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J Am Coll Cardiol, 2002; 40:2182-2188
© 2002 by the American College of Cardiology Foundation
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CLINICAL STUDY

Left ventricular remodeling early after aortic valve replacement: differential effects on diastolic function in aortic valve stenosis and aortic regurgitation

Hildo J. Lamb, PhD*,*,1, Hugo P. Beyerbacht, MD{dagger}, Albert de Roos, MD*, Arnoud van der Laarse, PhD{dagger}, Hubert W. Vliegen, MD{dagger}, Ferre Leujes, MD{dagger}, Jeroen J. Bax, MD{dagger} and Ernst E. van der Wall, MD{dagger}

* Radiology, Leiden, The Netherlands
{dagger} Cardiology, Leiden University Medical Center, Leiden, The Netherlands

Manuscript received March 6, 2002; revised manuscript received August 16, 2002, accepted September 6, 2002.

* Reprint requests: Dr. Ernst E. van der Wall, Department of Cardiology, C5-P28, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
E.E.van_der_Wall{at}lumc.nl


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 Conclusions
 References
 
OBJECTIVES: The aim of this study was to evaluate the effect of aortic valve replacement (AVR) on left ventricular (LV) function and LV remodeling, comparing patients with aortic valve stenosis to patients with aortic regurgitation.

BACKGROUND: Aortic valve disease is associated with eccentric or concentric LV hypertrophy and changes in LV function. The relationship between LV geometry and LV function and the effect of LV remodeling after AVR on diastolic filling, in patients with aortic valve stenosis compared with aortic regurgitation, are largely unknown.

METHODS: Nineteen patients with aortic valve disease (12 aortic valve stenosis, 7 aortic regurgitation) were studied using magnetic resonance imaging to assess LV geometry and LV function before and 9 ± 3 months after AVR. Ten age-matched healthy males served as control subjects.

RESULTS: Before AVR, the ratio between left ventricular mass index (LVMI) and left ventricular end-diastolic volume index (LVEDVI) was only increased in patients with aortic valve stenosis (1.37 ± 0.16 g/ml) compared with control subjects (0.93 ± 0.08 g/ml, p < 0.05). After AVR, LVMI/LVEDVI decreased significantly in aortic valve stenosis (to 1.15 ± 0.14 g/ml, p < 0.0001), but increased significantly in aortic regurgitation (1.02 ± 0.20 g/ml to 1.44 ± 0.27 g/ml, p < 0.0001). Before AVR, diastolic filling was impaired in both aortic valve stenosis and aortic regurgitation. Early after AVR, diastolic filling improved in patients with aortic valve stenosis, whereas patients with aortic regurgitation showed a deterioration in diastolic filling.

CONCLUSIONS: Early after AVR, patients with aortic valve stenosis show a decrease in both LVMI and LVMI/LVEDVI and an improvement in diastolic filling, whereas in patients with aortic regurgitation, LVMI decreases less rapidly than LVEDVI, causing concentric remodeling of the LV, most likely explaining the observed deterioration of diastolic filling in these patients.

Abbreviations and Acronyms
  AVR
  aortic valve replacement
  CO
  cardiac output
  E
  early diastolic filling
  LV
  left ventricular
  LVEDVI
  left ventricular end-diastolic volume index
  LVEF
  left ventricular ejection fraction
  LVH
  left ventricular hypertrophy
  LVMI
  left ventricular mass index
  MR
  magnetic resonance

Patients with aortic valve stenosis and/or aortic regurgitation are subjected to increased pressure and/or volume load of the left ventricle, leading to either concentric or eccentric left ventricular hypertrophy (LVH) (1–3). Left ventricular hypertrophy is a recognized risk factor for cardiac morbidity and mortality (4) and is associated with systolic and/or diastolic function disturbances (5–13). In patients with aortic valve disease, diastolic and systolic function disturbances have important implications for morbidity and mortality before and after aortic valve replacement (AVR) (3,5,12–15). A previous study using left ventricular (LV) bi-plane angiography and high-fidelity pressure measurements has shown that diastolic function of patients with aortic valve stenosis deteriorates immediately after AVR. At follow-up, diastolic function improves gradually and may normalize completely long after AVR (13). The effect of AVR on diastolic function in patients with aortic regurgitation has not been studied extensively.

