Early Regression of Left Ventricular Wall Thickness following Percutaneous Aortic Valve Replacement (Full title below)

Early Regression of Left Ventricular Wall Thickness following Percutaneous Aortic Valve Replacement (Full title below)
Early Regression of Left Ventricular Wall Thickness following Percutaneous Aortic Valve Replacement (Full title below)
Early Regression of Left Ventricular Wall Thickness following Percutaneous Aortic Valve Replacement (Full title below)
Early Regression of Left Ventricular Wall Thickness following Percutaneous Aortic Valve Replacement (Full title below)
Early Regression of Left Ventricular Wall Thickness following Percutaneous Aortic Valve Replacement (Full title below)
Early Regression of Left Ventricular Wall Thickness following Percutaneous Aortic Valve Replacement (Full title below)
Early Regression of Left Ventricular Wall Thickness following Percutaneous Aortic Valve Replacement (Full title below)
Author(s): 

*Hasan Jilaihawi, MBChB, *Mohamed Jeilan, MD, §Tomasz Spyt, MD, *Derek Chin, MD,
§Elaine Logtens, BSc, *Jan Kovac, MUDr

From the *Department of Cardiology and the §Department of Cardiothoracic Surgery, Glenfield Hospital, Leicester, United Kingdom.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted November 17, 2008, provisional acceptance given December 2, 2008 and final version accepted December 31, 2009.
Corresponding author: Jan Kovac, MD, Department of Cardiology, Glenfield Hospital, Leicester United Kingdom LE3 9QP. E-mail: [email protected]

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Early Regression of Left Ventricular Wall Thickness following Percutaneous Aortic Valve Replacement with the CoreValve Bioprosthesis

ABSTRACT: Background/Aims. Severe aortic stenosis (AS) is associated with hypertrophy of the left ventricle (LVH), which is linked to adverse clinical outcomes. To date, the effects of the novel technology of percutaneous aortic valve replacement (PAVR) on LVH in severe AS have not been described. We sought to test the hypothesis that PAVR would result in regression of LVH associated with severe AS. Methods. Patients were recruited as part of a single-arm, prospective, safety, feasibility and clinical outcome study of the third-generation CoreValve percutaneous aortic bioprosthesis. To assess hypertrophy at baseline and at 1 month, the parasternal long-axis view in end-diastole was used to assess interventricular septal dimension and left ventricular posterior wall dimension. Results. 15 patients were studied. There were significant periprocedural reductions in peak (76.6 ± 28.1 mmHg to 16.3 ± 7.5 mmHg; p < 0.001) and mean (45.3 ± 18.4 mmHg to 8.2 ± 3.7 mmHg; p = 0.001) transvalvular gradients and increases in calculated aortic valve areas (0.73 ± 0.19 cm2 to 1.5 ± 0.3 cm2). Septal wall thickness regressed by 13% from 1.54 ± 0.30 cm at baseline to 1.35 ± 0.27 cm at 1 month (for difference; p = 0.002). Conclusion. We demonstrate an early regression of septal hypertrophy after PAVR for severe AS which is comparable to that seen at 1 year after conventional surgical aortic valve replacement.

J INVASIVE CARDIOL 2009;21:151–155

Degenerative calcific aortic stenosis (AS) is the most common form of valvular heart disease in adults in the Western world1 and is increasing in prevalence with an aging population. It is associated with left ventricular hypertrophy (LVH) and changes in ventricular geometry to preserve the relationship between intraventricular pressure and wall stress.2 This hypertrophy is linked to left ventricular diastolic dysfunction.3 Conventional aortic valve replacement reduces afterload, wall stress, and in turn, wall thickness.4 Following surgery, there is an early improvement in diastolic dysfunction that precedes regression of hypertrophy.5 LVH persisting late after aortic valve replacement is associated with impaired exercise tolerance and cardiac morbidity.6

