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  Page | 156 Vol. 8, July-September, 2009 Annals of African Medicine Blood pressure control and left ventricular hypertrophy in hypertensive Nigerians Babatunde L. Salako, Okechukwu S. Ogah 1 , Adewole A. Adebiyi, Olulola O. Oladapo,  Akinyemi Aje 2 , Adedeji K. Adebayo 3 , Dike B. Ojji 4 , Arinola Ipadeola, Chibuike E. Nwafor Department of Medicine, University College Hospital, Ibadan, PMB 5116 Ibadan, Oyo State, Nigeria, 1 Department of Medicine, Federal Medical Centre, PMB 3031 Sapon, Abeokuta, Ogun State, Nigeria, 2 Department of Accident and Emergency, University College Hospital, Ibadan, PMB 5116 Ibadan, Oyo State, Nigeria, 3 Department of Medicine, Lagoon Hospital, Lagos, Nigeria, 4 Department of Medicine, University of Abuja Teaching Hospital, FCT, Abuja, Nigeria. Correspondence to:  Dr. O. S. Ogah, Department of Medicine, Federal Medical Centre, PMB 3031 Sapon, Abeokuta, Ogun State, Nigeria- 110 001. E-mail: osogah56156@yahoo.com Abstract Background:  Hypertension is a disease characterized by end-organ complications, leading to high morbidity and mortality in many cases. People with untreated or uncontrolled hypertension often run the risk of developing complications directly associated with the disease. Left ventricular hypertrophy (LVH) has been shown to be a signi fi cant risk factor for adverse outcomes both in patients with hypertension and in the general population. We investigated the prevalence and pattern of LVH in a treated hypertensive population at the University College Hospital, Ibadan, Nigeria, using non-hypertensive subjects as control. Design and Setting:  A prospective observational study performed at the University College Hospital, Ibadan, Nigeria. Methods:  Patients had 6 visits, when at least one blood pressure measurement was recorded for each hypertensive subject and average calculated for systolic blood pressure (SBP) and diastolic blood pressure (DBP) separately. The values obtained were used for strati fi cation of the subjects into controlled and uncontrolled hypertension. Subjects also had echocardiograms to determine their left ventricular mass. Results:  LVH was found in 14 (18.2%) of the normotensive group, 40 (20.8%) of the uncontrolled hypertensive group and 14 (24.1%) of the controlled hypertensive group when left ventricular mass (LVM) was indexed to body surface area (BSA). When LVM was indexed to height, left ventricular hypertrophy was found in none of the subjects of the normotensive group, while it was found present in 43 (22.4%) and 14 (24.1%) subjects of the uncontrolled and controlled hypertensive groups, respectively. Signi fi cant difference in the prevalence of LVH was detected only when LVM was indexed to height alone. Conclusion:  Clinic blood pressure is an ineffective way of assessing BP control. Thus in apparently controlled hypertensive subjects, based on of  fi ce blood pressure, cardiac structural changes do remain despite antihypertensive therapy. This population is still at risk of cardiovascular events. Keywords:  Blood pressure control, hypertension, left ventricular hypertrophy Résumé arrière-plan:  l’hypertension est une maladie caractérisée par l’orgue de fi n complications menant à élevé de morbidité et mortalité dans de nombreux cas. Personnes avec l’hypertension non traitée ou non contrôlée souvent risquent de développer complications directement associées à la maladie. Laissé ventriculaire hypertrophie (LVH) a été démontré un facteur de risque signi fi catif pour les effets négatifs résultats tant chez les patients atteints de l’hypertension et de la population générale. Nous avons a enquêté sur la prévalence et le modèle de LVH dans un traité hypertendues population au University College Hospital, à l’aide Ibadan, Nigeria non-hypertendues des sujets comme contrôle. conception et la con fi guration:  A éventuel étude d’observation effectuée à la University College Hospital, Ibadan, Nigeria. méthodes:  Patients avaient six visites où au moins un sang mesure de pression a été enregistrée pour chaque sujet hypertendues et moyenne calculés séparément pour SBP et DBP. Les valeurs obtenues ont été utilisées pour  Annals of African MedicineVol. 