Abnormal regional myocardial deformation properties and increased aortic stiffness in normotensive patients with aortic coarctation despite successful correction: an ABPM, standard echocardiography and strain rate imaging study
Résumé
The long-term follow-up data subsequent to a successful repair of aortic coarctation (AoC) show that life expectancy remains reduced. Previous standard echocardiographic studies demonstrated normal or increased systolic cardiac function in patients after successful repair of AoC. Strain rate (SR) imaging is a new technique able to detect subclinical myocardial abnormalities. We investigated whether young patients late after successful AoC repair, without hypertension, as assessed by ABPM and exercise test, already show abnormal myocardial deformation properties and their relationship with aortic stiffness. We studied 166 subjects: 83 AoC non-hypertensive patients (mean age 12±4 years) late after successful repair of AoC; 83 age-sex comparable subjects as controls. Peak systolic SR (1/sec) for both regional longitudinal and radial function was assessed. Aortic (AO) stiffness index was calculated from the echocardiographically derived thoracic AO diameters and the measurement of blood pressure obtained by cuff sphygmomanometry. Left ventricular (LV) ejection fraction was significantly increased in AoC patients, while regional longitudinal SRs were significantly reduced (SR: -1.1±0.9 vs -2±0.5, p<0.0001) in patients. Ao stiffness index was significantly increased in AoC patients (12±9, p<0.0001). At multilinear regression analysis, age at repair (p:0.005; Coeff.: -0.201; SE; 0.027) and aortic stiffness index (p=0.0029; Coeff.: 0.334; SE: 0.423), predicted longitudinal SR. Despite the presence of a successful repair for AoC, in absence of hypertension, longitudinal deformation properties are significantly impaired. Moreover, the degree of longitudinal SR impairment is 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.
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