Asian Cardiovasc Thorac Ann 2007;15:459-462
© 2007 Asia Publishing EXchange Ltd
Left Ventricular Hypertrophy and Remodeling after Aortic Valve Replacement
Hikmet Iyem, MD,
Cevat Sekuri, MD1,
Mine Tavli, MD,
Suat Büket, MD
Cardiovascular Surgery Department,
1 Cardiology Department, Kent Hospital, Izmir, Turkey
For reprint information contact: Hikmet Iyem, MD, Tel: 90 232 386 7070, Fax: 90 232 386 7071, Email: hikmeti{at}hotmail.com, Kent Hastanesi Kalp ve Damar Cerrahi bölümü, Cigli Izmir 35580, Turkey.
 |
ABSTRACT
|
|---|
Left ventricular geometric remodeling and regression of hypertrophy were assessed after aortic valve replacement with a mechanical prosthesis in 37 patients with aortic stenosis and 39 with aortic insufficiency, aged 54.2 ± 14.3 and 52.6 ± 16.6 years, respectively. The follow-up period was 2 years. In patients with aortic insufficiency, ejection fraction increased from 54.4 ± 3.5 preoperatively to 59.6 ± 3.4 after 6 months and 61.7 ± 2.7 after 2 years. In patients with aortic stenosis, ejection fraction increased from 56.6 ± 5.1 preoperatively to 63.9 ± 4.4 after 6 months and 71.7 ± 4.1 after 2 years. Geometric remodeling, regression of hypertrophy, and increased ejection fraction of the left ventricle were similar in both groups at 6 months after surgery, but after 2 years of follow-up, greater improvement was found in patients who had undergone valve replacement for aortic stenosis.
|
INTRODUCTION
|
|---|
Left ventricular (LV) hypertrophy is an adaptive process that compensates for the pressure overload associated with aortic stenosis. This process is accompanied by LV remodeling that involves the muscular and nonmuscular compartments of the ventricle. Consequently, muscle fiber hypertrophy and abnormalities of the collagen network occur, which are responsible for the changes in systolic and diastolic function.1 Left ventricular hypertrophy is a recognized risk factor for cardiac morbidity and mortality.2 Pure aortic valve stenosis (AS) and aortic insufficiency (AI) are the most frequent reasons for prosthetic valve replacement in adults.3 Patients with AS and/or AI are subjected to increased LV pressure and volume load, leading to either concentric or eccentric LV hypertrophy.4 Left ventricular hypertrophy is associated with a 2 to 3-fold increase in cardiovascular-related mortality.5 Regression of LV hypertrophy was incomplete in > 50% of patients studied at 1 to 2 years after aortic valve replacement (AVR).6 Prognostic studies have given rise to the hypothesis that regression of LV hypertrophy is the underlying determinant of longevity after AVR.7–9 Others regard incomplete regression of hypertrophy as a consequence of suboptimal hemodynamic function of the prosthetic aortic valve.10 During 1.5 years of follow-up after AVR for AS, insufficient regression of LV hypertrophy was related to preoperative indices of advanced myocardial disease, which also precluded functional LV improvement despite successful AVR.11 The aim of this study was to compare LV geometric remodeling and regression of LV hypertrophy with ejection fraction (EF) after AVR in patients with pure AS or AI.
|
PATIENTS AND METHODS
|
|---|
The 76 patients who underwent AVR with a mechanical valve for pure AS or pure AI between March 2004 and December 2004 were prospectively enrolled in the study. Exclusion criteria were congenital heart disease, pulmonary or any other systemic disease. Suitable candidates were counseled before providing informed consent. The study was approved and monitored by the local human research ethics committee of our institute. The follow-up time was 2 years, and all patients were evaluated during this period by transthoracic echocardiography early preoperatively, at 6 months, and at 1 and 2 years after the operation by the same cardiology team. Three patients were excluded from the study: one in whom aortic root enlargement was performed, one who had a 19-mm valve implanted, and one who suffered paravalvular leakage during follow-up. The remaining 73 patients (aged 41–67 years) comprised 36 with pure AS and 37 with pure AI. The preoperative data of both groups are given in Table 1
.
All patients underwent AVR under cardiopulmonary bypass instituted with ascending aortic and right atrial cannulation using a 2-stage cannula. Cardioplegic arrest was achieved with 500 mL of cold (4°C) blood cardioplegia infused antegradely into the aortic root, followed by retrograde infusion of 500 mL via the coronary sinus, and maintained by retrograde infusion of 500 mL through the coronary sinus in every 20 min. We used the same types of valve (St. Jude Medical and Carbomedics mechanical prostheses) in both groups: 21–23 mm for AS and 23–27 mm for AI. Appropriate sizes of valves were chosen to avoid patient-prothesis mismatch.
