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ORIGINAL ARTICLE
Year : 2018  |  Volume : 21  |  Issue : 4  |  Page : 199-203

Target organ damage among subjects with high-normal blood pressure in a Nigerian tertiary health institution


1 Department of Medicine, Bayero University/Murtala Muhammad Specialist Hospital, Kano, Nigeria
2 Department of Medicine, Bayero University/Aminu Kano Teaching Hospital, Kano, Nigeria
3 Department of Medicine, Jos University Teaching Hospital, Jos, Nigeria

Date of Web Publication31-Dec-2018

Correspondence Address:
Dr. H Saidu
Department of Medicine, Bayero University/Murtala Muhammad Specialist Hospital, Kano
Nigeria
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DOI: 10.4103/smj.smj_66_17

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  Abstract 


Background: There is paucity of data on the relationship between high – normal blood pressure (BP) and target organ damage (TOD) in sub-Saharan Africa including Nigeria. This study therefore, aimed to assess target organ damage (TOD) among subjects with high – normal BP in comparison with hypertensives and subjects with optimal BP. Materials and Methods: The study was cross-sectional and comparative conducted at Aminu Kano Teaching Hospital, Kano on eligible subjects aged 18 years and above. Three groups comprising of randomly selected subjects (high -normal (group 1), hypertension (group 2) and optimal BP (group 3)), with each group having 100 in number were studied. Funduscopy and relevant investigations including transthoracic echocardiography were carried out. High – normal BP was defined as systolic BP of 130 -139mmHg and/or diastolic BP of 80-89mmHg. Results: The mean age of subjects in group 1 was 27.32 ± 8.20 years and 60% were female, 34.04±6.25 years for group 2 and 53% were female, and 52.81 ± 13.3 years for group 3 and 56% were female (P = < 0.001). The most prevalent TOD was left ventricular hypertrophy, present in 62% of hypertensives, 14% of those with high-normal BP and 2% of those with optimal BP(P = <0.001). Micro albuminuria and slight increase in creatinine were found in 12.9% and 6% of subjects with high-normal BP; 25.7% and 25% of hypertensives and 4.1% and 3% of subjects with optimal BP. The study found a significant progressive increase in both cardiovascular disease risk factors and target organ damage (TOD) as BP increased across the blood pressure categories from optimal BP to high – normal BP and to hypertension (P = <0.05). Conclusion: Subjects with high-normal BP had significantly higher prevalence of both TOD and cardiovascular disease risk factors than those with optimal BP but lower than hypertensives, suggesting that efforts to control BP should start early to reduce the complications of high BP.

Keywords: High-normal blood pressure, Nigeria, target organ damage


How to cite this article:
Saidu H, Karaye K M, Okeahialam B N. Target organ damage among subjects with high-normal blood pressure in a Nigerian tertiary health institution. Sahel Med J 2018;21:199-203

How to cite this URL:
Saidu H, Karaye K M, Okeahialam B N. Target organ damage among subjects with high-normal blood pressure in a Nigerian tertiary health institution. Sahel Med J [serial online] 2018 [cited 2019 Jan 16];21:199-203. Available from: http://www.smjonline.org/text.asp?2018/21/4/199/249082




  Introduction Top


High-normal blood pressure (BP) or prehypertension has been found to be associated with increased risk of cardiovascular (CV) events, including progression to hypertension.[1] It is associated with more than 2-fold increase in the relative risk of developing CV disease (CVD) in 10 years compared with optimal BP.[1] High-normal BP (HNBP) is associated more frequently than normal BP with other CVD risk factors and target organ damage (TOD) such as dyslipidemia, dysglycemia, overweight/obesity, microalbuminuria, and increased left ventricular mass (LVM).[2]

This clustering of risk factors is considered to be principally responsible for the TOD in subjects with HNBP. Identifying such subjects will thus provide an opportunity to modify the risk factors and avoid future complications in them. Data from the Sub-Saharan Africa that explore the relationship between HNBP and TOD are scarce. This study, therefore, aimed to assess TOD among subjects with HNBP in comparison with subjects with hypertension and those with optimal BP.


