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Table of Contents
CASE REPORT
Year : 2019  |  Volume : 4  |  Issue : 2  |  Page : 64-68

Primary orthostatic hypertension: A case report and literature review


1 Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China
2 Department of Cardiovascular Medicine; Jiangxi Key Laboratory of Molecular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China

Date of Submission22-May-2019
Date of Acceptance13-Jun-2019
Date of Web Publication26-Jun-2019

Correspondence Address:
Yi-Fei Dong
Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, No. 1, Minde Road, Nanchang, Jiangxi 330006
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cp.cp_12_19

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  Abstract 


Orthostatic hypertension (OHT) is a sudden elevation in blood pressure after standing, which is clinically easy to ignore. Most of these OHT patients do not have characteristic manifestations of hypertension and are often diagnosed during physical examination. Most of the blood pressure increase in OHT patients is due to diastolic blood pressure, and the fluctuation is large. An adult patient with OHT was diagnosed and treated, and possible underlying mechanisms were analyzed.

Keywords: Antihypertensive therapy, hypertension, orthostatic hypertension


How to cite this article:
Wang YX, Wang Y, Xu Y, Xu CC, Dong YF. Primary orthostatic hypertension: A case report and literature review. Cardiol Plus 2019;4:64-8

How to cite this URL:
Wang YX, Wang Y, Xu Y, Xu CC, Dong YF. Primary orthostatic hypertension: A case report and literature review. Cardiol Plus [serial online] 2019 [cited 2019 Aug 21];4:64-8. Available from: http://www.cardiologyplus.org/text.asp?2019/4/2/64/261429




  Introduction Top


Postural blood pressure abnormalities include orthostatic hypertension (OHT) and orthostatic hypotension (OH). At present, there are many studies on OH, but there are relatively few reports on OHT. We treated a patient with OHT in December 2018.


  Case Report Top


A 45-year-old male patient was found to have elevated blood pressure during physical examination, especially when standing. The highest standing blood pressure was 170/120 mmHg, and the home self-test standing blood pressure fluctuated between 120–140/90–100 mmHg. The patient had no previous history of major diseases, no family history of hypertension and occasional tinnitus, and no other obvious symptoms.

At admission, the office supine blood pressure was 114/78 mmHg (right arm) and the standing blood pressure was 154/107 mmHg (right arm). There were no positive signs. Auxiliary examinations revealed synchronous four-limb blood pressure (decumbent position): 113/82 mmHg (right arm), 145/89 mmHg (right ankle), 117/82 mmHg (left arm), and 141/81 mmHg (left ankle); 24-h ambulatory blood pressure: the whole day 134/93 mmHg, the daytime 139/98 mmHg, the night 119/81 mmHg, and dipping blood pressure rhythm; electrocardiogram: sinus rhythm and no left ventricular high-voltage performance; echocardiography: ventricular septum thickness 9 mm (8–11), left ventricular posterior wall thickness 8 mm (8–11), and left ventricular ejection fraction 57%; abdominal and bilateral renal artery computed tomography angiography: no obvious abnormalities; adrenal computed tomography: left adrenal junction nodular thickening; cervical Doppler sonography: carotid intima–media thickness of left 0.8 mm and right 0.7 mm; pulse wave velocity: 1631 cm/s on the left and 1626 cm/s on the right; ankle/arm blood pressure index: on the left 1.21 and on the right 1.24; fundus photography: bilateral retinal atherosclerosis; serum creatinine: 67.75 μmol/L; serum potassium: 3.75 mmol/L; and urinary microalbumin/creatinine: 6.89 mg/g, cortisol level and rhythm normal, and plasma aldosterone and renin activity levels in decubitus/standing positions as shown in [Table 1].
Table 1: Levels of plasma aldosterone and renin activity in decubitus/standing positions

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Overall, the patient's blood pressure level was slightly elevated (level 1), and there were no associated target organ damages. No secondary hypertension factors were found on the admission examinations. However, the aldosterone level and renin activity in the orthostatic position were significantly higher than that in the decumbent position [Table 1], suggesting that the overactivation of the circulating renin–angiotensin system during a postural change may be a potential cause of significant elevation of orthostatic blood pressure. In view of the above analysis, we prescribed allisartan isoproxil (240 mg/day), an angiotensin II receptor blocker, as an antihypertensive therapy. After taking the medicine for 3 weeks, the patient's office and home blood pressures returned to normal. [Figure 1] shows the results of office right/left arm systolic/diastolic blood pressure in decumbent and standing positions before and after 3 weeks of antihypertensive therapy. The mean difference of office systolic blood pressure of both arms between decumbent and standing positions decreased from 21.5 mmHg before taking medicine to 16 mmHg after taking medicine. The mean difference of office diastolic blood pressure of both arms between decumbent and standing positions decreased from 18.5 mmHg before taking medicine to 11 mmHg after taking medicine. [Figure 2] shows the results of home right/left arm systolic/diastolic blood pressure in decumbent and standing positions before and after 3 weeks of antihypertensive therapy. The mean difference of home systolic blood pressure of both arms between decumbent and standing positions decreased from 27.5 mmHg before taking medicine to 6.5 mmHg after taking medicine. The mean difference of home diastolic blood pressure of both arms between decumbent and standing positions decreased from 30.5 mmHg before taking medicine to 9 mmHg after taking medicine. [Figure 3] shows the office and home heart rates in decumbent and standing positions before and after antihypertensive therapy. The office standing heart rate increased from 8 times/min before taking medicine to 18 times/min after taking medicine [Figure 3]a. The home standing heart rate increased from 8 times/min before taking medicine to 15 times/min after taking medicine [Figure 3]b.
Figure 1: Office blood pressure of right/left arms in decumbent and standing positions before and after antihypertensive therapy. D: Decubitus position; RUE: Right upper extremity; SBP: Systolic blood pressure; S: Standing position