The LV geometrical shape also influences the outcome of AVR (3,14–18). Previous studies have focused on the postoperative regression of LV mass or LV volume (1,3,19,20). The relationship between LV remodeling and changes in LV diastolic filling properties after AVR and the differences between these changes in patients with aortic valve stenosis compared with patients with aortic regurgitation have not been studied previously.

Magnetic resonance (MR) imaging is a noninvasive, highly reproducible method for accurate measurement of LV mass and LV volume without the use of geometric assumptions (21–24). Magnetic resonance phase contrast flow velocity mapping allows measurement of flow-velocity as well as flow-volumes across the mitral valve orifice, providing a new means of diastolic function assessment which may even be a more sensitive method than Doppler echocardiography (25–27). The superior image quality and accuracy of MR imaging compared with echocardiography (21–24) has never been used to assess LV remodeling after AVR and to correlate the observed geometric changes to LV diastolic function. Therefore, the purpose of the present study was to assess the relationship between LV geometry and LV diastolic function in patients with either severe aortic valve stenosis or severe aortic regurgitation, before and early after AVR, using MR imaging.


   Methods
Top
 Abstract
 Methods
Results
 Discussion
 Conclusions
 References
 
Study population.   Nineteen patients (15 males, 4 females) with severe aortic valve disease and without significant coronary artery disease at cardiac catheterization were studied with MR imaging within a period of four weeks before aortic valve surgery. The baseline characteristics of patients and control subjects are listed in Table 1. Twelve patients had predominantly aortic valve stenosis with a peak-to-peak pressure gradient across the aortic valve of at least 60 mm Hg (mean 87.8 ± 22.6 mm Hg) without hemodynamically significant aortic regurgitation (grade 1 or 2; mean grade 1.1 ± 1.0). Seven patients had predominantly aortic regurgitation (grade 3 or 4, mean grade 3.9 ± 0.4) and a peak-to-peak pressure gradient across the aortic valve of <60 mm Hg (mean 22.6 ± 28.0 mm Hg). The MR imaging was repeated 9 ± 3 months after AVR in all 19 patients. A group of 10 healthy, age-matched males served as control subjects; they were normal at physical examination, had a normal electrocardiogram at rest and during exercise stress testing, and had no history of cardiac or any other major illness. The protocol was approved by the hospital’s Human Research Committee. All subjects gave informed consent before investigation.


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  		Table 1 Patient Characteristics Before Aortic Valve Replacement and Characteristics of Control Subjects

 
MR image acquisition
Magnetic resonance imaging was performed on a 1.5-T ACS-NT15 system (Philips Medical Systems, Best, The Netherlands) using prospective electrocardiographic triggering. A stack of short-axis images consisting of 10 to 12 slices (depending on heart size), with a thickness of 8 mm and an intersection gap of 1 mm was acquired using breath hold multishot echo planar imaging. Images encompassed the entire left ventricle. The imaging protocol was similar as reported previously (23).

Phase contrast flow velocity measurements across the mitral valve orifice were acquired using a gradient echo acquisition sequence with retrospective gating. Velocity maps were acquired across the mitral orifice using a flip angle of 20° and an echo time of 10 to 12 ms. The image section had a thickness of 8 mm, a field of view of 350 mm, and consisted of two measurements of a 128 x 128 acquisition matrix which was interpolated to a display matrix of 256 x 256 pixels. Depending on the actual heart rate, between 30 and 45 time frames were evenly distributed over the cardiac cycle, resulting in a temporal resolution of 25 to 30 ms. Total acquisition time was about 3 min. The maximum phase shift of 180° was set to occur at a velocity of 100 cm/s.

