Document Detail

Impact of prehypertension on left ventricular mass and QT dispersion in adult black Nigerians.
Jump to Full Text
MedLine Citation:
PMID:  24844553     Owner:  NLM     Status:  In-Data-Review    
BACKGROUND: Prehypertension has been associated with target-organ damage. This study sought to determine the impact of prehypertension (PHT) on QT dispersion and left ventricular hypertrophy (LVH) in adult black Nigerians.
METHODS: One hundred and one subjects with office blood pressure ( BP) < 140/90 mmHg were categorised according to their office BP into normotensive (normal BP < 120/80 mmHg, n = 57) and prehypertensive (prehypertensive BP 120-139/80-89 mmHg, n = 44) groups. Echocardiography and electrocardiography (ECG) were performed on the subjects.
RESULTS: Thirty-four males aged 53.65 ± 16.33 years and 67 females aged 52.42 ± 12.00 years were studied. The mean QT interval dispersion (QTd) of the normotensive (38.96 ± 11.06 ms) and prehypertensive (38.41 ± 11.81 ms) groups were similar (p = 0.81). Prehypertensive subjects had higher left ventricular mass (LVM) (165.75 ± 33.21 vs 144.54 ± 35.55 g, p = 0.024), left ventricular mass index 1 (LVMI-1) (91.65 ± 16.84 vs 80.45 ± 18.65 g/m(2), p = 0.021) and left ventricular mass index 2 (LVMI-2) (54.96 ± 10.84 vs 47.51 ± 12.00 g/m(2.7), p = 0.017). QTd was independent of echocardiographic and electrocardiographic LVH (p > 0.05).
CONCLUSIONS: Compared with normotension, prehypertension is associated with higher LVM but similar QTd. This suggests that structural remodelling precedes electrical remodelling in prehypertension.
O K Ale; J N Ajuluchukwu; D A Ok; A C Mbakwem
Related Documents :
3912053 - Distance running in the 1980s: cardiovascular benefits and risks.
8187123 - Long-term prognosis after a first myocardial infarction in turkey: determinants of mort...
16961673 - Effects on mortality of abciximab in st-elevation myocardial infarction treated with pe...
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Cardiovascular journal of Africa     Volume:  25     ISSN:  1680-0745     ISO Abbreviation:  Cardiovasc J Afr     Publication Date:  2014  
Date Detail:
Created Date:  2014-05-21     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101313864     Medline TA:  Cardiovasc J Afr     Country:  South Africa    
Other Details:
Languages:  eng     Pagination:  78-82     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): Cardiovasc J Afr
Journal ID (iso-abbrev): Cardiovasc J Afr
Journal ID (publisher-id): TBC
ISSN: 1995-1892
ISSN: 1680-0745
Publisher: Clinics Cardive Publishing
Article Information
Download PDF © 2010 Clinics Cardive Publishing
Received Day: 18 Month: 10 Year: 2013
Accepted Day: 20 Month: 2 Year: 2014
Print publication date: Month: 4 Year: 2014
Volume: 25 Issue: 2
First Page: 78 Last Page: 82
PubMed Id: 24844553
ID: 4026767
DOI: 10.5830/CVJA-2014-010

Impact of prehypertension on left ventricular mass and QT dispersion in adult black Nigerians
OK Ale, MD Email: Affiliation: Department of Medicine, College of Medicine, University of Lagos/Lagos University Teaching Hospital, Lagos, Nigeria
JN Ajuluchukwu, MD Affiliation: Department of Medicine, College of Medicine, University of Lagos/Lagos University Teaching Hospital, Lagos, Nigeria
DA Ok, MD Affiliation: Department of Medicine, College of Medicine, University of Lagos/Lagos University Teaching Hospital, Lagos, Nigeria
AC Mbakwem, MD Affiliation: Department of Medicine, College of Medicine, University of Lagos/Lagos University Teaching Hospital, Lagos, Nigeria


The heterogeneity of individuals with blood pressure (BP) < 140/90 mmHg in terms of cardiovascular (CV) risk was reported as early as 1939 by Robinson and Brucer.1 BP in the range of 120–139/80–89 mmHg (labelled then as prehypertension) was observed to be associated with high risk of progression to hypertension (HT) and cardiovascular disease (CVD) later in life when compared with BP < 120/80 mm Hg.1

The term prehypertension was adopted in May 2003 by the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High blood Pressure (JNC-7) to describe BP range of 120–139/80–89 mmHg.2 The resuscitation of this terminology/concept in JNC-7 was a sequel to the documentation of a higher morbidity in individuals with prehypertension in landmark publications.3-5 Prehypertension (PHT) was defined in JNC-7 not only to emphasise the excess risk associated with BP in this range, but also to focus increased clinical and public health attention on prevention.2,6,7

Prevalence rates of PHT among adults in the United States, Ghana and northern Nigeria have been reported to be 31, 40 and 58.7%, respectively.7-9 In most studies, including the ones above, PHT was more prevalent than hypertension.7-9 Though PHT is associated with increased risk of major CV events independently of other CV risk factors,10 most individuals (90%) with PHT have at least one cardiovascular risk factor such as dyslipidaemia, abdominal obesity, hyperinsulinaemia, impaired fasting glucose levels, insulin resistance, a prothrombotic state, tobacco use, endothelial dysfunction, and impaired vascular distensibility.6,7,9,10

QT interval dispersion (QTd) (the difference between the longest and the shortest QT intervals on a surface ECG), when excessive, is associated with increased risk of cardiovascular morbidity and mortality in population studies, and many clinical conditions, including hypertension.11,12 This has been related to ventricular electrical instability, providing the necessary substrate for lethal ventricular arrhythmias.12,13 Greater QTd and left ventricular mass have been demonstrated in hypertensive individuals compared with normal individuals.11,13,14

Considering the well-established, linear relationship between BP and the risk of cardiovascular events, the CV risk associated with PHT is intermediate between normotension and hypertension.2,3 Hence, electrocardiographic and echocardiographic indices of target-organ damage in PHT may also be intermediate between normotension and hypertension. The aims of this study were: (1) to compare the QTd and indices of left ventricular hypertrophy in adult black normal and prehypertensive subjects, and (2) to evaluate the relationship of QTd with electrocardiographic and echocardiographic indices in these subjects.