Preoperative and postoperative (6 months and 2 years) transthoracic echocardiography was carried out with the patient in the left lateral decubitus position using a HP Sonos 2500 (Hewlett-Packard, Palo Alto, CA, USA) with a 3.5-Mhz transducer in standard views. Echocardiographic evaluations were made by the same cardiologist (in a blinded fashion at follow-up). Left ventricular dimensions were determined in parasternal long-axis view using M-mode at the tips of the papillary muscles. Left ventricular diameters and volumes, and septal and posterior wall thicknesses were measured according to criteria provided by the American Society of Echocardiography. Pulsed and continuous Doppler interrogation of the aortic valve and the Bernoulli equation were used for calculation of peak and mean gradients in patients with aortic stenosis. Left ventricular mass was normalized for body surface area and for height.12 The continuity equation was used for aortic valve area calculation.
Statistical analysis was performed with SPSS software version 11.0 (SPSS, Inc., Chicago, IL, USA). Preoperative demographic data of both groups were compared using the nonparametric independent-samples t test. Functional capacity, EF, and etiologic factors were compared by the nonparametric chi-squared test. Nominal variables are presented as percentages or mean ± standard deviation, and compared using one-way analysis of variance with the Bonferroni correction. A p value < 0.05 was considered statistically significant.
|
RESULTS
|
|---|
There was no operative or hospital mortality. All preoperative symptoms were relieved in both groups after surgery, and the functional status improved as detailed in Table 2. During follow-up, one patient had warfarin-related gastrointestinal bleeding. There were no significant differences in blood pressure or heart rate between groups. Mean cardiopulmonary bypass times for AS and AI groups were 74 ± 7.5 and 76 ± 9.4 min, respectively, and mean cross clamp times were 51.8 ± 6.5 and 53.7 ± 5.8 min. Echocardiographic parameters are summarized in Table 3. Although the decrease in LV mass index during the first 6 months was similar in both groups, at 2 years postoperatively, it was significantly lower in the AS group than the AI group. The decrease in LV end-diastolic diameter after 2 years was also greater in the AS group. The increase in the EF was significant in both groups at 6 months, but the increase in the late follow-up period was greater for the AS group than the AI group. The increase in EF paralleled the LV geometric measurements (Table 3).
|
DISCUSSION
|
|---|
Gaasch and colleagues13 found that LV end-diastolic dimensions and volumes became near normal in most patients with aortic regurgitation within 2 weeks after AVR, whereas a significant regression of LV hypertrophy took at least 6 months. In our study, there were significant changes in LV remodeling parameters after 6 months in both groups. In the AS group, LV remodeling and improvement in EF were continuing processes, with further significant improvements in the 2nd year. In contrast, LV remodeling and improvement in EF in the AI group did not change significantly between 6 months and 2 years postoperatively.
Some studies have shown that certain patients with aortic regurgitation and severely depressed EF with critical LV dilatation before surgery, failed to achieve regression of LV hypertrophy after AVR.14–16 In patients with AS, the presence of supernormal EF and a disproportionally high increase in wall thickness before AVR was associated with excessive perioperative risks of morbidity and mortality.4,17 On the other hand, patients with AS and less increased wall thickness with eccentric hypertrophy showed decreased systolic function as well as symptoms of heart failure.18 Lamb and colleagues19 compared EF and LV geometric parameters in 19 patients before and after AVR with 10 control subjects. Left ventricular mass index decreased significantly from 126.3 ± 33.1 to 87.5 ± 23.6 g·m–2 in 12 patients with AS, and from 146.5 ± 38.2 to 119.1 ± 29.0 g·m–2 in 7 patients with AI. In both groups, LV mass index after surgery was still significantly higher than in the controls (68.6 ± 7.9 g·m–2), and it was significantly higher in patients with AR than in those with AS. This study was similar to ours, except that the measurements were made by magnetic resonance imaging. Lund and colleagues20 examined patients who underwent AVR for AS for 10 years postoperatively; LV mass index fell rapidly in the first 3 months postoperatively, followed by further slight decreases after 1.5 and 10 years. In our study, there was a similar decrease in LV mass index in the early postoperative period, but after 2 years, there was a further substantial decrease in the AS group and a smaller decrease in the AI group. This means there was gradual remodeling late after AVR for AS, whereas in patients with AI, the improvement was rapid during the first 6 months after the operation but slowed considerably so that there was no further significant change after 2 years.