MR image analysis
The MR images and velocity maps were analyzed on a remote workstation (Sun Microsystems Computer Corp., Mountain View, California). The LV short-axis acquisitions were used to assess LV dimensions, wall mass, ejection fraction, and cardiac output (CO). The endocardial, epicardial, and papillary muscle borders of the end-diastolic and end-systolic images from each short-axis slice were manually traced using the MR analytical software system developed at this institution (22). Measurements were performed on separate occasions by two independent experienced observers. Reported data represent the average value from both observers. Myocardial borders were detected in the same way as previously reported, with an intraobserver and interobserver variability of 4 ± 2% and 9 ± 3%, respectively (27). The left ventricular mass index (LVMI), left ventricular end-diastolic volume index (LVEDVI), CO, and left ventricular ejection fraction (LVEF) were calculated as described before (23). The ratio of LVMI and LVEDVI (LVMI/LVEDVI) was used as an indicator of LVMI normalized to chamber size. The classification in concentric or eccentric hypertrophy was based on comparison of patients with the control group: a statistically significant increase in LVMI, LVEDVI, and LVMI/LVEDVI is concentric hypertrophy, but a nonstatistically significant difference in LVMI/LVEDVI is eccentric hypertrophy.

Volumetric flow across the mitral valve was calculated by manually tracing the borders of the mitral valve in all time frames of the velocity map series, using the FLOW analytical software package (MEDIS Medical Imaging Systems, Leiden, The Netherlands) (28). Contour tracings were performed on two occasions by a different observer. Flow curves were automatically analyzed following a manual indication of the start of early (E) filling, peak E filling, peak atrial (A) contribution to filling, and the end of filling as described previously (26). To correct for differences in stroke volume and/or heart rate, the E-wave acceleration and deceleration slopes were also normalized for CO.

Statistical analysis
Reported data are expressed as mean values ± 1 SD. When applicable, paired two-tailed Student t tests were used, otherwise two-sample two-tailed Student t tests were used. A p value of <0.05 was considered statistically significant. Correlations were determined using linear regression analysis.


   Results
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 Abstract
 Methods
 Results
Discussion
 Conclusions
 References
 
LV geometry.   All patients with aortic stenosis exhibited an improvement in symptoms directly after surgery. In contrast, only three of seven patients with aortic regurgitation improved in symptoms after the procedure. Finally, in this cohort of patients perioperative mortality was 0% and in-hospital mortality was also 0%. Peripheral systolic and diastolic blood pressures and heart rate did not change significantly after surgery, changing to 127.1 ± 14.9 mm Hg, 74.8 ± 7.0 mm Hg, and 66.1 ± 10.4 beats/min respectively for patients with aortic valve stenosis, and to 121.2 ± 25.0 mm Hg, 65.9 ± 9.8 mm Hg, and 65.6 ± 12.9 beats/min respectively for patients with aortic regurgitation (all p > 0.05, see Table 1 for baseline characteristics). The results of all 19 patients regarding LV function and LV geometry before and after AVR are summarized in Table 2, together with the corresponding data obtained in 10 control subjects. In 12 patients with aortic valve stenosis, LVMI decreased from 126.3 ± 33.1 g/m2 to postoperatively 87.5 ± 23.6 g/m2 (p < 0.0001), and in 7 patients with aortic regurgitation, LVMI decreased from 146.5 ± 38.2 g/m2 to postoperatively 119.1 ± 29.0 g/m2 (p < 0.05). In both groups of patients, LVMI after surgery was still significantly higher than LVMI in control subjects (68.6 ± 7.9 g/m2, p < 0.05). After surgery, LVMI was significantly higher in patients with aortic regurgitation than in patients with aortic valve stenosis (p < 0.05).


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  		Table 2 LV Function and Geometry Before and After Aortic Valve Replacement Compared With Control Subjects

 
The changes in LV geometry after AVR were also assessed by calculation of the changes in LVMI/LVEDVI and are presented in Figure 1. Patients with aortic valve stenosis had concentric LVH, as compared with patients with aortic regurgitation and compared with control subjects. The LVMI/LVEDVI in control subjects was 0.93 ± 0.08 g/ml. Before surgery, this ratio in patients with aortic regurgitation was within the normal range (1.02 ± 0.20 g/ml), but it was elevated in patients with aortic valve stenosis (1.37 ± 0.16 g/ml, p < 0.001 vs. control subjects and vs. aortic regurgitation). After surgery, LVMI/LVEDVI in patients with aortic regurgitation increased from 1.02 ± 0.20 g/ml to 1.44 ± 0.27 g/ml (p < 0.0001), whereas in patients with aortic valve stenosis LVMI/LVEDVI decreased from 1.37 ± 0.16 g/ml to 1.15 ± 0.14 g/ml (p < 0.0001).



