Trends for prevalence and incidence of resistant hypertension: population based cohort study in the UK 1995-2015BMJ 2017; 358 doi: https://doi.org/10.1136/bmj.j3984 (Published 22 September 2017) Cite this as: BMJ 2017;358:j3984
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Re: Trends for prevalence and incidence of resistant hypertension: population based cohort study in the UK 1995-2015
we very much welcome this important contribution to the study of resistant hypertension. This is one of the first general practice record studies published in this area, as opposed to those derived from trial or observational cohorts, which greatly enhances the generalisability of the reported findings. This is an impressive study, with a nationally representative sample of 2.2 million patients followed over 10 years. The suggested prevalence of 6.5%, which is significantly lower than that which has been reported elsewhere (see Achelrod, Wenzel, & Frey, 2015), resonates clinically and suggests that this condition is being over-diagnosed. With regard to pseudo-resistance, the examination of adherence through prescribing records, albeit a limited measurement approach, is most welcome; however, consideration of white coat hypertension and maximal dosing are still overlooked. These are likely to reduce prevalence even further. A study of individual patient records, which we are currently undertaking, may be helpful in this regard.
Peter Hayes 1, Monica Casey 1, Gerry Molloy 2, Hannah Durand 2, Andrew W Murphy 1, 3.
1Discipline of General Practice, School of Medicine, National University of Ireland, Galway, Ireland
2 School of Psychology, NUI Galway, Ireland
3 HRB Primary Care Clinical Trials Network, Ireland
Achelrod, D., Wenzel, U., & Frey, S. (2014). Systematic review and meta-analysis of the prevalence of resistant hypertension in treated hypertensive populations. American Journal of Hypertension, 28(3), 355-361. https://doi.org/10.1093/ajh/hpu151
Competing interests: No competing interests
Uncontrolled hypertension “resistant” to three, concurrent, antihypertensive drugs is an alarming diagnosis with significant, subsequent cardiovascular morbidity (1). Treating the condition as a syndrome may suit contemporary pharmacological approaches but, in many cases, there is an historical, renal arteriolar injury that may better define the condition. In 1937, Moritz & Oldt reported arteriolar stenosis in kidney, spleen, pancreas and adrenal in hypertensive patients of both sexes, across the age range with an increasing incidence with advancing age (2). The aetiology of that injury had not been elucidated though their central question was; is this injury a cause or a consequence of hypertension ?
We find that injuries to vasomotor nerves in renal (and other visceral) arterioles leads to release of cytokines, regeneration of injured nerves with concurrent hyperplasia of the denervated-vessel walls (3). Injured arterioles express purinergic, P2X3 ”stretch” receptors, and, are susceptible to hyaline and fibrinoid changes. Salt, sugar, stress, smoking, and straining at stool may all contribute to hypertension associated with these vasomotor injuries (4). Subsequent narrowing of renal arterioles also plays into the development of “resistant” hypertension through classical, Goldblatt mechanisms associated with relative ischaemia. The arteriolar injury may, therefore, be both a “cause and consequence” of hypertension producing a downward spiral of deteriorating consequences that ends as the syndrome of resistant hypertension. Preventing the initial injuries by amending lifestyle choices to avoid peaks of high blood pressure that damage injured, renal arterioles, may further reduce the rate of resistant hypertension ?
(1) Sinnott SJ, Smeeth L, Williamson E, Douglas IJ.
Trends for prevalence and incidence of resistant hypertension: population based cohort study in the UK 1995-2015.
(2) Moritz A, Oldt M
Arteriolar Sclerosis in Hypertensive and Non-Hypertensive Individuals.
Am J Pathol. 1937 Sep;13(5):679-728.
(3) Wu XQ, Xu XX, Zhou ZY, Quinn MJ.
Potential mechanisms in pregnant and non-pregnant hypertension.
BJOG, 2017 (in press).
(4) Wu XQ, Cai YY, Xia WT, Quinn MJ.
The aetiology of preeclampsia, 1945-53.
BJOG 2016; 123(13):2130.
Figure: Features of injured renal arterioles and nerves in hypertension is at http://www.preeclampsiaexplained.com/publications/letter-to-bmj-october-...
[A] Narrowed, renal arterioles with medial hyperplasia, and, irregular layers of perivascular hyalinisation (“fried egg” appearance) created by raised intravascular pressures causing traumatic injuries to renal vasomotor nerves (x100, hematoxylin and eosin).
[B] Regenerating, injured vasomotor nerves in the perivascular layers that also regenerate in the arteriolar wall (x200, anti-S100).
[C] Expression of purinergic P2X3 “stretch” receptors (brown) in endothelial and perivascular layers in narrowed renal arterioles (x100, anti-P2X3) that correspond with the layers of hyaline change in Fig. 1A.
[D] Collateral sprouting of injured, renal nerve bundles with loss of individual nerve fibres within the bundle, adjacent to narrowed arterioles that are pathognomonic for traumatic injury, which in this case, was associated with prolonged and persistent, physical efforts during defaecation (x100, anti-S100).
Competing interests: No competing interests