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Publication - Professor Julian Paton

    Repaired coarctation of the aorta, persistent arterial hypertension and the selfish brain

    Citation

    Rodrigues, JCL, Jaring, MRF, Werndle, M, Mitrousi, K, Lyen, S, Nightingale, AK, Hamilton, MC, Curtis, SL, Manghat, NE, Paton, JFR & Hart, ECJ, 2019, ‘Repaired coarctation of the aorta, persistent arterial hypertension and the selfish brain’. Journal of Cardiovascular Magnetic Resonance.

    Abstract

    Background
    20-30% repaired aortic coarctation (CoA) patients develop hypertension, with significant cardiovascular morbidity and mortality. Vertebral artery hypoplasia with an incomplete posterior circle of Willis (VAH+ipCoW) is associated with increased cerebrovascular resistance before the onset of increased sympathetic nerve activity in borderline hypertensive humans, suggesting brainstem hypoperfusion may evoke hypertension to maintain cerebral blood flow: the “selfish brain” hypothesis. We now assess the “selfish brain” in hypertension post-CoA repair.

    Methods
    Time-of-flight magnetic resonance angiography from 127 repaired CoA patients (34±14 years, 61% male, SBP 138±19mmHg, DBP 76±11mmHg) was compared with 33 normotensive controls (42±14 years, 48% male, SBP 124±10mmHg, DBP 76±8mmHg). VAH was defined as <2mm and ipCoW as hypoplasia of one or both posterior communicating arteries.

    Results
    VAH+ipCoW was more prevalent in repaired CoA than controls (odds ratio: 5.795 [1.614–20.812], p=0.007), after controlling for age, sex and body mass index (BMI). VAH+ipCoW was an independent predictor of hypertension (odds ratio: 2.473 [1.173–5.212], p=0.017), after controlling for age, gender and BMI. Repaired CoA subjects with VAH+ipCoW were more likely to have difficult to treat hypertension (odds ratio: 3.286 [1.005–10.743], p=0.049). Neither age at time of repair nor any specific repair type were significant predictors of VAH+ipCoW in univariate regression analysis.

    Conclusions
    VAH+ipCoW predicts hypertension and difficult to treat hypertension in repaired CoA. It is unrelated to age at time of repair or repair type. CoA appears to be a marker of wider congenital cerebrovascular problems. Understanding the “selfish brain” in post-CoA repair may help guide management.

    Full details in the University publications repository