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Figure 2: Home blood pressure of right/left arms in decumbent and standing positions before and after antihypertensive therapy. D: Decubitus position; RUE: Right upper extremity; SBP: Systolic blood pressure; S: Standing position

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Figure 3: Office (a) and home (b) heart rates in decumbent and standing positions before and after antihypertensive therapy

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  Discussion Top


The patient was middle aged and hypertensive whose blood pressure was generally normal in decumbent position and significantly elevated in standing position. The patient had a short history of hypertension and a slight increase in blood pressure; no serious target organ damage and no secondary hypertension factors were found. OHT has no internationally accepted definition and is a clinical pathological phenomenon with high prevalence, but is not taken seriously. At present, most researchers define OHT as an increase in systolic blood pressure (>20 mmHg) after the patient is transposed from the supine position to the orthostatic position, regardless of the change in diastolic blood pressure.[1] Some scholars, such as Streeten et al.,[2] define OHT as the change of diastolic blood pressure from the decumbent position <90 mmHg to standing position >90 mmHg. According to different definitions, the overall prevalence rate is about 8.6%–20%.[3],[4],[5] OHT is often found unexpectedly in physical examinations because of its general absence of obvious clinical manifestations.

OHT is closely related to stroke, deep white matter damage, cardiovascular damage, kidney damage, and diabetes mellitus, and most scholars consider OHT to be “prehypertension.”[5],[6],[7],[8],[9] Yatsuya et al.[7] concluded after nearly 20 years of research on 12,000 people that the increase of postural systolic blood pressure and the incidence of lacunar stroke showed a J-shaped curve. With increased postural blood pressure, the incidence of lacunar infarction also increased gradually. Matsubayashi et al.[8] found that the cognitive ability and daily living ability were significantly reduced in elderly patients over 75 years old with OHT, and the degree of deep white matter damage was much higher than that of the elderly without OHT. After a long period of investigation, Japanese researchers[10] found that the increased rate of carotid intima–media thickness in OHT patients was higher than that in normal hypertensive patients. Through a study of more than 600 hypertensive patients, Hoshide et al.[9] found that OHT patients with urinary albumin/creatinine ratio significantly higher than ordinary hypertensive patients, suggesting that OHT and kidney damage exist close relationship. A recent study[6] found that the prevalence of OHT in newly diagnosed type 2 diabetes with hypertension was 20.4%. The study concluded that OHT is closely related to diabetes.

The pathogenesis of OHT has not yet been fully elucidated, and most scholars believe that it is associated with excessive excitation or activation of the sympathetic and/or renin–angiotensin–aldosterone system (RAAS). In patients with OHT, when the posture changes from position to position, the sympathetic nerve is overexcited by the stimulation of blood pressure fluctuations, resulting in excessive contraction of blood vessels, which makes the patient's standing blood pressure significantly higher than the supine blood pressure.[1] Streeten et al.[2] believed that there are veins and venous sinuses below the human heart plane. These veins and sinuses are called “gravity vascular pools,” in which a large amount of blood is stored. When the OHT patient is in the standing position, the blood in the vascular pool is more stagnate, which reduces the amount of blood returning to the heart, and the cardiac output decreases, which leads to excessive sympathetic excitation, small arterial contraction, and high blood pressure. Some scholars[11] have found that renal ptosis is closely related to OHT. When a patient with renal ptosis is standing, it can cause stretching and torsion of the renal artery, resulting in a significant decrease in renal blood flow and activation of RAAS, resulting in elevated blood pressure.

