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Discussion

Many factors that increase operative morbimortality in patients

undergoing aortic valve replacement have been identified byseveral studies: LV

dysfunction, associated coronaryartery disease, renal insufficiency, advanced

age, prior aorticvalve replacement, aortic regurgitation, atrial fibrillation,

patient-prosthesis mismatch, low body surface area, CPB time,type of

prosthesis, etc (Thomson et al., 1998 and Heet al., 2001).

Elevated LVMI has also been considered a risk factor for increased

morbimortality in several circumstances by other investigationsreported in the

literature (Orsinelli et al., 1993 and Mehta et al., 2001).

This study included 339 patients with aortic stenosis underwent aortic

valve replacement in the period from 1998 2006 in Mehalla Cardiac Center

and National Heart Institute.

Results of the current study showed that 83 patients (24.5%) had

increased LV mass and 256 patients (75.5%) had a non-increased LV mass

according to the definition of increased LV mass used in our study as mentioned

in the patients and methods. On comparing our results with the study ofRafael

et al., (2005) who analyzed the effect of increased leftventricular mass index on

outcomes in patients undergoing aorticvalve replacement. Left ventricular mass

index wasconsidered increased if higher than the value of the superiordecile

(226 g/m2 in males and 216 in females). Increasedindex was considered in 9.9%

of patients. The incidence of increased LVMI was more in our study patients

which could be explained by the difference in the etiology of AS as in our

patients the most common cause was rheumatic heart disease while in their

study the most common cause was atherosclerotic aortic valve disease.

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Results of the current study showed that LVEF%, and LVFS% was

significantly lower in patients with increased LVMI than patients with no

increased LVMI (P < 0.05). The LVID, PWT, IVST was significantly higher in

patients with increased LVMI than patients with no increased LVMI (P > 0.05).

There was no significant difference between the two groups regarding the max

gradient, mean gradient or effective orifice area (P > 0.05).

Our results are in agreement with that reported byRafael et al (2003)

who found that preoperative EF was lower in elevated LVMI group. But our

results disagreed with his results in that they fount that the EF was not

significantly associated to mortality inunivariable and multivariable analysis.

Our results showed that post-operative low cardiac output syndrome

occurred in 7 patients (8.4%) in the group of increased LVMI versus 4 patients

(1.6%) in the group with no increased LVMI and the difference between the two

groups was significant (P < 0.001). Post-operative stroke occurred in 9 patients

(10.8%) in the group of increased LVMI versus 11 patients (4.3%) in the groupwith no increased LVMI and the difference between the two groups was

significant (P < 0.05). The mean duration of hospital stay was significantly

higher in patients with increased LVMI (12.5 4.5 days vs. 10.5 4.5 days for

patients with no increased LVMI) (P < 0.05). The other post-operative morbid

conditions as acute renal failure, respiratory failure, pneumonia, pre-operative

bleeding and sepsis was not significantly different in the two groups (P > 0.05).

Our results are in concordance with that reported byRafaelet al., (2005)

who found that postoperative complications(low cardiac output syndrome,

respiratory failure, arrhythmias,pneumonia and mediastinitis), median length of

hospital stay:12 days (657) versus 11 days (551), and in-hospital mortality

(11.4, 3.2%, P

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Discussion

In our patients the overall mortality rate was 7.4% (25/339). The

mortality rate in patients with increased LVMI was significantly higher in

patients with increased LMI (15.7%, 13/83 patients) than patients with no

increased LVMI (4.7%, 12/256 patients (P < 0.001).

These results are similar to those ofMehta et al., (2001) and Orsinelli et

al., (1993) who showed that LV hypertrophy was a risk factorof postoperative

mortality after aortic valve replacement foraortic stenosis.Mehta and

colleagues (2001) studied 473 consecutivepatients undergoing elective aortic

valve replacement and theconclusion of their analysis was that increased LVMI

was associatedwith increased in-hospital clinical events, greater length ofstay

and increased in-hospital mortality. They called for specialattention to

perioperative management of such patients and hypothesizedabout the potential

benefit of earlier surgery in asymptomaticpatients with significant increased

LVMI.

In the subgroup of patients with increased LVMI had a very extensivehypertrophy. Similar values of LVMI were reportedbyNatsuaki and

colleagues (2000) on a Japanese patient population.Several factors could

explain this finding: demographic differencesin the severity of muscle

hypertrophy, a significant numberof patients who underwent surgery in an

advanced phase of thedisease, a population with an extremely low body surface

area

with very high values in LVMI, etc. A possible explanation could

be thatfor a given degree of LV hypertrophy, patients witha very low body surface

area may have a greater LVMI value (accordingto Devereux's formula). In the

article byNatsuaki and colleagues (2000) the authors reported an evaluation of

postoperative cardiacfunction and long-term results after aortic valve

replacementfor aortic valve disease in patients with increased left ventricular

mass. The mean value of LVMI was 272 g/m2. In spite of that Japanesepeople

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have a low mean body surface area, a demographic characteristicsimilar to our

Spanish elderly patients with aortic valve disease.

In the study ofRafael et al., (2003) they found that different degrees of

LVMIin four groups of our patients (divided in quartiles accordingto LVMI

values), mortality in group 4 (with increased LVMI:over 228 g/m2 in males and

199 g/m2 in females) was clearlyhigher and with a near statistical significance:

6.5 versus3.2% (P = 0.06).

Increased LVMI could be responsible of this higher operativerisk by

means of several mechanisms: contractile impairmentand pump dysfunction

associated to excessive LV hypertrophy (Wisenbaugh et al., 1986 and Vasan et

al., 1996), diastolic dysfunction with abnormal relaxation and reduced

distensibility (Murakami et al., 1986 and Otto et al., 1989), abnormalities of

coronary flow reserve, propensity for cardiac arrhythmias (Levy et al., 1987

and Polese et al., 1991).

