Blood pressure variability: An emerging target for risk reduction in the setting of hypertensive emergency

Hypertensive emergency is the combination of severely elevated blood pressure, generally defined as a systolic ≥ 180 mm Hg and diastolic ≥ 110 or 120 mm Hg, and end-organ damage. Up to one million hypertensive Americans will experience a hypertensive emergency during their lifetime,1 and the incidence continues to increase for reasons that are not fully understood.2 The most common end-organ damage seen in hypertensive emergency is cardiac, neurologic, and renal.3 The mortality rate approaches 11%, and for survivors, the readmission rate ranges from 18% to 37%, of which heart failure and stroke are among the most common causes.4 Prompt blood pressure reduction is the mainstay of treatment for patients with hypertensive emergency and achievable with the wide variety of intravenous antihypertensives readily available in modern emergency departments and hospitals. Despite this, outcomes for patients with hypertensive emergency could be further improved. In this issue, Cucci and Benken present a novel perspective on why blood pressure reduction alone may not be enough to optimize outcomes after identification of hypertensive emergency.5 After providing a clear and concise explanation describing the different methodologies used to quantify BPV, the authors drawn on the body of research showing an association between elevated blood pressure variability (BPV) and worse outcome for patients with two of the most common end organ sequalae of hypertensive emergency and hemorrhagic and ischemic stroke, to suggest that increased BPV may be a underappreciated contributory factor to the high rate of adverse outcomes in hypertensive emergency. Apart from hemorrhagic and ischemic stroke, there is limited research on BPV for the other end-organ dysfunctions seen in hypertensive emergency such as acute heart failure or aortic dissection, but the negative consequences of increased BPV have also been shown for other vascular beds, including the heart, eye, and kidney, in patients without hypertensive emergency.6-10 While the mechanism by which BPV may worsen neurologic outcome after stroke is not known, the brain and other vascular beds autoregulate to maintain consistent blood flow across a wide range of blood pressures.11 In disease states, such as hypertensive emergency, the ability to autoregulate blood flow may be reduced, which may cause these patients to suffer damage from the fluctuations in flow generated by increased variability of blood pressure.12, 13 Prospective research of BPV in a cohort of hypertensive emergency patients with a variety of end-organ issues, ranging from hemorrhagic stroke to myocardial infarction to aortic dissection, is needed to provide definitive evidence of a causal relationship with worse outcomes. The methods of reducing BPV have not been studied, but such an intervention could be beneficial for patients with hypertensive emergency. BPV reduction is likely to be an inexpensive and widely available intervention, which could be administered in a range of health care settings, including community hospitals and even outpatient settings. Hypertensive emergency is a viable patient population for studying BPV reduction given the high rate of morbidity and mortality. At present, there are no randomized controlled trials that have tried to therapeutically decrease BPV.14 When compared to other antihypertensive medications such as beta-blockers, calcium channel blockers and thiazide diuretics appear to reduce BPV.15 However, a medication class effect alone is not likely to produce a sufficient impact on BPV and more advanced protocol-based medication titration will be needed to achieve both an end organ-specific blood pressure goal and a desired BPV level. Closed-loop systems that use adaptive dosing strategies in response to real-time physiologic data have shown promise in surgical anesthesia and are viable with modern portable computers and continuous noninvasive blood pressure monitoring.16, 17 In the next decade, the story of BPV in a variety of vascular diseases will continue to evolve and, ultimately, will become treatable to improve patient outcome. None. None.