The long-term follow-up data subsequent to a successful repair of AoC (aortic coarctation) show that life expectancy remains reduced. Previous standard echocardiographic studies have demonstrated normal or increased systolic cardiac function in patients following successful repair of AoC. SR (strain rate) imaging is a new technique able to detect subclinical myocardial abnormalities. In the present study we investigated whether young patients (without hypertension, as assessed using ambulatory blood pressure monitoring and an exercise test) following successful AoC repair already have abnormal myocardial deformation properties, and the relationship of the deformation properties with aortic stiffness. We studied 166 subjects, 83 AoC non-hypertensive patients (mean age 12±4 years) a number of years after successful repair of AoC and 83 age- and sex-matched subjects as controls. Peak systolic SR (1/s) for both regional longitudinal and radial function was assessed. The aortic stiffness index was calculated from the echocardiographically derived thoracic aortic diameters, and the measurement of blood pressure was obtained by cuff sphygmomanometry. The LV (left ventricular) ejection fraction was significantly increased in AoC patients, whereas regional longitudinal SRs were significantly reduced (−1.1±0.9 compared with −2±0.5, P<0.0001) in patients. The aortic stiffness index was significantly increased in AoC patients (12±9, P<0.0001). At multilinear regression analysis, age at repair (P=0.005; coefficient, −0.201; S.E.M., 0.027) and the aortic stiffness index (P=0.0029; coefficient, 0.334; S.E.M., 0.423) predicted longitudinal SR. Despite the presence of a successful repair for AoC, in the absence of hypertension, longitudinal deformation properties were significantly impaired. Moreover, the degree of longitudinal SR impairment was correlated with age at repair and aortic stiffness. Early repair can delay the onset of hypertension in postcoarctectomy patients, but cannot prevent the innate structural and functional abnormalities of the aorta and their deleterious effect on myocardial deformation properties.

INTRODUCTION

The long-term follow-up data subsequent to a successful repair of AoC (aortic coarctation) show that life expectancy remains reduced in AoC patients [1,2]. Late arterial hypertension, more often systolic, which occurs in nearly one third of patients after repair, and atherosclerosis are the main determinants of cardiovascular events [13]. Coronary heart disease, stroke, sudden cardiac death and heart failure account for the majority of premature deaths [13], and prognosis is related to the age at intervention [13]. Other studies suggest that AoC might not simply be a mechanical obstruction of the aorta, but more probably a generalized disease of the cardiovascular system [4]. Despite this, previous studies based on standard echocardiography have demonstrated normal or increased systolic cardiac function in patients after successful repair of AoC [59]. New tools, such as ultrasonically derived SR (strain rate) imaging, have added to our capabilities [10,11] and it is now possible to detect early subclinical myocardial abnormalities [1217]. The myocardial deformation properties in patients after AoC repair have not yet been described. In the present study we have sought to evaluate the myocardial deformation properties in normotensive AoC children a number of years following successful AoC repair and to assess the relationship of the deformation properties with arterial stiffness.

MATERIALS AND METHODS

Study sample

We studied consecutive AoC patients regularly followed at our outpatient clinic from June 2003 to September 2006 without (i) major associated cardiovascular abnormalities (such as ventricular septal defect and aortic and mitral valve functional abnormalities); (ii) evidence of recoarctation (>20 mmHg pressure gradient at continuous Doppler in the aortic arch and the presence of a diastolic tail) [18,19]; (iii) evidence of aortic aneurysm at the last outpatient visit; and (iv) hypertension. A patient was assumed to be ‘normotensive’, if they (i) were without antihypertensive drug treatment; (ii) had SBP and DBP [systolic and diastolic BP (blood pressure) respectively] <90th percentile for age, sex and height at office measurements; (iii) had 24-h SBP and DBP <90th percentile for age, sex and height; and (iv) had no hypertension during exercise. If at least one of these signs was positive, the patient was classified as ‘hypertensive’ and excluded from the study.

Control group

Using an identical protocol, we also studied 83 age- and sex-matched subjects with no detectable cardiovascular risk factors. Volunteer controls were all recruited in Naples (Italy) and were selected from our departments of paediatric cardiology among children investigated for dizziness or minor orthostatic complaints, or for sport eligibility. None of the control subjects had a family history of cardiomyopathy, cardiovascular structural or functional abnormalities or received any medication. All studies were performed in accordance with the rules of the Ethics Committee of the Second University of Naples. All parents gave their written informed consent for their children to participate in the study.