Our results showed that the univariate analysis of the significant

predictors of mortality. Patient prosthesis mismatch (PPM) was the most

significant predictor of mortality (Odd's ratio 5.6 with 95% Confidence Interval

ranged between 1.31 22.3, P < 0.001), then age > 50 years (Odd's ratio 4.5

with 95% Confidence Interval ranged between 2.6 17.9, P < 0.001), then CPB

time > 120 minutes (Odd's ratio 4.1 with 95% Confidence Interval ranged

between 2.7 15.7, P < 0.001) and increased LVMI (Odd's ratio 3.9 with 95%

Confidence Interval ranged between 1.8 12.9, P < 0.001). Our results

disagreed with that reported byRafael et al., (2003) who found that the most

significant predictor of mortality in patients Undergoing aortic valve surgery

were increased left ventricular mass index (odds ratio:5.6; 95% confidence

interval: 1.225.0; P=0.02) and the otherthree variables: age (P=0.04), history

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of chronic renal failure(P=0.03) and cardiopulmonary bypass time (P=0.004),

as independentpredictors of early mortality.

Our results showed that the in-hospital mortality in patients with

increased LVMI and low ejection fraction was 31.8% (7/22 patients) and the in-

hospital mortality of patients with increased LVMI and normal ejection fraction

was 9.8% (6/61 patients). The difference between the two groups was

significant (P < 0.001). The in-hospital mortality of patients with no increased

LVMI and low EF was 9% (5/45 patients) while it was 3.3% (7/211 patients)

and the difference between patients with no increased LVMI and low EF and

patients with no increase in LVMI and normal EF was significant (P < 0.05). In

all patients, the mortality rate in patients with low EF was 10% (12/67) while it

was 4.8% (13/272) in patients with normal EF (P < 0.05).

Our results agreed with that reported byMehta and colleagues (2001)

who found that EF was a significant independentpredictor of mortality in the

final logistic regression model.

Results of the current study showed that in patients with low ejection

fraction LVEF% and LVFS% was significantly lower in patients with increased

LVMI than patients with no increased LVMI (P < 0.05). The LVID, PWT,

IVST was significantly higher in patients with increased LVMI than patients

with no increased LVMI (P > 0.05). There was no significant difference

between the two groups regarding the max gradient, mean gradient or effective

orifice area (P > 0.05). These results identified the extent of the problem of low

ejection fraction in patients with aortic stenosis especially if associated with

increased LVMI.

These results could be discussed according to the that: Aortic valve

replacement in patients with aortic stenosis and left ventricular dysfunction

continuesto be associated with a high mortality risk despite surgicaland

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cardiological improvements (Tarantini et al., 2003, Powell et al., 2000 and

Sharony et al., 2003).

Early referral forsurgery has largely solved the problem of high mortality

associatedto left ventricular dysfunction in the context of aortic valve disease

(Greenet al., 1997).

On the contrary, patients with severe aortic stenosis constitutea

challenging group with a more heterogeneous response. On one side, patients

with critical aortic stenosis and low ejectionfraction due to afterload mismatch

(depressedejection performance resulting from excessively high systolic

ventricular wall stress secondary to aortic stenosis) generallyrespond well to

surgery, which immediately normalizes left ventricularafterload. Conversely,

other patients with critical aortic stenosisand advanced left ventricular systolic

dysfunction, who usuallypresent with low gradients and cardiac output,

constitute ahigh operative risk subgroup (Green et al., 1997).

Other factors that increase morbimortality are:associated coronary artery

disease, renal insufficiency, advancedage, prior aortic valve replacement, aortic

regurgitation, atrialfibrillation, patient-prosthesis mismatch, low body surface

area, CPB time, type of prosthesis, etc. Elevated LVMI has alsobeen considered

(Mehta et al., 2001).

Unfortunately, many of previous studies

have included patients withaortic insufficiency or undergoingconcomitant procedures, which complicates

comparisons. We wereespecially restrictive with the selection criteria and we

haveonly considered patients with isolated aortic stenosis.

Increased LVMI could be responsible of higher mortality by meansof

contractile impairment, diastolic dysfunction, abnormalitiesof coronary flow

reserve or cardiac arrhythmias (Garcia et al., 2003).

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Thisfactor was the strongest predictor of death in our patientswith

LVEF

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associated to this inadequateadaptation are not completely known (Palta et al.,

2003).

Hypertension, diabetesand pharmacologic treatments may have a

significant role. Otherfactors include sex, race, genetic and neurohumoral such

aslevels of angiotensin and other trophic hormones that mightmodulate

hypertrophy. Several factors have been associated morefrequently to our

patients with low LVEF and not increased LVMI:female sex, hypertension,

diabetes, rheumatic disease or lowgrade mitral regurgitation.Palta et al. (2003)

concluded thatmitral regurgitation in severe aortic stenosis is associatedwith

larger ventricles and lesser wall thickness, and this mayresult from failure of

adequate hypertrophy. Grade 12mitral regurgitation was more frequent in not

increased LVMIgroup in our patients with LVEF50%. Higher grades of

regurgitationwere not found because concomitant surgical procedures were

excluded.

In these, challenging patients with severe aortic

stenosis and low LVEF,LVMI might discern two different situations:an advanced cardiomyopathy with

excessive hypertrophy (highLVMIlow LVEF) with worse outcome, and an

insufficientadaptive hypertrophy (low LVMIlow LVEF) in patients with

afterload mismatch and more favorable results. Future studiesare needed to find

the possible factors implicated in this differenthypertrophic response to

afterload increase.

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