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Interact CardioVasc Thorac Surg 2005;4:260-266. doi:10.1510/icvts.2004.098194
© 2005 European Association of Cardio-Thoracic Surgery
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Institutional report - Valves

Left ventricular mass index as a prognostic factor in patients with severe aortic stenosis and ventricular dysfunction{star}

Rafael García Fuster*, José A. Montero Argudo, Oscar Gil Albarova, Fernando Hornero Sos, Sergio Cánovas López, María Bueno Codoñer, José A. Buendía Miñano and Ignacio Rodríguez Albarran

Universitary General Hospital of Valencia, C/Artes Graficas no 4, esc. inq. pta. 3, 46010 Valencia, Spain

Received 11 September 2004; received in revised form 4 January 2005; accepted 8 February 2005

{star} Presented at the joint 18th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 12th Annual Meeting of the European Society of Thoracic Surgeons, Leipzig, Germany, September 12-15, 2004.

*Corresponding author. Tel.: +34 (96) 3622216; fax: +34 (96) 197 2163.

E-mail address: rgfuster{at}terra.com (R. García Fuster).


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Statistical analysis
 4. Results
 5. Discussion
 Appendix A. Conference...
 References
 
Ventricular dysfunction and high hypertrophy may influence surgical outcome in aortic stenosis. Our aim was to determine whether an excessive left ventricular mass index (LVMI) discriminates different risk profiles in aortic stenosis with low ventricular ejection fraction (LVEF). Three hundred and thirty-nine patients with severe aortic stenosis underwent valve replacement (Mar-1994 and Nov-2001). LVMI values over the superior quartile were considered increased. Mortality models were constructed in global and LVEF≤50% groups. In-hospital mortality was higher in increased LVMI group: 9.6 vs. 1.9%, P<0.01. In LVEF≤50%-increased LVMI patients this mortality was also higher: 26.3 vs. 2.4%, P<0.05. Patients without LV dysfunction and increased LVMI did not show significant difference: 4.7 vs. 1.8%, P=0.41. Chronic renal failure (OR: 11.72, P<0.05), cardiopulmonary bypass time (OR: 1.03, P<0.01) and LVMI (g/m2) (OR: 1.01, P<0.01) were associated with mortality. In patients with LVEF≤50%, LVMI was the strongest predictor of death. Cummulative mortality was higher with increasing LVMI and low LVEF. In conclusion, LVMI in patients with severe aortic stenosis and low LVEF might discern two different situations: an advanced cardiomyopathy with excessive hypertrophy (high LVMI–low LVEF) with poor prognosis, and an inadequate adaptive hypertrophy (low LVMI–low LVEF) in patients with afterload mismatch and more favorable outcome.

Key Words: Ventricular mass; Aortic valve replacement; In-hospital mortality


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Statistical analysis
 4. Results
 5. Discussion
 Appendix A. Conference...
 References
 
Patients with severe aortic stenosis and impairment of ventricular function constitute a high risk group for aortic valve replacement [1–4]. They are also a challenging group because of their heterogeneous response: some patients have favourable results and others have high operative mortality and lower late survival [5]. Ventricular hypertrophy is also a negative factor [6,7]. The association of both factors may impact surgical outcome.

Our aim was to determine whether an excessive left ventricular mass index (LVMI) discriminates among different risk profiles in patients with aortic stenosis and low ejection fraction (LVEF).


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Statistical analysis
 4. Results
 5. Discussion
 Appendix A. Conference...
 References
 
2.1. Study group

All patients who underwent aortic valve replacement between Mar-1994 and Nov-2001 were identified from our prospectively maintained database. From 605 patients only those with pure or predominant aortic stenosis were included (392 patients). Concomitant procedures, emergent operations and lack of preoperative echocardiographic data were exclusion criteria. Finally, 339 patients were considered.

2.2. Echocardiographic study

Preoperative Doppler Echocardiography was performed in all patients. Normal systolic function was considered if LVEF >50%. Conversely, systolic dysfunction was defined as LVEF ≤50%.