Clinical assessment

During a 1 day stay, anamnestic and anthropometric data were reviewed. Resting BP was measured at all extremities using an automatic oscillometric cuff device (Dinamap; Critikon).

ABPM (ambulatory BP monitoring)

ABPM over 24 h was measured on the right arm (Space Labs). BP measurements were recorded automatically every 15 min from 08.00 hours to 20.00 hours and every 30 min from 20.00 hours to 08.00 hours. BP studies were excluded if there was an interval of 2 h of invalid or absent measurements. Hypertension at ABPM was defined as 24-h SBP or 24-h DBP >90th percentile of the reference values provided by Soergel et al. [20]. To allow interpretation of data by ABPM normative data [20], only patients with a height between 115 and 185 cm were included.

Exercise test

An exercise test was performed on a bicycle in a sitting position according to international guidelines [21]. The WHO (World Health Organization) protocol was used starting with 25 W and increasing work load by 25 W every 2 min [22]. ECG was monitored continuously and the BP was measured manually every 2 min. Hypertension during exercise was present when the peak SBP (mmHg) was more than 2 S.D. above the age- and work-load-dependent reference value [23]:

 
formula

Standard echocardiographic evaluation

Echocardiography measurements were taken with a System Seven instrument (GE Medical Systems).

In the present studies two echocardiographers were involved. All of the echocardiographic examinations were performed by the same observer (echocardiographer 1). All the echocardiographic measurements were performed off-line on digitally stored raw data by another investigator (echocardiographer 2) who was blinded to the clinical status of the studied subjects. The ascending aorta and the aortic arch were visualized by means of high long-axis view and suprasternal view. LV (left ventricular) measurements were taken from two-dimensional-guided M-mode tracings.

Parameters measured by echocardiography were the pressure gradient throughout the former coarctation region and the LV and aortic morphology. LVMI (LV mass indexed for height2.7) was calculated [24]. LV end-diastolic and end-systolic volumes and LVEF (LV ejection fraction) at rest were computed from apical four- and two-chamber views using a modified Simpson's biplane method. Each representative value was obtained from the average of three measurements. The endocardial VCFc (mean velocity of circumferential fibre shortening corrected for the heart rate) and end-systolic circumferential stress [25] were calculated.

To assess global LV and RV (right ventricular) longitudinal function from the standard apical view, the atrioventricular ring displacement was measured for the septal and lateral mitral ring [MAPSE (mitral annulus peak systolic excursion)] and lateral tricuspid ring [TAPSE (tricuspid annulus peak systolic excursion)] by conventional M-mode methods.

Mitral inflow velocities, E (early diastolic transmitral peak velocity), A (late diastolic transmitral peak velocity), E/A ratio, DT (deceleration time of E), the duration of A and IVRT (isovolumic relaxation time) were measured using pulsed-wave Doppler.

Echocardiography of the aorta

Thoracic aortic diameters (mm/m2) were measured 3 cm above the aortic valve by two-dimensional-guided M-mode transthoracic echocardiography of the aortic root at the left parasternal long-axis view. AoS (aortic systolic diameter) was measured at the time of full opening of the aortic valve, and the AoD (aortic diastolic diameter) was measured at the peak of the QRS complex at the simultaneous ECG recording. The aortic stiffness index was calculated as follows:

 
formula

CDMI (colour Doppler myocardial imaging)

CDMI data to assess longitudinal function were recorded from the interventricular septal and the LV lateral walls from the standard apical view.

The radial function for the LV posterior wall was recorded using the parasternal long-axis view. All data were acquired at a frame rate of 200±15 frames/s (GE Vingmed System Seven; 3.5 MHz). This frame rate was necessary to resolve cardiac mechanical events and to average out the influence of any random noise in the Doppler velocity signal. An appropriate velocity scale was chosen in order to avoid CDMI data aliasing. The narrowest image sector angle possible (usually 30°) was used to achieve the maximum colour Doppler frame rate possible. For apical views, care was taken to maintain each wall in the centre of the ultrasound sector in an attempt to align it as near as possible to the direction of longitudinal motion. For the parasternal long-axis view, care was paid to keeping the posterior LV wall perpendicular to the ultrasound beam in order to be aligned as near as possible to radial motion.

As breath holding is not feasible in young patients data from three consecutive cardiac cycles (to be used for subsequent analysis) were recorded during normal quiet respiration. CDMI data were stored in digital format and transferred to a computer workstation for the off-line analysis of regional SR curves. This was carried out using dedicated software (GE Workstation). Longitudinal SRs were estimated by measuring the spatial velocity gradient over a computation area of 10 mm. LV regional longitudinal function was evaluated on the apical, mid and basal segments of septal and lateral LV walls. Those LV walls were chosen because they had the best alignment with the ultrasound beam.