8, No. 3; 2009:156-162  Original    Article  Page | 157 Annals of African Medicine Vol. 8, July-September, 2009 strati fi cation des sujets dans l’hypertension contrôlée et incontrôlée. Sujets ont également echocardiograms pour déterminer leur masse ventriculaire gauche. résultats:  LVH a été trouvé en 14(18.2%) de la groupe normotensive, 40(20.8%) de groupe de hypertendues non contrôlées et 14(24.1%) de hypertendues contrôlée groupe lorsque quitté masse ventriculaire (LVM) a été indexée à corps surface (BSA). Lorsque LVM a été indexé à hauteur, laissé ventriculaire hypertrophie a été trouvé dans aucun du groupe normotensive, bien qu’il a été constaté présents dans les 43(22.4%) et 14(24.1%) de hypertendues non maîtrisée et contrôlée groupes respectivement. Était de différence signi fi cative dans la prévalence de la LVH détectés uniquement lorsque LVM a été indexé à hauteur alone. conclusion:  clinique artérielle est un moyen inef  fi cace de mesurer le contrôle de BP. Ainsi en sujet hypertendues apparemment contrôlée basée sur la pression artérielle de bureau, des changements structurels cardiaques restent malgré thérapie antihypertensive. Cette population est toujours à risque de maladies cardiovasculaires événements. Mots cles:  contrôle de la pression sanguine, LVH, l’hypertension DOI:  10.4103/1596-3519.57237  PMID:  19884691 Introduction   Hypertension is a disease characterized by end-organ complications, leading to high morbidity/ disability and mortality in many cases. [1]  People with untreated and uncontrolled hypertension often run the risk of developing complications such as left ventricular hypertrophy (LVH), cardiomegaly, congestive cardiac failure, retinopathy, cerebrovascular disease and renal insufficiency. LVH alone has been identified to have adverse effect on survival of hypertensive patients. [2,3]  It has been shown to be an important predictor of cardiovascular morbidity and mortality in hypertensive patients and even in the general population. [4,5] It is an adaptive response to increased left ventricular wall stress, which is reversible by treatment.Studies performed in Nigeria to evaluate blood pressure control in Nigerian hypertensive patients have shown that blood pressure control is poor, since only a few of them achieve a clinic blood pressure that can be described as optimal. [6-8] This study sets out to investigate the prevalence and pattern of LVH in both controlled and uncontrolled hypertensive population using apparently normal subjects as control in an attempt to observe the effects of treatment on LVH in the groups. Methods Normotensive healthy individuals and patients diagnosed with primary hypertension being followed- up in the medical clinic of the University College Hospital, Ibadan, were recruited into the study. Informed consent was obtained from the subjects, and their blood pressures were measured according to standard guidelines. [9]  Recruitment into the study was spread over a period of 2  years. Blood pressure was measured in patients and controls after 5 minutes of rest and the average of two measurements taken each time. Six consecutive clinic BP values at an interval of 6 weeks were recorded for each hypertensive subject, and average was calculated for SBP and DBP separately. The average systolic and diastolic blood pressures were used in stratifying controlled and uncontrolled hypertensive subjects. A standard mercury sphygmomanometer (Accosson, London)  was used, and systolic blood pressure (SBP) and diastolic blood pressure (DBP) were taken as Korotkoff sound phases I and V, respectively. A cuff of appropriate size was applied to the exposed right upper arm and was rapidly inflated to 30 mm Hg above the level at which the pulse disappeared and then deflated gradually. Blood pressure was considered to be well controlled if it was less than 140/90 mm Hg and uncontrolled if higher than 140/90 mm Hg. [10,11]  Weight was measured to the nearest 0.5 kg with subjects in light clothing and  without shoes on a beam balance scale calibrated  with standard weights. Height was measured to the nearest centimeter using anthropometric plane with subjects not putting on shoes or headgear. Body-mass index (BMI) was calculated using the formula BMI = Weight (kg)/ ! Height (m) 2 ,   and body surface area (BSA) was measured by the formula of Dubois. Subjects with heart failure, cerebrovascular disease, ischemic heart disease, diabetes mellitus and renal failure were excluded from the study. Echocardiography   Two-dimensional guided M-mode echocardiography  with the use of commercially available echo-machine (ALOKA SSD-1, 700) and a 3.5-MHz linear array transducer was performed on each subject in the left lateral decubitus position. All