in patients with increased LVMI and LVEF50% has been very high (26.3%) (Fig. 3). This link between increased ventricular mass and depressed LVEF was observed in a multicenter study [20]. An increased left ventricular mass was found as an independent risk factor for depressed left ventricular function. Therefore, these three factors, significant PPM, increased LVMI and low LVEF, may be linked all together in close association with mortality.
Moreover, in absence of mismatch, postoperative absolute LVMI regression was proportional to the preoperative LVMI level, i.e. this regression was higher in patients with higher basal degree of left ventricular hypertrophy. On the contrary, if PPM was present, LVMI regression was impaired, especially in those patients with higher LVMI values. This worse regression was reflected on a higher residual hypertrophy at follow-up (100% incidence when both factors were present).
In conclusion, in patients with severe left ventricular hypertrophy it may be important to elude PPM after aortic valve replacement to avoid a significant increase in mortality and improve left ventricular mass regression. Particularly, high-risk patients with elevated LVMI and low LVEF may have a marked increase in this mortality. Therefore, this mismatch may be tolerable in patients with lesser degree of hypertrophy.
4.1. Limitations of the study
A number of limitations are inherent to this analysis design: a retrospective single institution study. Although strict selection criteria were used to obtain a homogeneous group of patients, a retrospective analysis is susceptible to various sources of bias which may have not been identified and controlled. Thus, the decision to implant a specific valve prosthesis was not based on well defined preoperative criteria, but solely on surgeon preference. A wide variety of prostheses have been used including bioprostheses and mechanical prostheses. This fact may be also considered as a major limitation.
Another limitation of the present study is the long time period of the analysis (8 years); changes in surgical techniques and intraoperative myocardial protection methods along time may influence outcome and prognostic factors.
A further study limitation may be the method of LVMI evaluation. Although echocardiography is a usual diagnostic tool for LVMI estimation, magnetic resonance imaging provides a more reliable quantification of left ventricular hypertrophy regression.
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Appendix A. Conference discussion |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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Dr Garcia-Fuster (Valencia, Spain): This mismatch has been estimated in all patients in the operative setting. These are predictive mismatches indeed. We have used the effective orifice area from the manufacturer information. Our study is in-hospital short-term mortality. Another way to estimate mismatch is in the postoperative period by echocardiography, but if our endpoint was in-hospital mortality, we cannot use this kind of estimation of mismatch in the postoperative period. So with respect to your question, I cannot answer it exactly because a correlation has not been performed in the statistical analysis between postoperative gradients and postoperative estimated mismatch by echocardiography.
Dr M.G. Hazekamp (Leiden, The Netherlands): I enjoyed your presentation, and I think it contributes more evidence to struggle against one of the fairy tales of cardiac surgery that mismatch is not important. I think mismatch exists, as you have demonstrated, and that it is dangerous for a subgroup of patients.
I have one question. Do you still use a 19mm prosthesis after this presentation?
Dr Garcia-Fuster: Yes, because our demographic population is a very low body-surface area population; me, for example. A small aortic annulus is very frequent in our daily practice. So a 19mm prosthesis is one of the most frequent prostheses we use. And the important thing is that bioprostheses have a higher incidence of mismatch with respect to mechanical prostheses. But I think the impact of mismatch is relative. We cannot talk about mismatch in absolute terms. I think several kinds of patients can have a very deleterious effect if mismatch is present, but perhaps mismatch may be tolerable in other kinds of patients.
Dr R. Deac (Tirgu-Mures, Romania): I just want to congratulate on the contributions of your group on two important things. One is patient-prosthesis mismatch and, as yesterday, with subvalvular mitral apparatus.
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Acknowledgments |
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Footnotes |
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References |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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