LVMI was calculated by Devereux's formula [8,9] considering the diastolic measurements of left ventricular internal diameter (LVID), interventricular septal thickness (IVST) and posterior wall thickness (PWT):

LVMI (g/m2)=(1.04 [(IVST+LVID+PWT)3–LVID3]–14 g)/Body surface area.

According to this formula, LVMI is increased if >134/m2 in men and >110 g/m2 in women. We have evaluated higher degrees of LVMI and a new cut-off point was established arbitrarily at the first value of the superior quartile on the frequency distribution of LVMI values in both sexes.

2.3. Operative technique

Standard techniques with extracorporeal circulation were used. Myocardial protection was similar during the study: moderate hemodilution and multidose intermittent cold blood cardioplegia through the aortic root or into the coronary ostia. Antegrade/retrograde delivery was also routinely used. Prosthesis size and type were used to the discretion of the surgeon (Table 1).


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  		Table 1 Implanted prosthetic valves

 
2.4. Variables and definitions

The variables were based on demographics, clinical data, comorbidity and cardiac risk factors, cause of valvular lesion, echocardiographic, surgical and postoperative data.

Severe LV dysfunction was defined as LVEF≤35%. Previous stroke was defined as history of a central neurologic deficit >72 h. Chronic renal insufficiency was defined as creatinine ≥2 mg/dl. Chronic Obstructive Pulmonary Disease was defined as the need for pharmacologic therapy for chronic pulmonary compromise or as a preoperative espirometry with a moderate or severe obstruction. Urgent operation was considered when the surgical procedure was performed during the hospital stay of an acute episode. Respiratory failure was considered as the need for respiratory support for >48 h and postoperative renal failure as the increase in baseline creatinine value >2 mg/dl in the absence of end-stage renal failure on dialysis. Low cardiac output when postoperative inotropic support was used >24 h. Finally, in-hospital mortality was defined as death at any time before hospital discharge.


   3. Statistical analysis
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Statistical analysis
4. Results
 5. Discussion
 Appendix A. Conference...
 References
 
Statistical analysis was performed using SPSS 10.0 for Windows (SPSS Inc, Chicago, IL). Continuous variables were summarized as mean±standard deviation if normally distributed, on the contrary, median and inter-quartile ranges were used. Nominal data were presented as frequencies and percentages. Continuous variables were compared by unpaired t-test. Mann–Whitney test was used to compare not normally distributed data. Associations among categorical variables were compared by Pearson's {chi}2 test, continuity correction or two-sided Fisher exact test as appropriate.

Cummulative mortality associated to increasing LVMI values was calculated by hazard-function analysis. Comparison of hazard functions according to LVEF group was performed by Mantel-Cox and Breslow tests. Logistic regression was used to predict in-hospital mortality. Several stepwise logistic-regression models predicting in-hospital death associated to LVMI were obtained: one considering LVMI as a continuous variable, and the other considering the superior quartile as increased LVMI. A final model was performed in patients with LVEF≤50%. The receiver-operating characteristic (ROC) curve was obtained and its extrapolation to sensitivity–specificity curves gave us the best discriminant LVMI value for mortality prediction (curves crossing point). Models fit was evaluated using the Hosmer and Lemeshow goodness-of-fit statistic and the area under the ROC curve was calculated.


   4. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Statistical analysis
 4. Results
5. Discussion
 Appendix A. Conference...
 References
 
4.1. Preoperative characteristics and surgical data

Mean LVMI was 192.92±53.67 g/m2 (196.84±50.85 g/m2 in males and 187.86±56.87 g/m2 in females). The first value of the superior quartile was 226 g/m2 in males and 216 g/m2 in females. According to this, 83 patients (47 males and 36 females) had increased LVMI. Univariate comparisons of preoperative and surgical variables between increased and not increased LVMI groups are presented in Table 2. Patients with elevated LVMI were older and with lower LVEF. Rheumatic disease and previous atrial fibrillation were more frequent in not increased LVMI group. Other demographic characteristics, symptoms, comorbidities and cardiovascular risk factors were similar, except for a higher percentage of hypertension, hyperlipidemia and CCS angina class ≥III in not increased LVMI group.


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  		Table 2 Preoperative characteristics and surgical data

 
Urgent operations and mean ischemic and cardiopulmonary bypass times were similar. Ninety-eight bioprostheses and 241 mechanical prostheses were implanted and bioprostheses were more frequent in increased LVMI group.

