The Pressure Is On: Implications of Blood Pressure After Aortic Valve Replacement

T herapeutic control of blood pressure (BP) in an “allcomer” patient population is associated with a reduction in cardiovascular mortality. Recent evidence and contemporary guidelines suggest that the benefit of strict therapeutic reduction in BP (systolic BP [SBP] <120 mm Hg and diastolic BP [DBP] <80 mm Hg) confers additional benefit in patients with diabetes mellitus and/or those with a prior cardiovascular event. Such BP control has also been shown to be beneficial in those without diabetes mellitus and aged >75 years. However, in patients with aortic valve disease, a large proportion of whom are elderly patients, it is unclear whether this level of intensive BP control further improves prognosis. Guidance for BP control in patients with significant aortic stenosis has been confusing, particularly with the fear of afterload reduction causing syncope. To date, most of the evidence for BP control before aortic valve replacement (AVR) has involved alterations to the renin-angiotensin system. The renin-angiotensin system has been thought to have an influence on myocardial physiological characteristics, left ventricular hypertrophy, and extent of myocardial fibrosis. There is early evidence of potential benefits in angiotensinconverting enzyme inhibition, potentially reducing the progression of aortic stenosis without causing harm. Similar prognostic benefits have been found after AVR. The observation that BP after AVR is an independent predictor of outcome was first described by Perlman et al, who made the association that postprocedural hypertension after transcatheter AVR (TAVR) was a predictor of a better prognosis. In their study of 105 consecutive patients after TAVR, 51% had sustained increases in BP after TAVR, requiring intensification of antihypertensive treatment. Patients with increased BP had an increase in stroke volume and cardiac output independent of other factors and, thereafter, a better prognosis. Lindman et al, before their most recent publication, evaluated the effects of post-TAVR hypertension using the Edwards Balloon expandable system. Analyzing the Partner I trial data, they demonstrated that postprocedural hypertension was independently associated with improved survival. So if hypertension after AVR indicates a good prognosis, can we deduce that hypotension is a bad thing? In this issue of the Journal of the American Heart Association (JAHA), Lindman et al demonstrate that low BP (both SBP and DBP) is linked to poorer outcomes after AVR via both surgical and transcatheter approaches. Patients enrolled in the Medtronic intermediate, highand extreme-risk trials receiving either TAVR with a self-expanding valve or surgical AVR were analyzed (Figure). They concluded that a DBP of 30 to <60 mm Hg compared with a DBP of 60 to <80 mm Hg was associated with increased all-cause (HR, 1.62; 95% CI, 1.23–2.14) and cardiovascular mortality (HR, 2.13; 95% CI, 1.52–3.00). A similar association was shown for SBP, where SBP of 90 to <120 mm Hg compared with SBP of 120 to <150 mm Hg was again associated with increased all-cause (HR, 1.63; 95% CI, 1.21–2.21) and cardiovascular mortality (HR, 1.81; 95% CI, 1.25–2.61). Why is this phenomenon observed and what are the biological explanations for this association? There is no doubt that replacement of the aortic valve in the setting of long-standing and incrementally severe aortic stenosis brings about dramatic hemodynamic changes in the cardiovascular system. The abrupt relief of excess afterload causes immediate alterations in systolic and diastolic function, ventriculoarterial interactions, coronary blood flow, and, thus, cardiac output. These changes are now no longer masked by the confounding effects of cardiopulmonary bypass with the widespread introduction of TAVR as a mainstream therapy. The implications of changes in SBP and DBP early after AVR, which are crude markers of this complex hemodynamic environment, are likely to be different from those in the long-term setting. The rules governing optimal BP management, therefore, may well be different after AVR, The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From King’s College Hospital National Health Service Foundation Trust, London, United Kingdom. Correspondence to: Philip MacCarthy, MBChB, PhD, King’s College Hospital National Health Service Foundation Trust, London SE59RS, United Kingdom. E-mail: philip.maccarthy@nhs.net J Am Heart Assoc. 2019;8:e014631. DOI: 10.1161/JAHA.119. 014631. a 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.