doi: 10.1161/01.STR.0000014412.54558.B8
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(Stroke. 2002;33:1180.)
© 2002 American Heart Association, Inc.
Letters to the Editor |
Cerebral Atherosclerosis Causes Neurogenic Hypertension
Hospital Santa Teresa Zacatecas, Mexico City, Mexico
To the Editor:
Su et al1 presented an excellent report regarding "the hypothesis that hypertension has a major role in the pathogenesis of atherosclerosis." The results of their study were very similar to other findings previously reported.2 Both groups defended that essential arterial hypertension (EAH) is the major risk factor in the development of atherosclerosis. However, I offer some opposing comments upheld by many authors, based on clinical and neurosurgical evidences. First, EAH represents 90% to 95% of all cases of hypertension and is the main factor of risk in the generation of cerebrovascular and cardiovascular diseases. Second, generally there is a close correlation between age (about 35 years) and the incidence of essential hypertension3 as well as the onset of cerebral atherosclerosis.4,5 Third, 5 areas are associated with EAH6,7: denervation of the baroreceptors from the carotid sinus and aortic arc by atherosclerosis, and ischemia in the posterior hypothalamus and medulla oblongata (A1/C1 cell column, commissural portion of the nucleus solitarius, and A2/C2 cell column). Fourth, microvascular decompression of the left rostral ventrolateral medulla8 or the omental transplantation on the anterior perforated space6,9 can improve or normalize EAH—by restitution of the blood flow in the A1/C1 cell column using the first surgical technique, and because of revascularization in the lateral and posterior hypothalamus produced with the last technique. Therefore, ischemia in the posterior hypothalamus and nuclei of the medulla oblongata are the specific causes of neurogenic hypertension.
Based on the above-mentioned factors and the efficacy of both neurosurgical techniques in the treatment of EAH, we think that neurogenic hypertension represents the great majority of patients with essential hypertension.7 Therefore, as the specific cause is proven, this neurogenic hypertension type is defined as secondary. Moreover, as the onset of neurogenic hypertension and cerebral atherosclerosis are associated with age (about 35 years), these clinical findings suggest that in the pathogenesis of atherosclerosis, there exist a primary factor and a secondary factor.10 In my opinion, the primary factor is the main cause of atherosclerosis during the first decades of life; mechanical stresses generated by blood flow provoke a reactive biological response of the intima, ie, atherosclerotic changes.
For these reasons, we believe9,10 that the primary cause of neurogenic hypertension is of microvascular origin related to vascular anomalies and that atherosclerotic plaques located at the mouths of the arterial branches vascularize to the posterior hypothalamus and medulla oblongata. In other words, neurogenic hypertension is caused by atherosclerosis, and later on, arterial hypertension constitutes the most important risk factor that accelerates the development of atherosclerosis.
References
1.
Su TC, Jeng JS, Chien KL, Sung FC, Hsu HC, Lee YT. Hypertension status is the major determinant of carotid atherosclerosis: a community-based study in Taiwan. Stroke. 2001; 32: 2265–2271.
2.
Sander D, Kukla CH, Klingehofer J, Winbeck K, Conrad B. Relationship between circadian blood pressure patterns and progression of early carotid atherosclerosis: a 3-year follow-up study. Circulation. 2000; 102: 1536–1541.
3.
Stamler J, Stamler R, Riedlinger WF, Algera G, Roberts RH. Hypertension screening of 1 million Americans: community hypertension evaluation clinic (CHEC) program, 1973 through 1975. JAMA. 1976; 235: 2299–2306.
4.
Hass WK, Fields WS, North RR, Kricheff II, Chase NE, Bauer RB. Joint study of extracranial arterial occlusion, II: arteriography, techniques, sites, and complications. JAMA. 1968; 203: 961–968.
5.
Baker AB, Resch JA, Loewenson RB. Hypertension and cerebral atherosclerosis. Circulation. 1969; 39: 701–710.
6. Rafael H. Microvascular decompression of the left lateral medulla oblongata for severe refractory neurogenic hypertension. Neurosurgery. 1999; 44: 691–692.Letter.[Medline] [Order article via Infotrieve]
7. Rafael H. Hipertension arterial esencial: un analisis neurologico sobre su etiologia. Hipertensión (Méx). 2000; 20: 7–10.
8. Jannetta PJ, Segal R, Wolfson SK, Dujovny M, Semba A, Cook EE. Neurogenic hypertension: etiology and surgical treatment. Ann Surg. 1985; 202: 253–261.[Medline] [Order article via Infotrieve]
9. Rafael H, Mego R, Correa F, Moromizato P, Espinoza M. Transplante de epiplón en hipertensos con isquemia hipotalámica: reporte de 3 casos. Hipertensión (Perú). 2000; 5: 26–28.