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  		Figure 1 The left ventricular mass index (LVMI)/left ventricular end-diastolic volume index (LVEDVI) of 12 patients with aortic valve stenosis and 7 patients with aortic regurgitation, before (PRE) and after (POST) valve replacement, compared with 10 control subjects. Mean values are displayed with standard deviation bars. *p < 0.05 versus control subjects; {dagger}p < 0.05 before surgery versus after surgery (paired two-tailed t test); {ddagger}p < 0.05 aortic stenosis versus aortic regurgitation (pre vs. pre or post vs. post).

 
LV function
Before AVR, ejection fraction was not changed in patients compared with control subjects; LVEF was 60.2 ± 13.2% in patients with aortic valve stenosis, 53.2 ± 10.7% in patients with aortic regurgitation, and 59.0 ± 4.3% in control subjects (p = NS). After AVR, LVEF was significantly higher in patients with aortic valve stenosis than in patients with aortic regurgitation (62.9 ± 5.2% vs. 53.0 ± 8.7%, p < 0.01).

Before AVR, diastolic function was impaired in both groups of patients. For example, the E-wave acceleration peak normalized for CO was lower in patients with aortic valve stenosis and aortic regurgitation (0.046 ± 0.017 s–1 x 10–3 and 0.048 ± 0.008 s–1 x 10–3, respectively) than in control subjects (0.081 ± 0.033 s–1 x 10–3). In patients with aortic valve stenosis, E-wave acceleration peak and deceleration peak slopes normalized for CO improved after AVR, whereas these parameters deteriorated postoperatively in patients with aortic regurgitation (Fig. 2, Table 2).



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  		Figure 2 (A) The maximum acceleration slope of early diastolic filling corrected for cardiac output (E accel peak/CO), and (B) the maximum deceleration slope of early diastolic filling corrected for cardiac output (E decel peak/CO) of 12 patients with aortic valve stenosis and 7 patients with aortic regurgitation, before (PRE) valve replacement and 9 ± 3 months after (POST) valve replacement, compared with 10 control subjects. The mean values are displayed with standard deviation bars. *p < 0.05 versus control subjects; {dagger}p < 0.05 before surgery versus after surgery (paired two-tailed t test); {ddagger}p < 0.05 aortic stenosis versus aortic regurgitation (pre vs. pre or post vs. post).

 
Correlation between LV geometry and LV function
From the data obtained in all 19 preoperative patients and in 10 control subjects, we investigated whether LV geometry and LV function parameters were correlated. To that purpose, baseline LVMI, LVMI/LVEDVI, and LVEDVI were correlated to selected baseline functional parameters. A significant correlation was observed between LVMI and E-wave acceleration (r = –0.49, p < 0.01) and deceleration (r = 0.45, p < 0.05) slopes after normalization for CO. A good correlation was also found between LVMI/LVEDVI and E-wave acceleration and deceleration slopes after normalization for CO (r = –0.50 and r = 0.47 respectively, p < 0.01). The E/A peak did not correlate significantly to LVMI, nor to LVMI/LVEDVI (r = 0.12 and r = 0.31, respectively, p = NS).


   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
Conclusions
 References
 
LV geometry.   Before AVR, we found that patients with aortic valve stenosis had typical concentric LVH, because their LVMI and LVMI/LVEDVI were significantly higher than those of control subjects. After surgery, with relief of pressure overload, LVMI and LVMI/LVEDVI decreased significantly towards values observed in control subjects. However, in patients with aortic regurgitation, preoperative LVMI was significantly increased but LVMI/LVEDVI was comparable to the values in control subjects. After AVR, in these patients LVMI decreased less rapidly than LVEDVI, causing an increase in LVMI/LVEDVI. As a result, these patients showed concentric remodeling of the LV.

