High blood pressure

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High blood pressure

Hypertension (HTN) or high blood pressure, sometimes called arterial hypertension.

Elevated BP increases the risk of developing stroke, particularly in the absence of routine BP measurements and hypertension treatment. A strict BP management target (SBP, <120 mmHg; DBP, <80 mmHg) should be adopted for young and middle-aged men 1).

Epidemiology

Hypertension affects more than a quarter of the world’s adult population.

Types

Essential, or primary, or idiopathic hypertension is historically defined as a rise in blood pressure (BP) without any known causes, which still accounts for ≈95% of all hypertension 2).

Etiology

Ever since the identification of hypertension in 1872, researchers have struggled to find its cause(s) with only minor successes 3).

Whereas multiple risk factors for hypertension, including genetic variations, obesity, insulin resistance, high alcohol intake, and stress, have been identified, primary causes for hypertension remain elusive. Also, the predictive factors for its development are unclear 4) 5) 6).

Despite medical advancements, no underlying cause can be found in more than 9 out of 10 patients with hypertension. Although elevated sympathetic nervous activity contributes to the development of hypertension, the mechanism by which this occurs remains poorly understood 7).

The so-called Cushing reflex has been suggested to explain arterial hypertension. According to this mechanism, hypoperfusion of the rostral ventrolateral medulla induces sympathetic nervous system activation and a pressor response. The pressor response then increases perfusion of a primary brain area regulating sympathetic activity, but in doing so heightens systemic blood pressure. The initial hypoperfusion could arise as a result of narrowed vertebral arteries—evident as high resistance and low flow in these arteries. Although systemic hypertension might lead via remodeling to a narrowing of vertebral arteries, it has been suggested that hypertension is the result of narrowed vertebral arteries rather than the cause 8).

There are anatomical and physiological evidences that the ventrolateral (VL) region of the medulla plays an important role in blood pressure regulation and that dysfunction at this level may generate hypertension (HT). Vascular compression by a megadolicho-artery from the vertebrobasilar arterial system at the root entry/exit zone (REZ) of the glossopharyngeal (IXth) and vagal (Xth) cranial nerves (CNs) and the adjacent VL aspect of the medulla has been postulated as a causal factor for HT from neurogenic origin. The first attempts at microvascular decompression (MVD) of the IX-Xth CNs together with the neighbouring VL brainstem was revealed promising.

Established criteria for indication of MVD as an aetiological treatment of apparent essential HT are still needed 9).

Renovascular disease is a well-described cause of hypertension, which is caused by the increase in renin secretion with subsequent increase in angiotensin and aldosterone but is found to be a primary cause in a minority of cases 10).

Outcome

Hypertension is refractory to treatment in ≤20% to 30% of cases despite the availability of numerous classes of antihypertensives, and finding primary cause could improve treatment of refractory hypertension 11)..

Complications

Elevated blood pressure (BP), which presents in approximately 80 % of patients with acute intracerebral hemorrhage (ICH), is associated with increased risk of poor outcome.

Hypertension is the most important risk factor for the formation of cerebral aneurysm, as well as aneurysm rupture 12) 13) 14) 15) 16).

Hypertension as hemodynamic management of subarachnoid hemorrhage

Volume expansion and hypertension are widely used for the hemodynamic management of patients with subarachnoid hemorrhage to prevent delayed cerebral ischemia.

Given the suggestion of possible worse neurobehavioral outcome with augmented blood pressure (ABP), a larger trial to determine the optimal blood pressure management in this patient population is warranted (ClinTrials.gov NCT01414894.) 17).

Hypertension is an independent risk factor for intracranial aneurysm.

Complications

Lenticulostriate artery are particularly susceptible to damage from hypertension. They may either rupture, producing an intracerebral hemorrhagethat is initially centered in the region they supply, or become occluded producing a lacunar infarct in the tissue they supply.

Treatment

see Arterial hypertension treatment.