  Materials and Methods Top


The study was carried out in Aminu Kano Teaching hospital, a tertiary health institution in Kano State, Nigeria. Ethical Approval was obtained on 4th January 2010 by the Research Ethics Committee of Aminu Kano Teaching Hospital. (NUREC /21/08/2008/AKTH/EC/194). It conformed to the Declaration of Helsinki on investigations involving human subjects.[3]

Patient selection

The study population comprised of patients at least 18 years of age, attending the cardiology and general outpatient (GOP) clinics of the hospital. There were three subject groups: Group 1 – subjects with optimal BP who presented to the GOP with minor ailments; Group 2 – subjects with HNBP who also presented to the GOP with minor ailments; and Group 3 – hypertensives on treatment attending the cardiology clinic. Three hundred patients were recruited and evaluated, 100 in each group. The sample size was estimated using the prevalence of HNBP of 16.9% in a community-based study in Edo State, Nigeria.[4] Subjects in groups 1 and 2 were consecutively selected, while the hypertensive patients were selected using simple random sampling after satisfying the inclusion criteria. Exclusion criteria include subjects <18 years of age, pregnant women, and those on drugs known to increase BP such as steroids and contraceptive pills. Furthermore, excluded among the subjects with HNBP and normotensives were subjects with previous history of hypertension or known to have established diabetes mellitus (DM), chronic renal failure, or other forms of heart diseases.

In a standardized manner, information was obtained on relevant sociodemographic characteristics such as age, gender, drug history, and history of hypertension and DM with the aid of an interviewer-administered semistructured questionnaire. The weight (taken with patients in light clothing) and height (without cap/head gear/shoes) of the patients were measured using a stadiometer. The body mass index (BMI) was then calculated using the following formula: BMI = weight (kg)/height (m2). BP was measured according to the recommendations of the American Society of Hypertension.[5] The average of two readings taken 15 min apart was recorded.

All subjects were fasted overnight for 10–12 h after which venous samples were obtained for fasting plasma glucose, total cholesterol (TC), and creatinine. The samples were analyzed in the hospital chemical pathology laboratory using the auto-analyzer machine (Chiron Diagnostic – Bayer, made in England).

The CVD risk factors and TOD assessed were recognized in the 2003 World Health Organization (WHO)/International Society of Hypertension guidelines for the management of hypertension.[6] HNBP was defined as systolic BP (SBP) of 130–139 mmHg and/or diastolic BP (DBP) of 85–89 mmHg. Hypertension was defined as SBP ≥140 mmHg and/or DBP of ≥90 mmHg whereas optimal BP was defined as SBP of <120 mmHg and/or DBP of <80 mHg. The diagnosis of DM was based on the WHO criteria.[7] TC was considered to be high if it was >200 mg/dl (5.2 mmol/L).[8]

The presence of TOD is defined as the presence of any or all of the following:[6]

  1. LV hypertrophy (LVH): This was determined using echocardiography. Transthoracic echocardiography was performed using Aloka SSD 4000 machine with 3.5 MHz transducer. The procedure was performed according to the recommendations of the American Society of Echocardiography.[9] LVM was calculated using the formula (Devereux modified ASE cube formula).[10] LVM was indexed to the allometric power of height.[11] LVH was considered present if LVM index>46 g2.7
  2. Proteinuria and/or slight elevation of plasma creatinine concentration: It was defined as protein excretion >300 mg/days. It was determined with the use of urine dip stick and was considered present when more than or equal to 1+ was detected on the dip stick on the urine sample
  3. Microalbuminuria: It was defined as persistent albumin excretion between 30 and 300 mg/day.[12] It was determined with the use of Micral strips and was considered positive when a reaction color appears on the test pad of the strip[12]
  4. Slight elevation of plasma creatinine: It was defined by the presence of 1.2–2 mg/dl (105.6–176 umol/L) of creatinine in the patient's plasma[6]
  5. Early hypertensive retinopathy: This was determined with the use of ophthalmoscope. Fundoscopy was done in a darkened room. Assistance was sought from the ophthalmologists when necessary. It was considered to be present if there is generalized or focal narrowing of retinal arteries with or without arteriovenous nipping.[13]