Because the mechanism of OHT is not clear, there is no “specific drug” for its treatment at present. Studies have found that the administration of α1-blocker (doxazosin) before bedtime can reduce the systolic pressure of the standing position, but has no effect on the systolic pressure of the sitting position.[12] It has also been reported that a novel calcium channel blocker (azadipine) and an alpha-2 receptor agonist (clonidine) are effective in the treatment of OHT.[13]

In this patient, the renin activity was significantly higher than that in the supine position [Table 1], suggesting that postural changes activate RAAS, and after 3 weeks of treatment with angiotensin II blocker (allisartan isoproxil), the patient's standing blood pressure decreased significantly [Figure 1] and [Figure 2]. We also observed the changes in the patient's heart rate before and after treatment to evaluate the sympathetic system activation. It was found that the patient's standing heart rate increased more obviously after treatment, but the elevated blood pressure was effectively controlled. The observation showed that the excessive activation of RAAS might be the main mechanism under this OHT case.

The diagnosis and treatment of this patient suggested that the test of renin activity/aldosterone in both decumbent position and standing position can provide useful information for the treatment of OHT patients. An RAAS blocker is effective for controlling blood pressure in OHT patients with significantly increased renin activity in the standing position.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

This study was funded by Jiangxi Province “5511” Science and Technology Innovation Talents Project, Jiangxi Science and Technology Department (20165BCB18020); Jiangxi Science and Technology Department Key Research and Development Project (20171BBG70088).

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Kario K. Orthostatic hypertension: A measure of blood pressure variation for predicting cardiovascular risk. Circ J 2009;73:1002-7.  Back to cited text no. 1
    
2.
Streeten DH, Auchincloss JH Jr., Anderson GH Jr., Richardson RL, Thomas FD, Miller JW, et al. Orthostatic hypertension. Pathogenetic studies. Hypertension 1985;7:196-203.  Back to cited text no. 2
    
3.
Lili W, Zhandong L, Yingying Z, Jian Z, Jimei L. Postural blood pressure changes and their effects on neurocognitive impairment in elderly patients with hypertension. J Clin Exp Med 2012;11:241-6.  Back to cited text no. 3
    
4.
Xiaohan F, Haiying W, Rutai H. Postural hypotension and cardiovascular and cerebrovascular diseases. Chin J Hypertens 2009;17:858-62.  Back to cited text no. 4
    
5.
Thomas RJ, Liu K, Jacobs DR Jr., Bild DE, Kiefe CI, Hulley SB. Positional change in blood pressure and 8-year risk of hypertension: The CARDIA study. Mayo Clin Proc 2003;78:951-8.  Back to cited text no. 5
    
6.
Nibouche-Hattab WN, Lanasri N, Zeraoulia F, Chibane A, Biad A. Orthostatic hypertension in normotensive type 2 diabetics: What characteristics? Ann Cardiol Angeiol (Paris) 2017;66:159-64.  Back to cited text no. 6
    
7.
Yatsuya H, Folsom AR, Alonso A, Gottesman RF, Rose KM; ARIC Study Investigators. Postural changes in blood pressure and incidence of ischemic stroke subtypes: The ARIC study. Hypertension 2011;57:167-73.  Back to cited text no. 7
    
8.
Matsubayashi K, Okumiya K, Wada T, Osaki Y, Fujisawa M, Doi Y, et al. Postural dysregulation in systolic blood pressure is associated with worsened scoring on neurobehavioral function tests and leukoaraiosis in the older elderly living in a community. Stroke 1997;28:2169-73.  Back to cited text no. 8
    
9.
Hoshide S, Matsui Y, Shibasaki S, Eguchi K, Ishikawa J, Ishikawa S, et al. Orthostatic hypertension detected by self-measured home blood pressure monitoring: A new cardiovascular risk factor for elderly hypertensives. Hypertens Res 2008;31:1509-16.  Back to cited text no. 9
    
10.
Kario K, Eguchi K, Hoshide S, Hoshide Y, Umeda Y, Mitsuhashi T, et al. U-curve relationship between orthostatic blood pressure change and silent cerebrovascular disease in elderly hypertensives: Orthostatic hypertension as a new cardiovascular risk factor. J Am Coll Cardiol 2002;40:133-41.  Back to cited text no. 10
    
11.
Buddineni JP, Chauhan L, Ahsan ST, Whaley-Connell A. An emerging role for understanding orthostatic hyp'er'tension in the cardiorenal syndrome. Cardiorenal Med 2011;1:113-22.  Back to cited text no. 11
    
12.
Hoshide S, Parati G, Matsui Y, Shibazaki S, Eguchi K, Kario K, et al. Orthostatic hypertension: Home blood pressure monitoring for detection and assessment of treatment with doxazosin. Hypertens Res 2012;35:100-6.  Back to cited text no. 12
    
13.
Magkas N, Tsioufis C, Thomopoulos C, Dilaveris P, Georgiopoulos G, Doumas M, et al. Orthostatic hypertension: From pathophysiology to clinical applications and therapeutic considerations. J Clin Hypertens (Greenwich) 2019;21:426-33.  Back to cited text no. 13
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1]



 

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