LV radial SRs were estimated using a computation area of 5 mm from the mid segment of the LV posterior wall. To derive SR profiles from the different segments, the region of interest was maintained in a constant position within the segment being interrogated using a semi-automatic tracking algorithm.

The timing of ventricular ejection and relaxation was obtained using an anatomic greyscale M-mode cursor positioned visually in the underlying greyscale data set. The timing of these events was measured by placing the cursor at the level of aortic cusps and the mitral valve. From the averaged SR data, the peak systolic SR was measured. We decide to measure only SR because this is the less load-dependent contractility index obtained using CDMI data [27,28].

Pulsed-wave tissue Doppler of the septal annulus was used for the measurement of e′ (early diastolic mitral annular peak velocity). The E/e′ ratio was calculated.

Statistical analysis

All of the analyses were performed using a commercially available package (Rel 11.0 2002, SPSS).

Values are presented as means±S.D. The normality Kolmogorov–Smirnov test was performed to determine whether continuous variables were normally distributed. Age at the time of repair, which had a skewed distribution, is provided as the median value (range). Qualitative data were compared using the Mantel–Haenszel test. Continuous variables were compared using a paired Student's t test and Wilcoxon matched-pairs test. The correlations were studied by linear regression analysis. In addition, to identify significant predictors of average LV peak systolic SR in AoC patients, their individual association with clinically relevant variables was assessed by multiple regression analyses. Included in the analysis were clinical data (age, age at repair and 24-h SBP) and echocardiographic Doppler indexes (LVMI, aortic stiffness index, DT, A wave duration and E/e′). These variables were selected according to results of univariate analysis and to their clinical relevance and potential impact on prognosis, as shown by earlier studies [19]. The assumption of linearity was checked graphically by studying the smoothed margingal residuals from the null model plotted against the covariate variables. The linearity assumptions were satisfied. The Hosmer–Lemeshow goodness-of-fit test was used to check that the model adequately fitted the data. The model was cross-validated by the bootstrap technique (200 runs) [29].

The null hypothesis was rejected for a P-value <0.01. Reproducibility between the two echocardiographers was determined in 60 randomly selected subjects (30 patients and 30 controls). Inter- and intra-observer variability was examined using both Pearson's bivariate two-tailed correlations and Bland–Altman analysis. Pearson's correlations for peak systolic SR were r=0.88, P=0.0001 and for peak systolic strain were r=0.92, P=0.00001. For Bland–Altman analysis the 95% confidence limit and the percentage error for peak systolic SR were +3.1 and 3.5% respectively, and for peak systolic strain were +2.5 and 2.3% respectively.

RESULTS

In the present study 83 AoC normotensive patients were included and, of these, 45% had a bicuspid aortic valve without significant functional abnormalities (only trivial to mild aortic regurgitation, or peak pressure gradient at continuous Doppler <20 mmHg). AoC repair had been performed at a median age of 4 months (range 0.1–156 months), with 58% of subjects undergoing surgery within the first 4 months of life (mean age 12±4 years, 70% male). All were in the typical juxtaductal position. Repair was by end-to-end anastomosis in 48% of patients, by subclavian flap in 15%, by patch angioplasty in 18% and by primary percutaneous stent implantation in 19%. The median time from coarctation repair to the present study was 100 months (range 16–216 months).

Clinical characteristics of the study sample are shown in Table 1.

Table 1
General characteristics of the subjects studied

BSA, body surface area.

AoC patients (n=83)Controls (n=83)P-value
Age (years) 12±4 12±4 0.9 
Male (%) 70 70 0.9 
BSA (m21.2±0.3 1.2±0.3 0.9 
SBP (mmHg) 118±17 115±10 0.15 
DBP (mmHg) 66±9 65±6 0.38 
24-h SBP (mmHg) 114±10 111±12 0.0001 
24-h DBP (mmHg) 66±6 64±10 0.10 
Resting heart rate (beats/min) 85±8 85±5 0.9 
Peak exercise SBP (mmHg) 156±16 140±16 0.0001 
Exercise duration (min) 9±3 11±3 0.0001 
AoC patients (n=83)Controls (n=83)P-value
Age (years) 12±4 12±4 0.9 
Male (%) 70 70 0.9 
BSA (m21.2±0.3 1.2±0.3 0.9 
SBP (mmHg) 118±17 115±10 0.15 
DBP (mmHg) 66±9 65±6 0.38 
24-h SBP (mmHg) 114±10 111±12 0.0001 
24-h DBP (mmHg) 66±6 64±10 0.10 
Resting heart rate (beats/min) 85±8 85±5 0.9 
Peak exercise SBP (mmHg) 156±16 140±16 0.0001 
Exercise duration (min) 9±3 11±3 0.0001 