The mean indexed Effective Orifice Area (iEOA) was: 1.01±0.28 vs. 1.00±0.27 cm2/m2 and the prevalence of patient-prosthesis mismatch (iEOA≤0.85 cm2/m2) was similar. Preoperative echocardiographic data are presented in Table 3.


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  		Table 3 Preoperative echocardiographic data

 
4.2. Postoperative outcome

Univariate comparisons of postoperative morbidity are presented in Table 4. Hospital stay was slightly longer in increased LVMI group.


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  		Table 4 Postoperative morbidity and hospital stay

 
4.3. In-hospital mortality

Thirteen patients died (3.8%). In-hospital mortality in LVEF≤50% subgroup (n=60) was 10.0% (6 patients) in contrast to 2.5% (7 patients) in the subgroup with LVEF>50% (P<0.05). Mortality was also higher in patients with increased LVMI: 9.6% (8 patients) vs. 1.9% (5 patients) (P<0.01). Mortality according to preoperative LVEF and LVMI is summarized in Table 5.


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  		Table 5 In-hospital mortality in strata of left ventricular ejection fraction and left ventricular mass index

 
Univariate associations to mortality are presented in Table 6 (A). Independent predictors of mortality are presented in Table 6 (B). The first model showed that LVMI (continuous variable) was significantly associated to mortality. Increased LVMI was also identified as an independent predictor (Table 6, model 2). We added a LVEF-LVMI interaction term (Table 6, model 3) obtaining a high statistical significance. So, patients with increased LVMI and LVEF≤50% were at high risk of mortality.


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  		Table 6 Predictors of mortality: uni-multivariable analyses

 
LVMI was the strongest predictor of death in LVEF≤50% subgroup (Table 6, model 4). An ROC curve was obtained and the calculated LVMI cut-off point from the intersection of sensitivity–especificity curves was around 220 g/m2.

Cummulative mortality associated to increasing LVMI values is presented in Fig. 1. Patients with LVEF≤50% had a higher cumulative mortality (Fig. 1b), but this was particularly true in the superior strata of LVMI (Fig. 1d).



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  		Fig. 1. Cummulative mortality associated to increasing LVMI values by hazard-function analysis: a) in the whole cohort of patients, b) in patients with LVEF≤50% versus LVEF>50%, c) in patients with LVEF≤50% versus LVEF>50% (inferior strata of LVMI values), d) in patients with LVEF≤50% versus LVEF>50% (superior strata of LVMI values).

 
4.4. Different risk profiles

Two subgroups of patients with LVEF≤50% have been obtained according to the LVMI cut-off point (220 g/m2). Comparisons are reflected in Table 7. Despite the small sample size, several differences have been observed. Patients with LVMI >220 g/m2 were slightly older and with low body surface area. Female sex was most prevalent in not increased LVMI group. Smoking, diabetes, hypertension, hyperlipidemia, chronic atrial fibrillation and rheumatic disease were also more frequent in this group. The same occurred with associated grade 1–2 mitral regurgitation (Table 7). Increased LVMI group had not only a higher ventricular hypertrophy but also a more dilated left ventricle and lower LVEF. Lower transvalvular gradients were also observed with more accentuated left ventricular dysfunction (Table 7). A higher mortality was the consequence of this higher risk: 26.3% (5 patients) vs. 2.4% (1 patient); P<0.05. Postoperative low cardiac output syndrome was also more frequent: 3 (15.8%) vs. 2 (4.9%) (P=0.35).


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  		Table 7 Risk profile in low LVEF patients: inter-group differences according to LVMI

 

   5. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Statistical analysis
 4. Results
 5. Discussion
Appendix A. Conference...
 References
 
Aortic valve replacement in patients with aortic stenosis or regurgitation and severe left ventricular dysfunction continues to be associated with a high mortality risk despite surgical and cardiological improvements [1–5]. Early referral for surgery has largely solved the problem of high mortality associated to left ventricular dysfunction in the context of aortic regurgitation [5]. On the contrary, patients with severe aortic stenosis constitute a challenging group with a more heterogeneous response. On one side, patients with critical aortic stenosis and low ejection fraction due to ‘afterload mismatch’ (depressed ejection performance resulting from excessively high systolic ventricular wall stress secondary to aortic stenosis) generally respond well to surgery, which immediately normalizes left ventricular afterload. Conversely, other patients with critical aortic stenosis and advanced left ventricular systolic dysfunction, who usually present with low gradients and cardiac output, constitute a high operative risk subgroup [5].