Statistical analysis

Statistical analysis was performed with Statistical Package for Social Sciences (SPSS software version 19, Inc, Chicago, IL, USA). software version 19.0. Data are reported as mean ± standard deviation for continuous variables and as frequency for categorical variables. One-way analysis of variance was used to compare means across the three groups (optimal BP, HNBP and hypertension). P ≤ 0.05 was considered statistically significant.


  Results Top


The mean age of subjects in group 1 was 27.86 ± 8.6 years, 34.04 ± 6.25 years for group 2 and 52.62 ± 11.8 years for group 3. The subjects in group 2 were significantly older than those in group 1 (P ≤ 0.001) and those in group 3 were significantly older than those in group 2 (P ≤ 0.001). There were 60% females in group 1, 53% in group 2, and 56% in group 3. There were, however, no significant differences in the gender distribution between the three groups (P = 0.3) for each comparison. Subjects with HNBP had higher mean SBP, DBP, BMI, fasting plasma glucose, and TC when compared with those with normal BP [Table 1]. LVH was the most common TOD among the subjects with HNBP and hypertensives followed by proteinuria and microalbuminuria. The pattern of TOD among study and comparative groups is shown in [Table 2]. Among subjects with HNBP, 22% had 1 TOD and 8% had 2 TOD. [Figure 1] shows the number of TOD among the study groups. Comparison of TOD across the three BP categories showed a statistically significant increasing trend [Table 3].
Table 1: Comparison of cardiovascular disease risk factors across the blood pressure categories

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Table 2: Comparison of target organ damage of subjects with high-normal, hypertension, and optimal blood pressures

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Figure 1: Number of target organ damage in the affected subjects. BP: Blood pressure; HNBP: High-normal blood pressure; TOD: Target organ damage

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Table 3: Comparison of target organ damage across the blood pressure categories

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  Discussion Top


In the present study, subjects with HNBP had higher burden of TOD, than subjects with optimal BP, but lower than with hypertensives. The relationship between TOD and hypertension has been well established, and the presence of TOD is associated with increased CV mortality.[14] HNBP is also associated with TOD and other CVD risk factors, and their presence of which may contribute to the development of the TOD.[15],[16],[17] LVH was the most prevalent TOD followed by proteinuria, microalbuminuria, and slight increase in creatinine.

Subjects with HNBP had increased left ventricular mass index than subjects with optimal BP, with LVH detected in only 2% of subjects with optimal BP, but in up to 14% of subjects with HNBP. This finding is consistent with previous reports.[17],[18],[19] Jugal et al. reported LVH in up to 17% of prehypertensives while Segura et al. reported a lower prevalence of 10%.[19],[20] The reason for these observations is not clear. The high prevalence of LVH observed among the hypertensives (66%) is also consistent with previous reports.[19],[20],[21],[22],[23],[24]

We found a prevalence of 12.9% of microalbuminuria among subjects with HNBP, 25.7% among subjects with hypertension, and 4.1% among subjects with optimal BP. Some other studies reported a prevalence of 10% and 4.9% among subjects with HNBP.[16],[21] Microalbuminuria is a widely identified marker of vascular dysfunction including endothelial dysfunction, and it is associated with other CVD risk factors. Its presence markedly increases the risk for CV morbidity and mortality.[25],[26],[27],[28],[29],[30] Urinary albumin excretion has also been reported as a predictor of developing hypertension and BP progression, irrespective of the baseline BP level and other predisposing factors.[28]