Our findings are in agreement with Carroll et al. (17) who found that in most patients with aortic regurgitation LV end-diastolic dimensions and volumes became near normal within two weeks after AVR, whereas a significant regression of LVH took at least six months. However, other studies have shown that several patients with aortic regurgitation who had a severely depressed LVEF and a strongly dilated LV before surgery, failed to achieve regression of LVH after AVR (29,30). These studies also recognized relative wall thickness as an important prognostic parameter in patients with aortic regurgitation (3,29,30).

An increase in LV wall thickness proportional to the increase in LV radius preserves LV systolic wall stress and can prevent irreversible cardiac dilation and failure (3). In patients with aortic valve stenosis, the presence of a supernormal ejection fraction and "disproportionally high" relative wall thickness before AVR is associated with an excessive perioperative risk of morbidity and mortality (2,15,16). Alternatively, aortic valve stenosis patients with a low relative wall thickness and eccentric hypertrophy showed decreased systolic function as well as symptoms of heart failure (18). The clinical implications associated with the contrasting changes in LVMI/LVEDVI after AVR in patients with aortic valve stenosis compared with patients with aortic regurgitation, as observed in the present study, merit future investigation. In the present study, follow-up was relatively short (9 ± 3 months) and only associated with partial regression of LVMI. Complete regression of LVH may take many years (1,3,13,19,20), but it is important because incomplete regression of LVH after AVR is also associated with decreased survival (29).

Diastolic function
Before AVR, all patients with aortic valve disease demonstrated abnormal diastolic filling, resulting from impaired LV relaxation, increased chamber stiffness, and/or chamber dilation (11,31,32). After AVR, in patients with aortic valve stenosis, LV geometry and diastolic properties both showed a trend towards normalization, illustrated by a decrease in both LVMI and LVMI/LVEDVI and an increase of the E-wave acceleration peak and deceleration peak normalized for CO (Table 2, Figs. 1 and 2). However, in patients with aortic regurgitation, the decline of LVEDVI after AVR occurs faster than normalization of LVMI, resulting in concentric remodeling. Concentric LVH is associated with impaired LV relaxation and increased chamber stiffness (5–10,31) and, therefore, may have contributed to the observed worsening of diastolic filling parameters illustrated by a decrease of the E-wave acceleration peak and deceleration peak normalized for CO in patients with aortic regurgitation after AVR. The decrease of the E-wave deceleration peak normalized for CO in patients with aortic regurgitation after AVR is probably largely due to a reduction in left atrial pressure.

The importance of assessment of diastolic function before aortic valve surgery was underlined by two studies of Lund et al. (12,33) who found that impaired diastolic function in patients with aortic valve stenosis is associated with increased mortality in the period before AVR, and is an independent risk factor for early and late postoperative mortality. Other studies have addressed the early and late changes in diastolic function after AVR, both in patients with aortic valve stenosis and in patients with aortic regurgitation (5,8,10,13,14). Patients with aortic valve stenosis had increased diastolic stiffness early after AVR, parallel to the relative increase in interstitial fibrosis (13). Moreover, diastolic stiffness and relaxation normalized late (81 ± 24 months) after AVR owing to regression of both muscular and nonmuscular tissue. Relaxation was correlated to the extent of hypertrophy, whereas passive elastic properties were correlated to changes in nonmuscular tissue (13).

In the present study, MR phase contrast flow velocity mapping was used to assess diastolic function. The studied groups represented a wide range of LV sizes and corresponding stroke volumes. Usually, the shape of the LV filling curve is influenced by LV relaxation, left atrial pressure, elastic properties of the LV, but also by stroke volume, ventricular size, and heart rate (11,31,32). Mirsky (34) suggested inclusion of LV volume in the chamber stiffness-pressure relationship and introduced the term "volume elasticity." To follow the concept of volume elasticity, we normalized the E acceleration peak and E deceleration peak for CO. As demonstrated in Table 2, the differences in diastolic properties of the LV between patients and control subjects, but also between aortic valve stenosis and aortic regurgitation patients, only became fully apparent after normalization of early diastolic filling (E) for CO.