A limitation of this study was that we compared the regression of LV parameters in patients given mechanical valves only, and did not consider other types of prosthesis. However, it was concluded that after AVR, LV geometric remodeling, regression of LV hypertrophy, and increase in EF were similar in patients with AS and those with AI at 6 months postoperatively, but in the 2nd year of follow-up, the improvement was more marked in the AS group.
|
REFERENCES
|
|---|
- Villari B, Campbell SE, Hess OM, Mall G, Vassalli G, Weber KT, et al. Influence of collagen network on left ventricular systolic and diastolic function in aortic valve disease. J Am Coll Cardiol 1993;22:1477–84.[Abstract]
- Beyerbacht HP, Lamb HJ, van Der Laarse A, Vliegen HW, Leujes F, Hazekamp MG, et al. Aortic valve replacement in patients with aortic valve stenosis improves myocardial metabolism and diastolic function. Radiology 2001;219:637–43.[Abstract/Free Full Text]
- Flachskampf FA, Daniel WG. Aortic valve stenosis. Internist (Berl) 2004;45:1281–90.[Medline]
- Monrad ES, Hess OM, Murakami T, Nonogi H, Corin WJ, Krayenbuehl HP. Time course of regression of left ventricular hypertrophy after aortic valve replacement. Circulation 1988;77:1345–55.[Abstract/Free Full Text]
- Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990;322:1561–6.[Abstract]
- Lund O, Kristensen LH, Baandrup U, Hansen OK, Nielsen TT, Emmertsen K, et al. Myocardial structure as a determinant of pre- and postoperative ventricular function and long-term prognosis after valve replacement for aortic stenosis. Eur Heart J 1998;19:1099–108.[Abstract/Free Full Text]
- Lund O, Vaeth M. Prediction of late results following valve replacement in aortic stenosis. Seventeen years of follow-up examined with the Cox regression analysis. Thorac Cardiovasc Surg 1987;35:295–303.[Medline]
- Lund O. Preoperative risk evaluation and stratification of long-term survival after valve replacement for aortic stenosis. Reasons for earlier operative intervention. Circulation 1990;82:124–39.[Abstract/Free Full Text]
- Lund O, Magnussen K, Knudsen M, Pilegaard H, Nielsen TT, Albrechtsen OK. The potential for normal long-term survival and morbidity rates after valve replacement for aortic stenosis. J Heart Valve Dis 1996;5:258–67.[Medline]
- Krayenbuehl HP, Hess OM, Monrad ES, Schneider J, Mall G, Turina M. Left ventricular myocardial structure in aortic valve disease before, intermediate, and late after aortic valve replacement. Circulation 1989;79:744–55.[Abstract/Free Full Text]
- Lund O, Erlandsen M. Changes in left ventricular function and mass during serial investigations after valve replacement for aortic stenosis. J Heart Valve Dis 2000;9:583–93.[Medline]
- Gaudino M, Alessandrini F, Glieca F, Luciani N, Cellini C, Pragliola C, et al. Survival after aortic valve replacement for aortic stenosis: does left ventricular mass regression have a clinical correlate? Eur Heart J 2005;26:51–7.[Abstract/Free Full Text]
- Gaasch WH, Carroll JD, Levine HJ, Criscitiello MG. Chronic aortic regurgitation: prognostic value of left ventricular end-systolic dimension and end-diastolic radius/thickness ratio. J Am Coll Cardiol 1983;1:775–82.[Abstract]
- de Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, de Divitiis O, et al. Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight. J Am Coll Cardiol 1992;20:1251–60.[Abstract]
- Bech-Hanssen O, Wallentin I, Houltz E, Beckman Suurkula M, Larsson S, Caidahl K. Gender differences in patients with severe aortic stenosis: impact on preoperative left ventricular geometry and function, as well as early postoperative morbidity and mortality. Eur J Cardiothorac Surg 1999;15:24–30.[Abstract/Free Full Text]
- Roman MJ, Klein L, Devereux RB, Kligfield P, Niles NW, Hochreiter C, et al. Reversal of left ventricular dilatation, hypertrophy, and dysfunction by valve replacement in aortic regurgitation. Am Heart J 1989;118:553–63.[Medline]
- Aurigemma GP, Silver KH, McLaughlin M, Mauser J, Gaasch WH. Impact of chamber geometry and gender on left ventricular systolic function in patients > 60 years of age with aortic stenosis. Am J Cardiol 1994;74:794–8.[Medline]
- Bonow RO, Dodd JT, Maron BJ, O’Gara PT, White GG, McIntosh CL, et al. Long-term serial changes in left ventricular function and reversal of ventricular dilatation after valve replacement for aortic regurgitation. Circulation 1988;78:1108–20.[Abstract/Free Full Text]
- Lamb HJ, Beyerbacht HP, de Roos A, van der Laarse A, Vliegen HW, Leujes F, et al. Left ventricular remodeling early after aortic valve replacement: differential effects on diastolic function in aortic valve stenosis and aortic regurgitation. J Am Coll Cardiol 2002;40:2182–8.[Abstract/Free Full Text]
- Lund O, Emmertsen K, Dorup I, Jensen FT, Flo C. Regression of left ventricular hypertrophy during 10 years after valve replacement for aortic stenosis is related to the preoperative risk profile. Eur Heart J 2003;24:1437–46.[Abstract/Free Full Text]
TOP
ABSTRACT
INTRODUCTION