Prehypertension increases the risk of renal arteriosclerosis which can lead to gradual decline renal function that may lead to rise in serum creatinine. Levels of serum creatinine tend to rise with increasing SBP and DBP, starting from prehypertensive to full-blown hypertension.[31] We however report in this study the prevalence of slight increase in creatinine 6%, 25%, and 3% hypertensive subjects and nonhypertensive controls. This finding is similar to previous reports.[20],[32] In another study, normal serum creatinine was found in all 771 participants of African descent with prehypertension, suggesting that the condition is not an independent risk factor for renal disease.[33]

Recent studies using quantitative measurements of retinal vascular caliber have demonstrated a graded association of narrowed retinal arterioles with increasing BP in different populations.[34],[35],[36],[37] Findings from some studies showed that retinal arteriorlar narrowing is a preclinical marker of hypertension risk.[35],[36],[37] All the studies reported that, among persons without hypertension at baseline, those with narrowed retinal arterioles had a higher risk of hypertension in the subsequent 3–7 years, independent of baseline BP levels, BMI, and other known hypertension risk factors.[35],[36],[37] Retinal arteriolar narrowing may therefore be considered as surrogate marker of an individual's genetic predisposition to hypertension development.[38] In this study, none of the subjects with HNBP or optimal BP had retinopathy. This finding suggest that HNBP plays little role in mediating retinal TOD in the population studied although an association could be demonstrated in future larger studies. The limitations of the present study, thus, include the modest sample size and cross-sectional approach. A community-based cohort study could reveal some novel risk factors in our population, which is still in epidemiologic transition.


  Conclusion Top


The present study suggests that subjects with HNBP had higher prevalence of target organ changes than subjects with optimal BP but lower than those of hypertensives, with LVH being the most prevalent TOD. Individuals in the HNBP category should therefore be identified and screened for other CVD risk factors and TOD which should be corrected to prevent them from developing hypertension and related complications.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Valsan RS, Baiser A, D'Agostino RB, Seshadri S. Residual life time risk for developing hypertension in middle aged men and women. The Framingham Study. JAMA 1996;275:1571-6.  Back to cited text no. 1
    
2.
World Health Report. Reducing Risks, Promoting Healthy Life. Geneva, Switzerland: World Health Organization; 2002.  Back to cited text no. 2
    
3.
World Medical Association. World medical association declaration of Helsinki: Ethical principles for medical research involving human subjects. J Postgrad Med 2002;48:206-8.  Back to cited text no. 3
[PUBMED]    
4.
Omuemu VO, Okojie OH, Omuemu CE. Blood pressure pattern and prevalence of hypertension in a rural community in Edo state. J Med Biomed Res 2006;52:79-86.  Back to cited text no. 4
    
5.
Recommendations for routine blood pressure measurement by indirect cuff sphygmomanometry. American Society of Hypertension. Am J Hypertens 1992;5:207-9.  Back to cited text no. 5
    
6.
Whitworth JA. World Health Organization – International Society of Hypertension guidelines on the management of hypertension. J Hypertens 2003;21:1983-92.  Back to cited text no. 6
    
7.
World Health Organization. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications: Report of a WHO Consultation Part I. Geneva: World Health Organization; 1999.  Back to cited text no. 7
    
8.
National Cholesterol Education Programme. Third report of the expert panel on the detection, evaluation and treatment of high blood cholesterol in adults (Adult treatment Panel III) National Heart Lung and Blood Institute, National Institute of Health. Circulation, 2002; 106:3143.  Back to cited text no. 8
    
9.
Sahn DJ, De Maria A, Kissio J, Weyman A. The committee on M – Mode standardization of the American Society of Echocardiography. Recommendations regarding quantitation in M – Mode echocardiography. Results of survey of echocardiographic measurements. Circulation 1978;58:1072-83.  Back to cited text no. 9
    
