Why the study?
Does early versus late surgery for aortic coarctation prevent long-term left ventricular hypertrophy and systolic dysfunction?
Does early versus late surgery for aortic coarctation prevent long-term left ventricular hypertrophy and systolic dysfunction?
Despite successful aortic coarctation repair, residual LV hypertrophy persists long-term regardless of age at surgery, driven by residual exercise pressure gradients, though systolic function remains normal.
Residual LV hypertrophy after coarctation repair persists irrespective of surgical age; leaves open optimal timing and adjunctive strategies to mitigate remodeling.
The study was designed to assess non-invasively the long-term effect of coarctation repair on systemic blood pressure, left ventricular (LV) muscle mass (LMM) and LV systolic function. Blood pressure and pressure gradients across the coarctation site were measured at rest and during exercise. LV systolic function and LMM were assessed by echocardiography. Twenty-eight patients late after successful coarctation repair were divided according to their age at surgery into two groups: group 1: < 1 year (10 days-12 months, mean 0.2 years) and group 2: > 1 year (1-19 years, mean 9.7 years). A group of age- and sex-matched patients with normal LV function served as controls. LMM was increased late postoperatively in both groups irrespective of the age at surgery and was correlated significantly with the elevated systolic blood pressure and the residual pressure gradient at exercise. End-systolic wall stress was normal at rest and the stress/velocity relationship revealed normal contractility in all patients. Despite successful operation of aortic coarctation, residual LV hypertrophy persists 2 to 19 years after surgery irrespective of the age at surgery. LV systolic function is normal. Hypertrophy can be explained by the residual arm-leg pressure gradient during exercise which persists even after successful repair.
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Krogmann et al. (1993) studied this question.
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