10. Rafael H, Pérez-Carranco M, Valadez MT. El climaterio como factor de riesgo para la enfermedad de Alzheimer. Climaterio. 2001; 4: 202–205.
Department of Internal Medicine, National Taiwan University Hospital
Department of Neurology, National Taiwan University Hospital
College of Public Health, National Taiwan University, Taipei, Taiwan
Response
We would like to thank Dr Rafael for his interest and valuable comments on our recent article in Stroke.1 In our article, we did not address the mechanism of essential hypertension and the relationship between carotid atherosclerosis with neurogenic hypertension. We agree that neurogenic mechanisms may be important for the maintenance of most forms of hypertension. However, there are still insufficient evidences to implicate abnormal central nervous system (CNS) function as the primary cause of essential hypertension.2 The effect of lowering blood pressure by microvascular decompression of the left rostral ventrolateral medulla3 may be similar to blockade of the sympathetic nervous system, leading to vasodilatation. Our previous study revealed that thoracic sympathectomy might reduce blood pressure and elevate blood flow volume of carotid arteries4; that may partly explain one of the neurogenic mechanisms. However, the etiologies of essential hypertension are multifactorial: environmental, genetic, pathological, and so on.5 The relief of hypertension from microvascular decompression surgery at the rostral ventrolateral medulla does not indicate CNS atherosclerosis as the unique cause of essential hypertension. The immediate postprocedural hemodynamic complications in patients receiving carotid stenting for severe carotid stenosis, including hypotension (22.4%) and hypertension (38.8%),6 indicate that release of compression from severe internal carotid artery stenosis does not always reduce blood pressure.
The causal relationship between hypertension and carotid atherosclerosis was reinforced by the findings of the dose-response effect of hypertension on carotid intima-media thickness and carotid atherosclerosis.1 Furthermore, the analysis of subjects with extracranial carotid atherosclerotic plaque scores 
4 showed that 27.6% cases are normotensives.1 There are bodies of evidence demonstrating that hypertension may play a major role in carotid atherosclerosis1,7 and its progression.8,9 A recent study provided convincing data that treatment for hypertension has a beneficial effect on the regression of carotid atherosclerosis.10
Thus, the hypothesis raised by Dr Rafael that neurogenic hypertension is caused by atherosclerosis, which is considered to be the primary cause of essential hypertension, seems to lack strong and direct evidence. Further studies by cohort and prospective designs may be conducted to delineate the sequential and causal relationship between hypertension and atherosclerosis at the vascular beds of CNS.
References
1. Su TC, Jeng JS, Chien KL, Sung HC, Hsu HC, Lee YT. Hypertension status is the major determinant of carotid atherosclerosis: a community-based study in Taiwan. Stroke. 2001; 32: 2265–2271.
2.
Reis DJ. The brain and hypertension. Arch Neurol. 1988; 45: 180–182.
3. Levy EI, Scarrow AM, Jennetta PJ. Microvascular decompression in the treatment of hypertension: review and update. Surg Neurol. 2001; 55: 2–11.[CrossRef][Medline] [Order article via Infotrieve]
4. Jeng JS, Yip PK, Huang SJ, Kao MC. Changes in hemodynamics of the carotid and middle cerebral arteries before and after endoscopic sympathectomy in patients with palmar hyperhidrosis: preliminary results. J Neurosurg. 1999; 90: 463–467.[Medline] [Order article via Infotrieve]
5.
Carretero OA, Oparil S. Essential hypertension, I: definition and etiology. Circulation. 2000; 101: 329–335.
6.
Qureshi AI, Luft AR, Sharma M, Janardhan V, Lopes DK, Khan J, Guterman LR, Hopkins LN. Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting. Stroke. 1999; 30: 2086–2093.
7.
Psaty BM, Furberg CD, Kuller LH, Borhani NO, Rautaharju PM, O’Leary DH, Bild DE, Robbins J, Fried L, Reid C. Isolated systolic hypertension and subclinical cardiovascular disease in the elderly: initial findings from the Cardiovascular Health Study. JAMA. 1992; 268: 1287–1291.
8.
Lakka TA, Salonen R, Kaplan GA, Salonen JT. Blood pressure and the progression of carotid atherosclerosis in middle-aged men. Hypertension. 1999; 34: 51–56.
9.
Delcker A, Diener HC, Wilhelm H. Influence of vascular risk factors for atherosclerotic carotid plaque progression. Stroke. 1995; 26: 2016–2022.
10.
Lonn E, Yusuf S, Dzavik V, Doris C, Yi Q, Smith S, Moore-Cox A, Bosch J, Riley W, Teo K, SECURE Investigators. Effects of ramipril and vitamin E on atherosclerosis: the study to evaluate carotid ultrasound changes in patients treated with ramipril and vitamin E (SECURE). Circulation. 2001; 103: 919–925.
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