Why the study?
Is arterial-left ventricular-left atrial coupling impaired late after repair of aortic coarctation and interruption compared to controls?
Is arterial-left ventricular-left atrial coupling impaired late after repair of aortic coarctation and interruption compared to controls?
Adolescents and young adults late after repair of aortic coarctation and interrupted aortic arch exhibit impaired arterial function and abnormal arterial-LV-LA interaction.
Supports impaired arterial-LV-LA coupling late after coarctation repair; hypothesis-generating and requires prospective validation.
AIMS: This study aimed to explore the arterial-left ventricular (LV)-left atrial (LA) interaction in adolescents and young adults late after intervention for coarctation of the aorta (CoA) and interrupted aortic arch (IAA). METHODS AND RESULTS: Thirty-one (16 males) patients aged 23.4 ± 6.3, at 20.6 ± 5.2 years after intervention, and 31 controls were studied. Carotid arterial stiffness and intima-media thickness (IMT) and brachial-ankle pulse wave velocity were determined by radiofrequency-based echocardiography and oscillometry, respectively. Tissue Doppler and speckle tracking echocardiography (STE) were performed to assess, respectively, LV myocardial tissue velocities and linear and torsional deformation. Left atrial positive, negative, and total strain and strain rate at ventricular systole (aSRs), early diastole (aSRed), and atrial contraction (aSRac) were also determined using STE. Patients had significantly greater arterial stiffness and IMT than controls (all P < 0.05). Mitral annular systolic and diastolic velocities, LV longitudinal and radial strain and early diastolic strain rates, peak torsion and untwisting velocity, and LA peak positive and total strain, aSRs, aSRed, and aSRac were significantly lower in patients than in controls (all P < 0.05). Arterial stiffness correlated inversely with LV longitudinal strain and systolic and early diastolic strain rate (all P < 0.05), while LA total strain and aSRed were associated positively with LV diastolic annular velocity, longitudinal SRe, and peak untwisting velocity (all P < 0.05). Multiple linear regression further revealed arterial stiffness as an independent determinant of LA total strain (β = -1.3, P = 0.034). CONCLUSION: Our findings suggest impairment of arterial function and LV and LA mechanics in patients after CoA and IAA repair and implicate an abnormal arterial-LV-LA interaction.
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Li et al. (2015) studied this question.