Standard echocardiography (Table 2) demonstrated an increased wall thickness and a significant increase in LVMI in AoC patients. LVEF and VCFc were significantly increased in AoC patients. End-systolic stress was significantly reduced in AoC patients (Table 2).

Table 2
Standard echocardiographic characteristics of the subjects studied

IVS, interventricular septum; PW, posterior wall.

AoC patients (n=83)Controls (n=83)P-value
IVS end-diastole (mm) 11±2 7±2 <0.0001 
LV end-diastole (mm) 40±7 40±7 0.9 
LVPW end-diastole (mm) 9±2 7±2 <0.0001 
LVEF (%) 68±8 64±7 0.0001 
LVMI (g/m2.749±20 33±14 <0.0001 
VCFc (circ/s) 1.3±0.2 1.1±0.2 <0.0001 
End-systolic stress (g/cm238±14 46±12 0.001 
MAPSE-septal wall (mm) 12±5 13±3 0.05 
MAPSE-lateral wall (mm) 12±4 15±6 0.11 
TAPSE (mm) 24±5 22±6 0.14 
E/A 1.8±0.6 1.7±0.1 0.06 
DT (ms) 239±57 150±15 <0.0001 
A duration (ms) 97±22 86±17 0.001 
E/e′ 7±2 5±1 <0.0001 
IVRT (ms) 48±19 50±16 0.36 
Aortic stiffness index 12±9 6±4 <0.0001 
AoC patients (n=83)Controls (n=83)P-value
IVS end-diastole (mm) 11±2 7±2 <0.0001 
LV end-diastole (mm) 40±7 40±7 0.9 
LVPW end-diastole (mm) 9±2 7±2 <0.0001 
LVEF (%) 68±8 64±7 0.0001 
LVMI (g/m2.749±20 33±14 <0.0001 
VCFc (circ/s) 1.3±0.2 1.1±0.2 <0.0001 
End-systolic stress (g/cm238±14 46±12 0.001 
MAPSE-septal wall (mm) 12±5 13±3 0.05 
MAPSE-lateral wall (mm) 12±4 15±6 0.11 
TAPSE (mm) 24±5 22±6 0.14 
E/A 1.8±0.6 1.7±0.1 0.06 
DT (ms) 239±57 150±15 <0.0001 
A duration (ms) 97±22 86±17 0.001 
E/e′ 7±2 5±1 <0.0001 
IVRT (ms) 48±19 50±16 0.36 
Aortic stiffness index 12±9 6±4 <0.0001 

Among the studied diastolic parameters, E, DT and A wave duration were significantly prolonged in AoC patients. The E/e′ ratio was significantly increased in patients. The stiffness of the aortic wall as assessed by the aortic stiffness index was also significantly increased in patients (P<0.0001). Radial peak systolic SR was significantly increased in AoC patients (Table 3), whereas regional longitudinal peak systolic SRs were significantly reduced in AoC patients (Table 3). Among AoC patients, 16 (19%) were outside the 95% lower confidence limits in the normal group.

Table 3
Peak systolic SR (1/s) values of the subjects studied
AoC patients (n=83)Controls (n=83)P-value
Posterior wall    
 Parasternal short-axis view 3.1±0.7 2.8±0.5 0.001 
 Parasternal long-axis view 3.2±0.6 2.7±0.5 0.001 
Apical four-chamber view    
 Basal septum −1.1±0.9 −2±0.5 <0.0001 
 Mid septum −1.2±0.5 −1.9±0.4 <0.0001 
 Apical septum −1.3±0.7 −2.1±0.7 <0.0001 
 Basal LV lateral wall −1.4±0.7 −1.9±0.7 0.001 
 Mid LV lateral wall −1.3±0.6 −1.9±0.5 0.001 
 Apical LV lateral wall −1.6±0.6 −2.0±0.6 0.001 
AoC patients (n=83)Controls (n=83)P-value
Posterior wall    
 Parasternal short-axis view 3.1±0.7 2.8±0.5 0.001 
 Parasternal long-axis view 3.2±0.6 2.7±0.5 0.001 
Apical four-chamber view    
 Basal septum −1.1±0.9 −2±0.5 <0.0001 
 Mid septum −1.2±0.5 −1.9±0.4 <0.0001 
 Apical septum −1.3±0.7 −2.1±0.7 <0.0001 
 Basal LV lateral wall −1.4±0.7 −1.9±0.7 0.001 
 Mid LV lateral wall −1.3±0.6 −1.9±0.5 0.001 
 Apical LV lateral wall −1.6±0.6 −2.0±0.6 0.001 