Other factors [10–12] that increase morbimortality are: associated coronary artery disease, renal insufficiency, advanced age, prior aortic valve replacement, aortic regurgitation, atrial fibrillation, patient-prosthesis mismatch, low body surface area, CPB time, type of prosthesis, etc. Elevated LVMI has also been considered [6,7,13]. Unfortunately, many of previous studies have included patients with aortic insufficiency or undergoing concomitant procedures, which complicates comparisons. We were especially restrictive with the selection criteria and we have only considered patients with isolated aortic stenosis.

Increased LVMI could be responsible of higher mortality by means of contractile impairment, diastolic dysfunction, abnormalities of coronary flow reserve or cardiac arrhythmias [6,7]. This factor was the strongest predictor of death in our patients with LVEF≤50%. In the global group, preoperative LVEF was associated with mortality in univariate analysis and it was also an independent predictor when increased LVMI-LVEF≤50% interaction was tested. But some patients with low LVEF have not increased LVMI and they had a better survival (Table 5). So, LVMI in patients with aortic stenosis and low LVEF might discern two groups of patients with different outcomes.

In valvular aortic stenosis, concentric hypertrophy maintains left ventricular chamber size and ejection fraction within normal limits, but in late stages, function can deteriorate as preload reserve is lost. Even when the ejection fraction is markedly reduced, it can improve to normal after surgery, suggesting that afterload mismatch rather than irreversibly depressed myocardial contractility was responsible for left ventricular failure. This mismatch occurs when an inadequate adaptive hypertrophy is present [14]. These patients have a low LVEF and a ‘not increased LVMI’ because adaptative hypertrophy has been insufficient. But in other patients without afterload mismatch, the operative risk is high and the improvement of left ventricular function may not be complete. An irreversibly depressed contractility may be the result of excessive hypertrophy and fibrosis [2]. These patients have a low LVEF and a severely increased LVMI. Survival is still improved with the possible exception of patients with severe ventricular dysfunction caused by coronary disease [2,4]. Therefore, patients with severe aortic stenosis should not be denied operation because of impaired cardiac function, but it would be important to unmasked this irreversibly depressed myocardial contractility. The evaluation of the hypertrophic response might be a useful tool.

We must consider a real ‘dysfunction’ in this adaptive mechanism to afterload increase. It should be secondary to an inadequate hypertrophy (insufficient or excessive) with respect to the increased afterload. The factors associated to this inadequate adaptation are not completely known [15]. Hypertension, diabetes and pharmacologic treatments may have a significant role. Other factors include sex, race, genetic and neurohumoral such as levels of angiotensin and other trophic hormones that might modulate hypertrophy. Several factors have been associated more frequently to our patients with low LVEF and not increased LVMI: female sex, hypertension, diabetes, rheumatic disease or low grade mitral regurgitation. Palta et al. [15] concluded that mitral regurgitation in severe aortic stenosis is associated with larger ventricles and lesser wall thickness, and this may result from failure of adequate hypertrophy. Grade 1–2 mitral regurgitation was more frequent in not increased LVMI group in our patients with LVEF≤50%. Higher grades of regurgitation were not found because concomitant surgical procedures were excluded.

In summary, in these, challenging patients with severe aortic stenosis and low LVEF, LVMI might discern two different situations: an advanced cardiomyopathy with excessive hypertrophy (high LVMI–low LVEF) with worse outcome, and an insufficient adaptive hypertrophy (low LVMI–low LVEF) in patients with afterload mismatch and more favourable results. Future studies are needed to find the possible factors implicated in this different hypertrophic response to afterload increase.

