Patients with surgically corrected aortic coarctation have increased proximal aortic stiffness that might contribute to the known worse cardiovascular outcomes. We examined the effect of stenting on the mid-term ascending aortic elastic properties and its relation to cardiac structure and function in adults with native coarctation of the aorta. A total of 20 consecutive patients (13 men, age at stenting 30 ± 8 years) were prospectively studied before and 14 ± 2 months after coarctation stenting. The aortic stiffness index was calculated using the ascending aortic diameters and right arm blood pressure values. The ventricular long-axis function was assessed using pulsed-wave tissue Doppler imaging at the septal site. The results were compared to those from 31 normal controls. Statistically significant improvement was found in aortic narrowing (catheter-derived gradient 32 ± 11 vs 10 ± 6 mm Hg), left ventricular mass index (132.8 ± 50.1 vs 114.7 ± 47.7 g/m 2 ), long-axis function, and left atrial volume index (26.5 ± 5.3 vs 23.7 ± 5.6 mm 3 /m 2 ). The patients continued to have a thicker left ventricle, reduced long-axis function, and larger left atrium after intervention than did the controls. They also had impaired proximal aortic function with respect to the controls that remained unchanged after stenting (aortic stiffness index 10.7 ± 4.5 to 10.1 ± 3.0). The poststenting aortic stiffness index correlated modestly with the left ventricular mass index and reduced long-axis velocity. In conclusion, aortic stenting resulted in partial mid-term improvement in cardiac structure and function in adults with coarctation of aorta but the ascending aortic elastic properties remained abnormal. Such a degree of impairment was related to residual left ventricular hypertrophy and dysfunction. Early identification of such patients and optimum management might avoid these irreversible ventriculoaortic disturbances and their known consequences.
Patients with apparently successful repair of coarctation of the aorta have increased proximal aortic stiffness that might contribute to the known significant cardiovascular mortality and morbidity. The increase in such large artery stiffness reduces the aortic reserve and creates stronger reflected waves, which, themselves, can lead to adverse left ventricular (LV) remodeling and functional disturbances. Arterial stiffness is histologically related to increased collagen and elastin and reduced smooth muscle cell content in the prestenotic aortic wall. Such a loss of proximal aortic function has been reported at birth and has been shown to be related to the presence of bicuspid aortic valves, suggesting that it is an intrinsic primary arterial wall disease “aortopathy.” Although difficult to dispute such a suggestion, recent data have shown a selective increase in proximal, but not poststenotic, aortic stiffness in adolescences after surgery, implying that aortic stiffness could be acquired. Patients with coarctation and suitable anatomy have recently undergone endovascular aortoplasty and/or stenting. The effect of stenting on the proximal aortic elastic properties and its relation to cardiac structure and function in such patients is not known. We hypothesized that the increase in arterial stiffness secondary to long-standing coarctation might not improve, despite correction of the mechanical obstruction and might be related to the residual LV functional disturbance previously reported in this condition.
Methods
A total of 20 consecutive patients with native coarctation of the aorta who had been referred to the Royal Brompton Hospital for endovascular stenting from October 2002 to March 2005 were prospectively studied. All patients had a reduced femoral pulse and the following Doppler echocardiographic evidence of significant aortic coarctation: (1) the presence of a diastolic tail (anterograde flow in the descending aorta during diastole) and (2) diastolic velocity measured at the end of T-wave on the electrocardiogram of >193 cm/s. All studied patients provided informed consent, and the local ethics committee approved the study. The patient demographics, including gender, associated bicuspid aortic valves, history of hypertension, and medication use, were recorded. Blood pressure (BP) measurements, transthoracic echocardiography, and cardiac catheterization were performed at baseline and at 12 months after stenting. The patients’ BP was measured at the right arm, with the patient lying supine and using an automatic oscillometric device (Dinamap PRO 300, Critikon Inc., London, United Kingdom). Patients were considered to have hypertension if the BP readings were >140/90 mm Hg on more than one occasion. A history of antihypertensive treatment was documented if it had been unchanged for 12 weeks before stenting. All procedures were performed with the patient under general anesthesia using previously described techniques. The peak to peak pressure gradients across the coarctation sites were recorded during cardiac catheterization at baseline and during follow-up. Patients with suboptimal echocardiographic windows, Turner syndrome, poorly controlled BP, pacemakers, atrial fibrillation, bundle branch block, hypoplastic or abnormal aortic arch, previous surgical coarctation repair, and other hemodynamically significant cardiac lesions (more than mild valvular disease) were excluded from the present study. The patients’ results were compared to those of 31 age- and gender-matched healthy subjects.
Echocardiograms were obtained using a Philips Sonos 5500 system (Philips, Andover, Massachusetts). At least 3 consecutive beats in sinus rhythm were recorded, and the average values were calculated.
The LV dimensions and wall thickness were measured from M-mode recordings from the parasternal long-axis view. The LV mass and left atrial volumes were derived using the Devereux formula and area–length method, respectively, and indexed to the body surface area. The LV ejection fraction was measured using Simpson’s volume estimates. The LV filling velocities were obtained by placing a 2-mm pulsed-wave Doppler sample volume at the tips of the mitral valve leaflets from the apical 4-chamber view. The peak early LV filling velocity (E wave), peak atrial filling velocity (A wave), E/A ratio, and E wave deceleration time were all measured. Segmental myocardial function was assessed by recording the long-axis motion at septal annulus using pulsed-wave tissue Doppler imaging technique. The long-axis peak systolic (Sa), early diastolic (Ea), and late diastolic (Aa) velocities were measured. The E/Ea ratios were then calculated. All recordings were made using a sweep speed of 100 mm/s, with an electrocardiogram (lead II) and a phonocardiogram superimposed.
Continuous-wave Doppler recordings were obtained from the suprasternal view to assess the maximum systolic velocity (V) and diastolic velocity across the coarctation site and the presence of a diastolic tail. The peak systolic pressure gradients were calculated using the simplified Bernoulli equation (peak systolic pressure gradient 4 V 2 ).
The difference between the systolic and diastolic BP was taken as an estimation of the central aortic pulse pressure. The accuracy and reproducibility of this method have been previously reported. The thoracic aortic diameter was measured 3 cm above the aortic valve level using 2-dimensional guided M-mode recordings of the aortic root, taken from the left parasternal long-axis view. The aortic systolic diameter (AoS) was measured at the point of full opening of the aortic valve and the diastolic (AoD) diameter at the peak R wave of the superimposed electrocardiogram. From these measurements, the following indexes of aortic elastic properties were calculated, as previously described :
Aortic distensibility ( c m 2 / dyne / 10 6 ) = 2 × ( Aos − AoD ) / ( AoD × pulse pressure )
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