10.
Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, et al. Echocardiographic assessment of left ventricular hypertrophy: Comparison to necropsy findings. Am J Cardiol 1986;57:450-8.  Back to cited text no. 10
    
11.
de Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, de Divitiis O, et al. Left ventricular mass and body size in normotensive children and adults: Assessment of allometric relations and impact of overweight. J Am Coll Cardiol 1992;20:1251-60.  Back to cited text no. 11
    
12.
Parikh CR, Fischer MJ, Estacio R, Schrier RW. Rapid microalbuminuria screening in type 2 diabetes mellitus: Simplified approach with micral test strips and specific gravity. Nephrol Dial Transplant 2004;19:1881-5.  Back to cited text no. 12
    
13.
Keith NM, Wagener HP, Barker NW. Some different types of essential hypertension: Their course and their prognosis. Am J Med Sci 1939;197:332-43.  Back to cited text no. 13
    
14.
Nadar SK, Tayebjee MH, Messerli F, Lip GY. Target organ damage in hypertension: Pathophysiology and implications for drug therapy. Curr Pharm Des 2006;12:1581-92.  Back to cited text no. 14
    
15.
Lonati L, Cuspidi C, Sampieri L, Boselli L, Bocciolone M, Leonetti G, et al. Ultrasonographic evaluation of cardiac and vascular changes in young borderline hypertensives. Cardiology 1993;83:298-303.  Back to cited text no. 15
    
16.
Kimura Y, Tomiyama H, Nishikawa E, Watanabe G, Shiojima K, Nakayama T, et al. Characteristics of cardiovascular morphology and function in the high-normal subset of hypertension defined by JNC-VI recommendations. Hypertens Res 1999;22:291-5.  Back to cited text no. 16
    
17.
Manios E, Tsivgoulis G, Koroboki E, Stamatelopoulos K, Papamichael C, Toumanidis S, et al. Impact of prehypertension on common carotid artery intima-media thickness and left ventricular mass. Stroke 2009;40:1515-8.  Back to cited text no. 17
    
18.
Drukteinis JS, Roman MJ, Fabsitz RR, Lee ET, Best LG, Russell M, et al. Cardiac and systemic hemodynamic characteristics of hypertension and prehypertension in adolescents and young adults: The strong heart study. Circulation 2007;115:221-7.  Back to cited text no. 18
    
19.
Jugal KB, Sahay AP, Agarwal AK, Bindu G, Ashish G. Impact of left ventricular structure, function and geometry. J Clin Diagn Res 2014;8:BC07-10.  Back to cited text no. 19
    
20.
Segura J, Sierra DL, Fernandez S, Ruilope M. High prevalence of target organ damage in hypertensive and pre – Hypertensive patients with associated cardiovascular risk factors. Journal of Hypertension 2010;28: e466.  Back to cited text no. 20
    
21.
Karaye KM, Habib AG. Left ventricular geometric pattern among hypertensives: A study of a hypertensive population in Nigeria. Sahel Med J 2009;12:148-54.  Back to cited text no. 21
  [Full text]  
22.
Adamu UG, Kolo PM, Katibi IA, Opadijo GO, Omotosho AB, Araoye MA, et al. Relationship between left ventricular diastolic function and geometric patterns in Nigerians with newly diagnosed systemic hypertension. Cardiovasc J Afr 2009;20:173-7.  Back to cited text no. 22
    
23.
Shipilova T, Pshenichnikov I, Kaik J, Volozh O, Abina J, Kalev M, et al. Echocardiographic assessment of the different left ventricular geometric patterns in middle-aged men and women in Tallinn. Blood Press 2003;12:284-90.  Back to cited text no. 23
    
24.
Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Relation of arterial structure and function to left ventricular geometric pattern in hypertensive adults. J Am Coll Cardiol 1995;25:83-90.  Back to cited text no. 24
    