Patients surgically treated had an LVEF of 72±8%, an MAPSE-septal wall of 13±3mm, an LVMI of 47±17 g/m2.7 and an average peak systolic longitudinal SR of 1.4±0.5 1\s. AoC patients who underwent primary stent implantation had an LVEF of 74±7%, an MAPSE-septal wall of 13±5 mm, an LVMI of 55±16 g/m2.7 and an average peak systolic longitudinal SR of 1.5±0.6 1\s.

Determinants of diastolic function

E/A was significantly correlated with age at repair (P=0.004; r=−45), LVMI (P=0.001; r=−36) and 24-h DBP (P=0.002; r=−48). E/e′ ratio was significantly correlated with age at surgery (P=0.003; r=−34), LVMI (P=0.004; r=−33) and the aortic stiffness index (P=0.001; r=−55).

Determinants of myocardial deformation properties

Following univariate analysis, average peak systolic longitudinal SR was significantly correlated with age at repair (P< 0.001; r2=0.68), age (P<0.001; r2=0.13), LVMI (P<0.001; r2=0.20), aortic stiffness index (P<0.001; r2=0.61) and 24-h SBP (P<0.001; r2=0.15) (Figure 1).

Linear regression analyses

Figure 1
Linear regression analyses

Linear regression between (A) average peak systolic longitudinal SR and age (years), (B) average peak systolic longitudinal SR and LVMI, (C) average peak systolic longitudinal SR and age at repair (months), (D) average peak systolic longitudinal SR and aortic stifness, and (E) average peak systolic longitudinal SR and 24-h SBP.

Figure 1
Linear regression analyses

Linear regression between (A) average peak systolic longitudinal SR and age (years), (B) average peak systolic longitudinal SR and LVMI, (C) average peak systolic longitudinal SR and age at repair (months), (D) average peak systolic longitudinal SR and aortic stifness, and (E) average peak systolic longitudinal SR and 24-h SBP.

Following multilinear regression analysis, the only independent predictors of LV average peak systolic longitudinal SR were age at correction (P=0.005; coefficient, −0.201; S.E.M., 0.027) and aortic stiffness index (P=0.0029; coefficient, 0.334; S.E.M., 0.423).

DISCUSSION

To the best of our knowledge, the present study is the first to report SR imaging in AoC patients. Regional longitudinal systolic myocardial deformations are significantly reduced in a large sample of young AoC patients, despite a successful correction and in the presence of a (super) normal LVEF and an increased VCFc/stress. The degree of this impairment is significantly related to age at correction and aortic stiffness.

LV function in AoC patients

Increased systolic function and enhanced standard echocardiographic indexes of contractility have been reported in patients after successful repair of AoC during childhood [58], a group known to have an increased incidence of LV hypertrophy, systemic hypertension and a significant late mortality risk [14]. However, the mechanism underlying this apparent persistent elevation of myocardial contractility is difficult to explain. Chronic ventricular hypertrophy is known to be associated with contractile dysfunction [3033], thus the enhanced myocardial contractility found in AoC patients may be artifactual [34]. Indeed, all those studies [59] suggesting elevation of myocardial contractility after successful repair of AoC are in contrast with results from both animal models with experimentally induced pressure overload [3537] and studies in humans with hypertension [38,39]. In those studies, LV hypertrophy is commonly associated with a gradual deterioration in LV function and contractility.

Many of the previous studies assessing myocardial contractility in AoC patients used endocardial stress–velocity indexes which can overestimate myocardial performance and contractility, especially in hypertrophied hearts [27,29,31,39,40]. This misrepresentation of fibre mechanics by those standard echocardiographic-derived indexes has been found to be clinically important in subjects with LV hypertrophy caused by systemic hypertension [30,32,34,39,40], resulting in a failure to recognize depressed fibre shortening.

Other studies using a midwall index of contractility, thus providing a physiological correction, still showed evidence of an unexplained hypercontractile state in AoC patients [34]. However, it has been demonstrated that the midwall stress–velocity relationship at low afterload has a similar behaviour to the endocardial stress–velocity relationship [39].