5.1. Limitations of the study

A retrospective, non-randomized analysis in a single center is subjected to the effects of selection bias. Another limitation is the reduced number of patients with LVEF≤50%, because severe aortic stenosis and ventricular dysfunction is not a frequent association (a common limitation in previous studies). The comparison in this subgroup is limited by the small sample size. Thus, further research in larger series is needed to elucidate mechanisms of ventricular remodelling in patients with aortic stenosis and ventricular dysfunction.


   Appendix A. Conference discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Statistical analysis
 4. Results
 5. Discussion
 Appendix A. Conference...
References
 
Dr A. Laczkovics (Bochum, Germany): I have realized that you have adapted the Morrow procedure in both groups, however, it was only 2% in the Leiden and the Seville group. Would it be logical that in the group with the massive left ventricular hypertrophy you would apply the Morrow procedure more often? It should have an impact on the echocardiographic findings and do you speculate it would have an impact on the outcome?

Dr Garcia-Fuster: Other procedures?

Dr Laczkovics: The Morrow procedure. You have had it on your slide.

Dr Garcia-Fuster: This variable was not shown in the slide.

Dr Laczkovics: Oh, yes, it was. It was in both groups, 2.2 and 2.6%.

Dr Garcia-Fuster: Exactly. We have performed septal myectomy or Morrow procedure in both groups, and curiously the proportion of patients was similar in both groups. I cannot have an explanation for this. Perhaps it depends on the surgeons. Eight surgeons along the study period have performed all the operations, and the experience of the surgeon is probably important. But it is curious, effectively, because in patients with increased left ventricular mass, septal thickness was higher, of course.

Dr R Frater (Bronxville, New York): I may have missed this, but was there a difference in hypertension in these two groups of patients?

Dr Garcia-Fuster: Hypertension was higher in absolute terms in the whole group in patients with no increased left ventricular mass, but there was no statistical significance. This is another curious result. But hypertension is not an important factor, I think, in this gorup of severe aortic stenosis patients in order to cause a significantly important left ventricular mass. But curiously, in absolute terms, hypertension was more prevalent in patients with no increased left ventricular mass, but not with statistical significance.

Dr P. Sergeant (Leuven, Belgium): From the clinical experience in coronary surgery, we are always cautious when patients undergo coronary surgery in the presence of massive left ventricular hypertrophy. The variables that we usually carry in our analysis are hypertension or left ventricular hypertrophy, but we would never carry variables like the left ventricular mass index. Have you tested the hypothesis or just observed the hypothesis in coronary bypass patients?

Dr Garcia-Fuster: Left ventricular mass index has been calculated in these patients with Devereux's formula by echocardiography. Magnetic resonance imaging is probably a better test. But in coronary patients, it has not been our policy to test this parameter. Perhaps it would be good, I ---think. But in coronary patients we have not been looking for the impact of left ventricular hypertrophy in the results. So it is not establised in this study in coronary patients.

S. Nashef (Cambridge, UK): You have shown a very powerful relationship between left ventricular mass index and early in-hospital mortality. Do you have any idea what the mode of death in these patients was, and have you considered at all the possibility that you might be missing systolic anterior motion of the mitral valve as a cause for the deterioration?

Dr Garcia-Fuster: Increased left ventricular mass index has been evident as an important factor in increased short-term mortality, in-hospital mortality, and I think the myocardium is susceptible in the early phase after extracorporeal circulation of several insults, for example, great hypertrophy or in the presence of prosthetic-patient mismatch, and this is a very critical phase.

Of couse, myocardial protection is a very important thing, but we have no evidence of anterior systolic motion of the mitral valve in these patients in the perioperative period. I think left ventricular hypertrophy can cause a severe impact on in-hospital mortality by means of several mechanisms, for example, ischemic insult and deficiency in protection.

On the other hand, arrhythmias are more frequent. And a diastolic dysfunction can be responsible for low cardiac output in the postoperative period in early phases. So I think, of course, that myocardial protection is very important in these patients and to assess the probability of complications if we know that increased left ventricular mass index in our patients is a very important factor to consider.

Dr P. Sergeant (Leuven, Belgium): You have very nicely shown how the performance of your mathematical modeling improved by transforming the original variable. Have you tested other transformations like exponential transformations and square transformations, or have you restricted yourself to the transformations shown?