25.
Knight EL, Kramer HM, Curhan GC. High-normal blood pressure and microalbuminuria. Am J Kidney Dis 2003;41:588-95.  Back to cited text no. 25
    
26.
Kim BJ, Lee HJ, Sung KC, Kim BS, Kang JH, Lee MH, et al. Comparison of microalbuminuria in 2 blood pressure categories of prehypertensive subjects. Circ J 2007;71:1283-7.  Back to cited text no. 26
    
27.
Dinneen SF, Gerstein HC. The association of microalbuminuria and mortality in non-insulin-dependent diabetes mellitus. A systematic overview of the literature. Arch Intern Med 1997;157:1413-8.  Back to cited text no. 27
    
28.
Gerstein HC, Mann JF, Yi Q, Zinman B, Dinneen SF, Hoogwerf B, et al. Albuminuria and risk of cardiovascular events, death, and heart failure in diabetic and nondiabetic individuals. JAMA 2001;286:421-6.  Back to cited text no. 28
    
29.
Hillege HL, Janssen WM, Bak AA, Diercks GF, Grobbee DE, Crijns HJ, et al. Microalbuminuria is common, also in a nondiabetic, nonhypertensive population, and an independent indicator of cardiovascular risk factors and cardiovascular morbidity. J Intern Med 2001;249:519-26.  Back to cited text no. 29
    
30.
Hillege HL, Fidler V, Diercks GF, van Gilst WH, de Zeeuw D, van Veldhuisen DJ, et al. Urinary albumin excretion predicts cardiovascular and noncardiovascular mortality in general population. Circulation 2002;106:1777-82.  Back to cited text no. 30
    
31.
Ninomiya T, Kubo M, Doi Y, Yonemoto K, Tanizaki Y, Tsuruya K, et al. Prehypertension increases the risk for renal arteriosclerosis in autopsies: The Hisayama Study. J Am Soc Nephrol 2007;18:2135-42.  Back to cited text no. 31
    
32.
Usman W, Muhammad MH. Detection of nephropathy in prehypertensive subjects. JRMC 2014;18:186-9.  Back to cited text no. 32
    
33.
Norton GR, Maseko M, Libhaber E, Libhaber CD, Majane OH, Dessein P, et al. Is prehypertension an independent predictor of target organ changes in young-to-middle-aged persons of African descent? J Hypertens 2008;26:2279-87.  Back to cited text no. 33
    
34.
Hubbard LD, Brothers RJ, King WN, Clegg LX, Klein R, Cooper LS, et al. Methods for evaluation of retinal microvascular abnormalities associated with hypertension/sclerosis in the atherosclerosis risk in communities study. Ophthalmology 1999;106:2269-80.  Back to cited text no. 34
    
35.
Wong TY, Islam FM, Klein R, Klein BE, Cotch MF, Castro C, et al. Retinal vascular caliber, cardiovascular risk factors, and inflammation: The multi-ethnic study of atherosclerosis (MESA). Invest Ophthalmol Vis Sci 2006;47:2341-50.  Back to cited text no. 35
    
36.
Kawasaki R, Wang JJ, Rochtchina E, Taylor B, Wong TY, Tominaga M, et al. Cardiovascular risk factors and retinal microvascular signs in an adult Japanese population: The Funagata Study. Ophthalmology 2006;113:1378-84.  Back to cited text no. 36
    
37.
Wong TY, Klein R, Klein BE, Meuer SM, Hubbard LD. Retinal vessel diameters and their associations with age and blood pressure. Invest Ophthalmol Vis Sci 2003;44:4644-50.  Back to cited text no. 37
    
38.
Wang JJ, Wong TY. Genetic determinants of retinal vascular caliber: Additional insights into hypertension pathogenesis. Hypertension 2006;47:644-5.  Back to cited text no. 38
    


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