Ejection fraction
Ejection fraction was largely unaffected in the present group of patients with severe aortic valve disease. Before and after AVR, LVEF was slightly lower in patients with aortic regurgitation compared with both control subjects and patients with aortic valve stenosis, although LVEF differed significantly only between postoperative patients with aortic valve stenosis and postoperative patients with aortic regurgitation. These findings confirm that diastolic function in aortic valve disease is affected at an earlier stage of the disease process than the ejection fraction. Therefore, deterioration of the ejection fraction should be considered as a sign of severe and advanced aortic valve disease (12,14).

Correlation between LV geometry and LV diastolic function
Increased LVMI and increased LVMI/LVEDVI were negatively correlated to the E acceleration peak normalized for CO. The acceleration peak of E is influenced by several determinants such as left atrial pressure, the LV relaxation constant, LV end-systolic volume, LV systolic function, and intrinsic myocardial stiffness (11,31,32). In patients with aortic valve stenosis before AVR, the depressed E acceleration peak is due to prolonged LV relaxation and increased myocardial stiffness (31). After surgery, LVMI and LVMI/LVEDVI both decreased, whereas the E acceleration peak increased, the latter largely due to improved myocardial relaxation and reduced myocardial stiffness (31). In patients with aortic regurgitation before AVR, the depressed E acceleration peak slope results from prolonged LV relaxation and increased myocardial stiffness (11,31,32). After surgery, LVMI decreased but LVMI/LVEDVI increased, leading to concentric remodeling. The further decrease of the E acceleration peak slope is most likely caused by a reduced left atrial pressure combined with a prolongation of myocardial relaxation and increment of myocardial stiffness (31).

The LVMI and LVMI/LVEDVI were positively correlated to the E deceleration peak normalized for CO. Concentric LVH increases intrinsic myocardial stiffness and is known to shorten the deceleration time and to increase the deceleration peak of E (11,31,32). In patients with aortic valve stenosis before AVR, the depressed E deceleration peak slope, therefore, is due to prolonged LV relaxation (11,31). After surgery, LVMI and LVMI/LVEDVI both decreased, whereas the E deceleration peak slope increased, most likely as a result of improved myocardial relaxation (31).

In patients with aortic regurgitation before AVR, the depressed E deceleration peak also results from prolonged LV relaxation (31). After surgery, LVMI decreased but LVMI/LVEDVI increased, leading to concentric remodeling. The further decrease of the E deceleration peak slope after AVR, therefore, is mainly caused by a reduction of left atrial filling pressure and a prolongation of myocardial relaxation (11,31,32).

Study limitations
Patient follow-up after surgery was performed at 9 ± 3 months, so early and late effects of surgery are mixed. Thus, changes in morphology and function are not completely uniform, which is reflected by the reported standard deviations.

The clinical definition for concentric and eccentric hypertrophy or remodeling, as described in the present study, may be different from the pathophysiologic definition. The main difference is that with the currently applied imaging technique it is not possible to evaluate sarcomere orientation. Therefore, the parallel sarcomere deposition in concentric hypertrophy cannot be discriminated from the serial deposition in eccentric hypertrophy.

In the present study, it was not clinically feasible to measure invasive left atrial pressures. Therefore, on the basis of previous reports, we only speculate on the effects of changes in left atrial pressures on diastolic filling characteristics.


   Conclusions
Top
 Abstract
 Methods
 Results
 Discussion
 Conclusions
References
 
Patients with aortic valve stenosis or patients with aortic regurgitation show a differential response in diastolic function early after AVR. Before AVR, patients with aortic valve stenosis show concentric LVH. Early after AVR, both LVMI and LVMI/LVEDVI decrease and diastolic filling improves. In patients with aortic regurgitation, preoperative LVMI and LVEDVI are about equally increased, resulting in a LVMI/LVEDVI within the normal range. Early after AVR, LVMI decreases less rapidly than LVEDVI, causing an increase in LVMI/LVEDVI. Despite the absolute decrease in LVMI, these patients at least temporarily show concentric remodeling of the LV, most likely explaining the observed deterioration of diastolic filling in these patients.


   Footnotes
 
1 Correspondence: Dr. Hildo J. Lamb, Department of Radiology, C2S, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands. Back


   References
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 Methods
 Results
 Discussion
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 References
 

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