measurements were made according to the leading edge–to–leading edge criteria of the American Society of Echocardiography. [12]  Left Ventricular Salako et al .: Blood pressure control and left ventricular hypertrophy  Page | 158 Vol. 8, July-September, 2009 Annals of African Medicine (LV) measurement was obtained at end diastole and end systole. The LV measurements taken include interventricular septal thickness at end-diastole (IVSTd), the posterior wall thickness at end-diastole (PWTd) and the LV internal dimensions at end-systole (LVIDs) and end-diastole (LVIDd). Measurements were taken in 3 cardiac cycles, and average of the 3 values was calculated. Two experienced echocardiographers performed all the echocardiographic examinations. In our laboratory, the intra-observer concordance correlation coefficient ranged from 0.76 to 0.98, while that of the inter-observer concordance ranged from 0.82 to 0.96. [13]   Calculation of derived variables and LV hypertrophy Left ventricular mass (LVM) was calculated using the following formula, which has been shown to yield  values closely related to necropsy LV weight and also has good inter-study reproducibility (r= 0.90) [14] : . LVM = LVM = 1.04 × [(LVID + IVS + LVPW)  3- (LVID)  3 )-13.6]Relative wall thickness was calculated as 2-x posterior wall thickness/LV internal dimension in diastole. [15]  LV hypertrophy was considered present  when LVM indexed to body surface area exceeded 116 g/m 2  in men and 104 g/m 2  in women, [16]  or LVM indexed to height exceeded 126 g/m in men and 105 g/m in women. [17]  Increased relative wall thickness  was present when RWT was greater than 0.43,  which represents the 97.5 th  percentile in normal subjects. [18]  LV geometry was defined using LV mass index and relative wall thickness. Normal geometry  was present when indexed LVM (LVMI) and RWT  were normal, whereas normal LVMI and increased RWT identified concentric remodeling. Increased LVMI but normal RWT identified eccentric LV hypertrophy, and increases of both variables identified concentric hypertrophy. [19] LV systolic performance (fractional shortening and ejection fraction) was calculated using the Teichholz’s formula. [20]   Data analysis SPSS software version 12.0 (SPSS, Inc., Chicago, Illinois) was used for statistical analysis. Continuous  variables were expressed as mean #  SD (standard deviation); and categorical variables, as percentages. Differences in categorical variables were assessed by chi-square analysis. Multiple comparisons were performed by analysis of variance (ANOVA). The Bonferroni post hoc test was used for comparison between groups. A 2-tailed P  value < .05 was considered to be significant. Results Patient characteristics Table 1 shows the baseline demographic and clinical characteristics of the subjects. Two hundred and fifty (250) hypertensive subjects and seventy seven (77) normotensive subjects (NT) were recruited into the study. Of the 250 hypertensive subjects, 122(48.8%) were men, and 128 (51.2%) were  women. As many as 192 (76.8%) hypertensive subjects had uncontrolled blood pressure (UH),  while 58 (23.2%) had controlled blood pressure (CH). Of the 77 normotensive subjects, 43 were males while 34 were females. Table 1: Baseline demographic and clinical characteristics VariableNormotensive Subjects (n = 77)Uncontrolled Hypertensive Subjects (n = 192)Controlled Hypertensive Subjects (n = 58)ANOVA P-valueGroup Comparison Gender (M/F)43/3494/9828/300.555NSAge (years)55.3 # 8.660.8 # 12.157.5 # 12.40.001*NT vs UHWeight (kg)67.8 #  15.070.3 # 11.669.4 #  13.10.726NSHeight (cm)164.4 # 7.5164.1 #  7.9164.9 #  8.30.784NSBM1 (kg/m 2 )25.5 #  5.526.1 #  3.625.5 #  4.20.495NSBSA (m 2 )1.75 #  0.181.77 #  0.181.76 #  0.180.746NSSBP (mmHg)120.3 #  9.4155.5 #  20.7 122.2 # 8.60.0001*NT vs UH, * UH vs CHDBP (mmHg)77.3 #  8.194.8 # 12.576.5 #  6.10.0001*NT vs UH, *UH vs CHPul Press (mmHg)42.9 #  8.360.7 #  18.745.7 # 8.70.0001*NT vs UH, *UH vs CHMAP (mmHg)91.6 #  7.6115.0 #   13.091.7 # 5.60.0001*NT vs UH, *UH vs CH M= male, F= female, BMI= body mass index, BSA= body surface area, Bpsys= systolic blood pressure, BPdiast= diastolic blood pressure, Pul Press= pulse pressure, MAP= mean arterial blood pressure, NT= normotensive, UH= uncontrolled hypertensive, CH= controlled hypertensive, NS= not significant. * = significant group comparison. Salako et al .: Blood pressure control and left ventricular hypertrophy  Page | 159 Annals of African Medicine Vol. 8, July-September, 2009 Subjects with uncontrolled blood pressure were significantly older than the normotensive subjects (60.8 #  12.1 vs.  55.3 # ,   P = 0.001). Otherwise, weight, height, BMI and BSA were similar in the 3 groups.  