References

1)

Zhao P, Liu J, Wang C, Zhao W, Zhang Y, Gu H, Tu J, Wang J, Ning X. Strict target blood pressure management for reducing the stroke risk according to 2017 ACC/AHA blood pressure guideline. Aging (Albany NY). 2019 Aug 27;11. doi: 10.18632/aging.102207. [Epub ahead of print] PubMed PMID: 31454794.
2)

Messerli FH, Williams B, Ritz E. Essential hypertension. Lancet. 2007 Aug 18;370(9587):591-603. Review. PubMed PMID: 17707755.
3)

Gull WW, Sutton HG. On the Pathology of the Morbid State commonly called Chronic Bright’s Disease with Contracted Kidney, (“Arterio-capillary Fibrosis.”). Med Chir Trans. 1872;55:273-330.1. PubMed PMID: 20896392; PubMed Central PMCID: PMC2150494.
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Ehret GB, Caulfield MJ. Genes for blood pressure: an opportunity to understand hypertension. Eur Heart J. 2013;34:951–961. doi: 10.1093/eurheartj/ehs455.
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he INTERSALT Co-operative Research Group. Sodium, potassium, body mass, alcohol and blood pressure: the INTERSALT study. J Hypertens Suppl. 1988;6:S584–S586.
6)

Sever PS, Poulter NR. A hypothesis for the pathogenesis of essential hypertension: the initiating factors. J Hypertens Suppl. 1989;7:S9–S12.
7)

Schlaich MP, Lambert E, Kaye DM et al. Sympathetic augmentation in hypertension: role of nerve firing, norepinephrine reuptake, and Angiotensin neuromodulation. Circ Res . 2004;43(2):1267-1269.
8)

DICKINSON CJ, THOMASON AD. Vertebral and internal carotid arteries in relation to hypertension and cerebrovascular disease. Lancet. 1959 Jul 18;2(7090):46-8. PubMed PMID: 13673588.
9)

Sindou M. Is there a place for microsurgical vascular decompression of the brainstem for apparent essential blood hypertension? a review. Adv Tech Stand Neurosurg. 2015;42:69-76. doi: 10.1007/978-3-319-09066-5_4. Review. PubMed PMID: 25411145.
10)

Black HR, Glickman MG, Schiff M Jr, Pingoud EG. Renovascular hypertension: pathophysiology, diagnosis, and treatment. Yale J Biol Med. 1978 Nov-Dec;51(6):635-54. Review. PubMed PMID: 377821; PubMed Central PMCID: PMC2595593.
11)

Calhoun DA, Jones D, Textor S, Goff DC, Murphy TP, Toto RD, White A, Cushman WC, White W, Sica D, Ferdinand K, Giles TD, Falkner B, Carey RM; American Heart Association Professional Education Committee. Resistant hypertension: diagnosis, evaluation, and treatment: a scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Circulation. 2008;117:e510–e526. doi: 10.1161/CIRCULATIONAHA.108.189141
12)

T. Inagawa, “Risk factors for the formation and rupture of intracranial saccular aneurysms in Shimane, Japan,” World Neurosurgery, vol. 73, no. 3, pp. 155–164, 2010.
13)

M. Clarke, “Systematic review of reviews of risk factors for intracranial aneurysms,” Neuroradiology, vol. 50, no. 8, pp. 653–664, 2008.
14)

J. Dubow and M. E. Fink, “Impact of hypertension on stroke,” Current Atherosclerosis Reports, vol. 13, no. 4, pp. 298–305, 2011.
15)

B. V. Nahed, M. L. DiLuna, T. Morgan et al., “Hypertension, age, and location predict rupture of small intracranial aneurysms,” Neurosurgery, vol. 57, no. 4, pp. 676–683, 2005.
16)

C. L. Taylor, Z. Yuan, W. R. Selman, R. A. Ratcheson, and A. A. Rimm, “Cerebral arterial aneurysm formation and rupture in 20,767 elderly patients: hypertension and other risk factors,” Journal of Neurosurgery, vol. 83, no. 5, pp. 812–819, 1995.
17)

Togashi K, Joffe AM, Sekhar L, Kim L, Lam A, Yanez D, Broeckel-Elrod JA, Moore A, Deem S, Khandelwal N, Souter MJ, Treggiari MM. Randomized Pilot Trial of Intensive Management of Blood Pressure or Volume Expansion in Subarachnoid Hemorrhage (IMPROVES). Neurosurgery. 2015 Feb;76(2):125-35. doi: 10.1227/NEU.0000000000000592. PubMed PMID: 25549192.

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