Myocardial deformation properties in AoC patients

Using for the first time peak systolic SR we demonstrated the presence of an abnormal longitudinal systolic function in AoC patients. SR is a parameter proposed to be a strong index of LV contractility [27,28]. In several studies the new ultrasonic-derived deformation indexes demonstrated a greater ability than standard echocardiography to unmask preclinical systolic abnormalities [1217]. In hypertensive patients with apparently normal systolic function and in the presence of a normal diastolic function, the application of SR imaging demonstrated the presence of preclinical LV systolic abnormalities [1317].

Of note, in the present study abnormal systolic function was detected by studying myocardial deformation along the longitudinal axis, whereas myocardial deformation properties along the radial axis were increased. Indeed, peak systolic radial SR is an expression of midwall fibre contraction and in the presence of low afterload has a similar behaviour to the endocardial stress–velocity relationship, showing evidence of an unexplained hypercontractile state in AoC patients [40]. This is in agreement with a recent report demonstrating increased midwall fractional shortening and decreased longitudinal shortening in 15 AoC patients late after successful correction, using magnetic resonance imaging [40]. In the present study sample, endocardial end-systolic stress, an index of afterload [4], was reduced. This finding is not surprising and is in agreement with previous studies [4,7]. In a mathematical model [10] keeping normal myocardial contractility and reducing afterload SR increased. Conversely in the present study, longitudinal peak systolic SR was significantly reduced even in presence of a reduced end-systolic stress, suggesting an impairment in myocardial longitudinal function. This finding may explain, at least in part, the reduced exercise duration in AoC patients compared with controls (Table 1).

Aortic stiffness in AoC patients

The aortic stiffness index was significantly increased in AoC patients in agreement with previous studies demonstrating abnormalities in vascular structure and function in patients after successful decoarctectomy.

These abnormalities are more frequently found in the precoarctation aorta and proximal arteries even in patients after early and successful repair [18,41,42].

In the present study, longitudinal deformation impairment was significantly correlated with the age at correction and the aortic stiffness index.

These findings suggest that, although early repair has a beneficial effect, it cannot change the innate structural and functional abnormalities of the proximal aorta and their deleterious effect on myocardial function [42]. Indeed, despite early repair, the estimated survival in postdecoarctectomy patients is still reduced, with 80% of the surgical patients alive at 40–50 years after surgery [1,43].

Study limitations

The present study has some limitations. (i) The patient sample included in the present study were AoC patients undergoing medical treatment corresponding to the usual clinical situation encountered in hospital practice. However, we excluded patients taking β-blockers to avoid any effect of drugs on myocardial contractility. (ii) The usual limitations inherent in the angle-dependency of all echocardiographic Doppler techniques also apply to ultrasound-derived SR imaging. In the present study, care was taken to always align the ultrasound beam with the direction of myocardial deformation to be interrogated and we included in the study only the walls with the best alignment.

Clinical implications

Our findings have potential implications for management strategies aimed at reducing late morbidity and mortality in this high-risk group.

AoC is associated with reduced life expectancy and increased morbid events even after successful repair. Aortic stiffness is increased in postcoarctectomy patients and myocardial deformation properties are significantly influenced by age at repair and the aortic stiffness index. The results of the present study suggest that AoC should be corrected early and the use of drugs able to improve aortic stiffness in postcoarctectomy patients, independently of BP values, should be considered.

Abbreviations

     
  • A

    late diastolic transmitral peak velocity

  •  
  • ABPM

    ambulatory blood pressure monitoring

  •  
  • AoC

    aortic coarctation

  •  
  • BP

    blood pressure

  •  
  • CDMI

    colour Doppler myocardial imaging

  •  
  • DBP

    diastolic BP

  •  
  • DT

    deceleration time of E

  •  
  • e

    early diastolic mitral annular peak velocity

  •  
  • E

    early diastolic transmitral peak velocity

  •  
  • IVRT

    isovolumic relaxation time

  •  
  • LV

    left ventricular

  •  
  • LVEF

    LV ejection fraction

  •  
  • LVMI

    LV mass indexed for height2.7

  •  
  • MAPSE

    mitral annulus peak systolic excursion

  •  
  • SBP

    systolic BP

  •  
  • SR

    strain rate

  •  
  • TAPSE

    tricuspid annulus peak systolic excursion

  •  
  • VCFc

    mean velocity of circumferential fibre shortening corrected for the heart rate

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