As expected, blood pressure measurements were significantly higher in the group with uncontrolled BP when compared with the controlled BP and normotensive subjects. Echocardiographic measurements Table 2 depicts the mean values of echocardiographic parameters of the 3 groups. Left atrial diameter was significantly higher in the hypertensive subjects compared with the normotensive subjects (UH, 3.41 #  0.65 vs.  CH, 3.57 #  0.62; as against NT, 3.15 #  0.47, P = 0.001).The aortic valve opening (AVO) and the interventricular septal wall thickness in diastole (IVSTd) were significantly higher in the subjects  with uncontrolled BP when compared with normal subjects but not when compared with the subjects of controlled BP group. The LVIDs and the LVM/ BSA were also significantly larger in the hypertensive subjects (UH and CH) when compared with normotensive subjects (NT). Relative wall thickness  was significantly higher in normal subjects (NT, 0.57 #  0.17; UH, 0.41 #  0.13; CH, 0.41 #  0.11, P = 0.0001).The LV posterior wall thickness, LV internal dimensions in diastole, LVM and LVM/BSA were similar in the 3 groups. Prevalence of LVH and LV geometric patterns Table 3 shows the prevalence of the LVH and the LV geometric patterns in the 3 groups. When LVM  was indexed to body surface area, LVH was found in 14 (18.2%) subjects of the NT group, 40 (20.8%) of the UH group and in 14 (24.1%) of the CH group. Forty-three (22.4%), 14 (24.1%) and none of the subjects in the UH, CH and NT groups, respectively, had LVH when LVM was indexed to height. This was statistically significant ( P = 0.0001). With respect to LV geometry, 52 (67.5%), 56 (29.2%) and 20 (34.5%) subjects of the NT, UH and CH groups, respectively, had concentric remodeling  when LVM was indexed to BSA. The corresponding numbers when LVM was indexed to height were 61 (79.2%), 52 (27.1%) and 20 (34.5%) for NT, UH and CH groups, respectively. Eccentric hypertrophy was found in 5 (6.5%), 25 (13.0%) and 8 (13.8%) subjects of the NT, UH and CH groups, respectively. The corresponding numbers when LVM was indexed to height were 0 (0.0%), 24 (12.5%) and 8 (13.8%) for NT, UH and CH groups, respectively. There were 9 subjects in the NT group with concentric LVH; 15, in the UH group; and 6, in the CH group when LVM  was indexed to body surface area. Nine (11.7%), 15 (7.8%) and 6 (10.3%) subjects in the NT, UH and CH groups, respectively, had concentric LVH  when LVM was indexed to height. Discussion Left ventricular hypertrophy is a common adaptive process that is induced by certain physiological and pathological stimuli that are naturally put in place to normalize the increase in left ventricular wall stress caused by hypertension. The findings from this study are that (1) absolute Table 2: Mean values for echocardiographic parameters VariableNormotensive Subjects n = 77)Uncontrolled Hypertensive Subjects (n = 192)Controlled Hypertensive Subjects (n = 58)P-valueGroup Comparison LA3.15 # 0.473.41 0.65 3.52 # 0.620.001*NT vs UH, *NT vs CHAoD2.80 # 0.372.80 # 0.42.84 # 0.590.751NSAVO1.98 # 0.271.89 # 0.271.93 # 0.310.041*NT vs UHIVSTd0.88 # 0.120.98 # 0.260.95 # 0.200.007*NT vs UHPWTd0.89 # 0.120.94 # 0.210.950.190.134NSLVIDd 4.61 # 0.584.78 # 0.884.84 # 0.910.207NSLVIDs3.04 # 0.513.28 # 0.943.40 # 0.960.036*NT vs UH, *NT vs CHFS33.7 # 8.431.5 # 8.231.3 # 8.30.115NSEF69.2 # 14.165.6 # 13.365.4 # 11.90.113NSLVM159.4 # 47.0165.9 # 73.5166.4 # 67.60.752NSLVM/BSA87.2 # 25.793.8 # 40.395.0 # 40.10.364NSLVM/HT53.1 # 15.7100.7 # 43.899.9 # 40.10.0001*NT vs UH, *NT vs CHRWT0.40 # 0.170.41 # 0.130.41 # 0.110.0001*NT vs UH, *NT vs CH LA= left atrial diameter, AoD= aortic root diameter, AVO= aortic valve opening, IVSTd= interventricular septal diameter in diastole, PWTd= posterior wall thickness in diastole, LVIDd= left ventricular internal diameter in diastole, LVIDs= left ventricular internal diameter in systole, LVM= left ventricular mass, BSA= body surface area, HT= height, RWT= relative wall thickness. NT= normotensive, UH= uncontrolled hypertensive, CH= controlled hypertensive. NS= not significant.* = significant group comparison. Salako et al .: Blood pressure control and left ventricular hypertrophy
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