Open surgical valve replacement is the treatment of choice for the majority of patients with AS, offering symptomatic relief and improving long-term survival, even in the elderly.7 However, up to a third of highly symptomatic patients with a significantly diseased valve are declined surgery due to associated comorbid conditions,1 which are known to carry a high operative mortality rate.8 Consequently, newer, less invasive techniques involving percutaneous aortic valve replacement (PAVR) are being evaluated. The short- and medium-term safety and efficacy of treating severe AS with PAVR (via both transfemoral and transapical approaches) has recently been demonstrated in several small case series.9–11

The early effects of PAVR on LVH have not yet been evaluated. Evidence suggests that different conventional surgical valves (stented and stentless bioprostheses and mechanical prostheses) differ to some extent in their effects on left ventricular wall thickness following aortic valve replacement.12,13 We studied the impact of PAVR on LVH and hypothesized that in patients with severe degenerative AS and concomitant LVH, PAVR with the CoreValve (CoreValve, Inc., Irvine, California) stented bioprosthesis would result in regression of LVH early post procedure.

Methods

The study cohort comprises patients with AS and LVH undergoing PAVR within a single-arm, prospective multicenter international safety, feasibility and clinical outcome study of the 18 Fr third-generation CoreValve aortic revalving system. Baseline operative risk was estimated by the logistic Euroscore.8 Inclusion criteria for the study were severe symptomatic AS (aortic valve area < 1 cm2) and age ≥ 75 years or logistic Euroscore ≥ 15%. Patients were also selected on a technical basis: 1) annulus size by echocardiography between 20 mm and 23 mm (for this time period, although a second, larger prosthesis exists currently); 2) peripheries at the level of the common femoral artery and proximal iliacs free of gross tortuosity and ≥ 6 mm as assessed by invasive quantitative angiography via the femoral route with a graduated pigtail; and 3) aorta at the sinotubular junction ≤ 43 mm. Patients with flow-limiting coronary artery disease received revascularization where appropriate prior to the PAVR procedure. The CoreValve aortic valve prosthesis consists of a trileaflet bioprosthetic porcine pericardial tissue valve, which is mounted and sutured in a self-expanding nitinol stent (Figure 1). The prosthetic frame (stent) is manufactured by laser cutting and has an overall length of 50 mm. Other details of the device and the procedure have been described previously.11 C-reactive protein (CRP) was measured preprocedure, early post procedure and pre-discharge.

Echocardiographic methods. A comprehensive two-dimensional and Doppler transthoracic echocardiogram was performed in the left lateral decubitus position on each patient at three timepoints: 1) immediately prior to the procedure; 2) predischarge; and 3) at 1-month follow up. Standard views were obtained with simultaneous electrocardiographic (ECG) monitoring. Second harmonic imaging (1.8–3.6 Mhz) was used to enhance endocardial border definition. All measurements were made using HeartLab imaging software (Agfa-Gevaert Group, New Jersey). At each time point, peak and mean aortic valve gradient, aortic valve area by continuity equation and biplane ejection fraction (EF) were calculated. End-diastolic measurements of interventricular septal dimension (IVSd) and LV posterior wall dimension (LVPWd) were taken from a parasternal long-axis view. Additional measurements of LV basal wall thickness were calculated:14 in the parasternal short-axis view at the mitral valve level, epicardial and endocardial borders were traced in end-diastole and a derived measure of wall thickness was calculated as (sqrt[epicardial area/pi]-sqrt[endocardial area/pi]). LV mass was calculated according to the Penn-Cube formula15 using values obtained in the two-dimensional parasternal long-axis view. End-diastole was defined by the onset of the R wave on the simultaneously recorded cardiac cycle. End-systole was identified as the smallest cavity size just before mitral valve opening. LV end-diastolic volume (EDV) and end-systolic volume (ESV) were calculated by the modified Simpson’s rule using the built-in quantitative programs; EF was calculated as EDV - ESV. Measurements were performed offline at each timepoint by two echocardiographers. The intraobserver correlation of echocardiographic measurements was assessed offline by the primary reader performing a second analysis of half of the studies7 selected at random. The interobserver correlation was tested for a second observer for the same randomly selected studies.

