Resistant hypertension

BMJ 2012; 345 doi: http://dx.doi.org/10.1136/bmj.e7473 (Published 20 November 2012)
Cite this as: BMJ 2012;345:e7473

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Hypertension is a global health issue. Observational studies have identified multifactorial characteristics of resistant hypertension. Genetic factor as aetiology is a reasonable thought. The pathogenesis of hypertension and organ damage is from altered activity of mineralocorticoid receptors. This can be classified as high or normal level of aldosterone. The former involves Conns (primary aldosteronism , aldosterone breakthrough phenomenon in presence of use of ACE-I or ACE-II (ARB) blocker [1]. The latter group involves chronic kidney disease, obesity, polycystic ovarian syndrome. In primary aldosteronism, about 20% lead to resistant hypertension [2]. The presentation can be insidious with hyperkalemia. In those patients plasma aldosterone concentration to plasma renin activity should be obtained. Other endocrine causes like Cushing’s, primary hyperparathyroidism and phaeochromocytoma are extremely uncommon. Those who have hypertension at a young age with systolic > 160 mm hg and diastolic > 100 mm hg should be confirmed with aldosterone suppression test with either oral or intravenous sodium loading.

Marked elevated blood pressure or hypertension can cause renal end organ damage. Poorly controlled hypertension will require more than 2- 3 antihypertensive medication. The future may lie with percutaneous renal denervation or carotid baroreflex activation. However, long term efficacy and safety data is yet to be ascertained.

Reference:
1. Shibata H, Itoh H. Mineralocorticoid receptor associated hypertension and its organ damage: Clinical relevance of resistant hypertension .American Journal of Hypertension, May 2012, Vol. /is. 25/5 (514 -23).
2. Mulatero P,Monticone S,Bertello C,Tizzani D, et al.Evaluation of primary aldosterone .Current opinion in Endocrinology, Diabetes and Obesity , June 2010 ,Vol./is. 17/3 (188 – 93).

Competing interests: None declared

Kaushik Sanyal, Specialist Registrar in Rheumatology / General Internal Medicine

East Surrey Hospital, Redhill , UK

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17 December 2012

I read with great interest the article BMJ 2012;345:e7473 doi: 10.1136/bmj.e7473 (Published 20 November 2012)1.

In Device Therapy section the Authors mention renal denervation as modern trend for the treatment of resistant hypertension in need of elaboration and better understanding of its mechanisms of action. Microvascular competition has been reported as another cause of resistant arterial hypertension. According to the hypothesis of Jannetta, an arterial compression of the left root entry zone of cranial nerves IX and X by looping arteries could play an important role in the pathogenesis of essential hypertension2. Jannetta et al. suggested that compression of the left lateral medulla oblongata and root entry zone (REZ) of CN IX and CN X may affect several parts of the neurogenic control system for BP and cause such a neural imbalance3.

To study the relationship of cranial nerves and neighboring vessels angiography and magnetic resonance has been implemented. In 80% of the angiograms of the hypertensive patients that could be evaluated, an artery crossed the left REZ of cranial nerves IX and X2. MRI has been used to investigate the presence of neurovascular conflict at REZ of the IX and X CN. Several authors declare different findings3,4. Several authors has reported isolated cases or short series of patients with resistant arterial hypertension treated with microvascular decompression of IX and X CN and left lateral medulla oblongata.

Reviewers of the method have concluded that multi-disciplinary evidence supports the hypothesis that a sub-population of hypertensive patients achieve significant relief of their hypertension after microvascular decompression4. Yet, a multi-institutional, prospective, randomized study is necessary to determine the efficacy of microvascular decompression for neurogenic hypertension5.

I suggest that in an updated review of resistant hypertension, microvascular decompression should be mentioned, as a still controversial, but possible invasive treatment in selected cases.

References

1. Myat A, Redwood SR, Qureshi AC, Spertus JA, Williams B. Resistant hypertension. BMJ. 2012 Nov 20;345:e7473. doi: 10.1136/bmj.e7473.

2. Kleineberg B, Becker H, Gaab MR, Naraghi R. Essential hypertension associated with neurovascular compression: angiographic findings. Neurosurgery.1992 Jun;30(6):834-41.

3. Jannetta PJ, Segal R, Wolfson SK Jr.. Neurogenic hypertension. Etiology and surgical treatment-observations in 53 Patients. Ann Surg 1985; 201: 391-8.

4. Säglitz SA, Gaab MR. Investigations using magnetic resonance imaging: is neurovascular compression present in patients with essential hypertension? J Neurosurg. 2002 Jun;96(6):1006-12.

5. Levy EI, Scarrow AM, Jannetta PJ. Microvascular decompression in the treatment of hypertension: review and update. Surg Neurol. 2001 Jan;55(1):2-10; discussion 10-1.

Competing interests: None declared

Ridvan Alimehmeti, Neurosurgeon

University Hospital Center "Mother Theresa", Dibra street, 370 - Tirana, Albania

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