Dr Garcia-Fuster: We have not performed mathematical transformations of our variables. The results were quite impressive at first glance and for statistical reasons we have not performed exponential transformations. There is direct management of our variables in the regression models and in the probit model.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Statistical analysis
 4. Results
 5. Discussion
 Appendix A. Conference...
 References
 

  1. Tarantini G, Buja P, Scognamiglio R, Razzolini R, Gerosa G, Isabella G, Ramondo A, Iliceto S. Aortic valve replacement in severe aortic stenosis with left ventricular dysfunction: determinants of cardiac mortality and ventricular function recovery. Eur J Cardiothorac Surg 2003;24:879–885.[Abstract/Free Full Text]
  2. Powell DE, Tunick PA, Rosenzweig BP, Freedberg RS, Katz ES, Applebaum RM, Perez JL, Kronzon I. Aortic valve replacement in patients with aortic stenosis and severe left ventricular dysfunction. Arch Intern Med 2000;160:1337–1341.[Abstract/Free Full Text]
  3. Sharony R, Grossi EA, Saunders PC, Schwartz CF, Ciuffo GB, Baumann FG, Delianides J, Applebaum RM, Ribakove GH, Culliford AT, Galloway AC, Colvin SB. Aortic valve replacement in patients with impaired ventricular function. Ann Thorac Surg 2003;75:1808–1814.[Abstract/Free Full Text]
  4. Conolly HM, Oh JK, Orszulak TA, Osborn SL, Roger VL, Hodge DO, Bailey KR, Seward JB, Tajik AJ. Aortic valve replacement for aortic stenosis with severe left ventricular dysfunction. Prognostic indicators. Circulation 1997;95:2395–2400.[Abstract/Free Full Text]
  5. Green GR, Miller DC. Continuing dilemmas concerning aortic valve replacement in patients with advanced left ventricular systolic dysfunction. J Heart Valve Dis 1997;6:562–579.[Medline]
  6. Mehta RH, Bruckman D, Das S, Tsai T, Russman P, Karavite D, Monaghan H, Sonnad S, Shea MJ, Eagle KA, Deeb GM. Implications of increased left ventricular mass index on in-hospital outcomes in patients undergoing aortic valve surgery. J Thorac Cardiovasc Surg 2001;122:919–928.[Abstract/Free Full Text]
  7. Garcia Fuster R, Montero JA, Gil O, Hornero F, Canovas S, Dalmau MJ, Bueno M, Buendia JA. Left ventricular mass index in aortic valve surgery: a new index for early valve replacement? Eur J Cardiothorac Surg 2003;23:696–702.[Abstract/Free Full Text]
  8. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man: anatomic validation of the method. Circulation 1997;55:613–619.
  9. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, Reichek N. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986;57:450–458.[CrossRef][Medline]
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  11. Bloomstein LZ, Gielchinsky I, Bernstein AD, Parsonnet V, Saunders C, Karanam R, Graves B. Aortic valve replacement in geriatric patients: determinants of in-hospital mortality. Ann Thorac Surg 2001;71:597–600.[Abstract/Free Full Text]
  12. Lytle BW, Cosgrove DM, Taylor PC, Goormastic M, Stewart RW, Golding LA, Gill CC, Loop FD. Primary isolated aortic valve replacement. Early and late results. J Thorac Cardiovasc Surg 1989;97:675–694.[Abstract]
  13. Orsinelli DA, Aurigemma GP, Battista S, Krendel S, Gaasch WH. Left ventricular hypertrophy and mortality after aortic valve replacement for aortic stenosis: a high risk subgroup identified by preoperative relative wall thickness. J Am Coll Cardiol 1993;22:1679–1683.[Abstract]
  14. Ross J Jr. Afterload mismatch in aortic and mitral valve disease: implications for surgical therapy. J Am Coll Cardiol 1985;5:811–826.[Abstract]
  15. Palta S, Gill KS, Pai RG. Role of inadequate adaptive left ventricular hypertrophy in the genesis of mitral regurgitation in patients with severe aortic stenosis: implications for its prevention. J Heart Valve Dis 2003;12:601–604.[Medline]



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