Statistical analysis. Data are presented as mean and standard deviation (SD) for continuous variables and absolute frequencies for categorical variables unless specified otherwise. Differences were assessed using a paired sample T-test for normally distributed data; where data did not follow a normal distribution, the paired Wilcoxon test was used. For interobserver and intraobserver correlation, the intraclass correlation coefficient was used. For other correlations, Pearson bivariate analysis was employed. A two-sided probability value of p < 0.05 was considered statistically significant. Statistical analyses were made using SPSS software (version 14) (SPSS, Inc., Chicago, Illinois).

Results

Baseline characteristics. The characteristics at baseline are summarized in Table 1. Fifteen patients with severe AS and LVH underwent PAVR between the 30th of January 2007 and the 17th of July 2007. Patients had a mean (SD) age of 85.8 (4.5) years and were predominantly female. All patients were symptomatic, with the majority (66.7%) having New York Heart Association (NYHA) Class II symptoms and the remainder Class III symptoms. Peak transvalvular gradient at baseline was 76.6 ± 28.1 mmHg and mean 45.3 ± 18.4 mmHg. Calculated aortic valve area at baseline was 0.73 ± 0.19 cm2. At 1-month follow up there were no case fatalities.

Hemodynamic results. A complete study dataset was available in 14 of the 15 patients. One patient with previous total pneumonectomy had unsuitable transthoracic echocardiographic windows, with poor endocardial definition preventing accurate measurement of wall thickness and chamber dimensions. In this patient, valve hemodynamic measurements were recorded. Significant periprocedural reductions were observed in peak (76.6 ± 28.1 mmHg to 16.3 ± 7.5 mmHg; p < 0.001; n = 15) and mean (45.3 ± 18.4 mmHg to 8.2 ± 3.7 mmHg; p = 0.001; n = 15) (Figure 2) transvalvular gradients. Calculated aortic valve areas increased from 0.73 ± 0.19 cm2 to 1.5 ± 0.3 cm2 (n = 15) (Figure 2). The majority of patients had preserved LV systolic function at baseline (EF > 55%). There was no change in EF from baseline to 1 month (54.8 ± 8.0 % to 57.5 ± 5.9 %; n = 14; p = 0.415). However, in patients with some degree of LV systolic impairment at baseline (EF < 55%), EF increased from 45.0 ± 8.5 % to 55.6 ± 9.9 % (p = 0.004; n = 7).

Changes in parameters of left ventricular hypertrophy. Preprocedural IVSd dimension at baseline was 1.54 ± 0.30 cm; a mild asymmetry of hypertrophy was observed with a relatively smaller LVPWd of 1.36 ± 0.36 cm (for difference p = 0.01; n = 14). A significant reduction in septal wall thickness (13%) was noted (1.54 ± 0.30 cm at baseline to 1.35 ± 0.27 cm at 1 month [p = 0.002; n = 14]). In contrast, LVPWd did not change (LVPWd at baseline: 1.36 ± 0.36 cm; at 1 month: 1.37 ± 0.31 cm; p = 0.856; n = 14). Derived thickness at the mitral valve level did not change significantly (1.10 ± 0.13 cm at baseline to 1.02 ± 0.14 cm at 1 month; p = 0.21). Similarly, LV mass remained constant (321.5 ± 78.4 g at baseline vs. 325.9 ± 49.9 g at 1 month; for difference, p = 0.811). For interobserver and intraobserver wall dimension measurements, the intraclass correlation coefficients were 0.96 and 0.97, respectively (significance level > 0.001). Data were available for 11 patients at the latest available follow up of 6–12 months; 3 died within this timeframe. IVSd dimension was 1.39 ± 0.21 cm (p = 0.02 for reduction relative to baseline). There was a nonsignificant trend toward a reduced LVPWd of 1.24 ± 0.19 cm at this later timepoint (p = NS relative to baseline).

Changes in C-reactive protein (CRP). CRP was minimally elevated at baseline at 7.8 mg/L (1.3). It increased dramatically to 96 mg/L (64.3) (p = 0.03) predischarge and partially recovered to 26.1 mg/L (28.4) at a median follow up of 30 days.

Discussion


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