One hundred and one consecutive, apparently healthy black Nigerian students, staff and retirees of the Lagos University Teaching Hospital and the College of Medicine, University of Lagos, aged between 26 and 86 years were recruited. They fulfilled the following criteria: age ≥ 18 years, no history of heart disease, including hypertension or other conditions known to affect QT interval and QTd (e.g. diabetes mellitus, dysautonomia), normal cardiac physical examination and fasting blood sugar level < 7 mmol/l. None of the subjects was on treatment with drugs known to affect QT interval (e.g. statins, macrolide antibiotics, halofantrine, amiodarone).15

Exclusion criteria were the presence of sustained non-sinus rhythm, intraventricular conduction defects and electrocardiograms in which the end of the T waves could not be reliably determined and/or QT interval from less than eight leads could be analysed.11 Subjects with suboptimal echo windows were also excluded from echocardiographic examination.

Ethical clearance was obtained from the ethics and research committee of the Lagos University Teaching Hospital. The study was conducted to conform to the ethical tenets developed by the World Medical Association, as espoused in the Declaration of Helsinki. All subjects provided informed consent.

All subjects were classified by office BP as either normotensive group: normal BP (< 120/80 mmHg) (n = 57) or prehypertensive group: prehypertensive BP (120–139/80–89 mmHg) (n = 44), according to the JNC-7 recommendations.2

A detailed medical history was obtained, physical examination was performed and anthropometric variables of height and weight were obtained. Trained personnel obtained measures of height and weight using a calibrated stadiometer and a weighing scale. Each subject’s height was measured without shoes, in the standing position, heels together, toes apart at a 45° angle and the head in the Frankfort horizontal plane. Weight was measured with the subject lightly clothed and without shoes. Body mass index (BMI) was calculated according to the formula:16 BMI = body mass (kg)/body height2 (m2). BMI < 25 kg/m2, 25 to < 30 kg/m2, and ≥ 30 kg/m2 were classified as normal, overweight and obese, respectively.16

Resting blood pressure was measured three times for each subject with a standard mercury sphygmomanometer on the right arm in a sitting position following a minimum of five minutes’ rest by a physician. Phases I and V Korotkoff sounds were used to determine systolic and diastolic BP measurements. The mean of the last two measurements was used in the analysis.


All subjects had a resting simultaneous 12-lead electrocardiogram (ECG) using an Esaote P80 Power electrocardiograph machine. At a paper speed of 25 mm/s with the machine control set at standard response, a standard lead II rhythm strip of 13–16 complexes and a minimum of three cardiac cycles per lead were recorded. All electrocardiograms were analysed by a single observer blinded to the clinical data.

QT and the preceding RR intervals were assessed manually with callipers and mean values were determined in three consecutive cycles. QT intervals were measured in all possible leads from the beginning of the QRS complex to the point of T wave offset, i.e. the point of the return of the T wave to the isoelectric line.11 In the presence of the U wave interrupting the T wave, the nadir between the T and U waves was used to define the point of T wave offset.

QT dispersion (QTd) in milliseconds was defined as the difference between the shortest (QTmin) and longest (QTmax) mean QT interval in each electrocardiogram.11 The QT interval was measured from the lead with the longest interval and was corrected for subjects’ heart rate using Bazett’s formula: 17


where QTc is the corrected QT interval, QTo is the observed QT interval in milliseconds, RR is the RR interval in milliseconds. QTc ≤ 440 ms and QTd = 30–60 ms were considered normal.18-20

ECG LVH was determined using the Araoye’s criteria21,22 for LVH in blacks [i.e. (1) SV2 + RV6 > 4.0 mV in males ≥ 30 years, SV2 + RV6 > 5.0 mV in males aged 15–29 years and SV2 + RV6 > 3.5 mV in females; (2) flat or inverted T waves in V5 or V6; (c) R1 amplitude > 1.2 mV. ECG LVH is diagnosed when any of the criteria is positive] and the Sokolow–Lyon voltage criteria.23 Araoye’s criteria has been shown to correlate well with echocardiographic LVH in Nigerians.24


Transthoracic echocardiography was performed on the first 60 consecutive subjects using a Hewlett Packard Sonos 2000 machine. Using the American Society of Echocardiography (ASE) recommendations,25 the following measurements were obtained: left ventricular internal diameter in diastole (LVIDd), left ventricular internal diameter in systole (LVIDs), interventricular septal thickness in diastole (IVSTd) and left ventricular posterior wall thickness in diastole (PWTd).

Left ventricular mass (LVM) was derived using the ASE formula:25

Estimated LVM (g) = 0.80 [1.04 (LVIDd + PWTd + IVSTd)3 – LVIDd)3] + 0.6 g

Left ventricular mass index was determined using two different methods. Left ventricular mass index 1 (LVMI-1) was calculated as the ratio of LVM to body surface area (g/m2).25 Subjects were was considered to have LVH if LVMI-1 was more than 134 g/m2 for men and more than 110 g/m2 for women.26

The second LVMI, i.e. LVMI-2 was derived by indexing LVM to height using the formula:27

LVMI-2 (g/m2.7 = LVM/height2.7.

However only LVMI-1 was used for the determination of the presence or absence of LVH in the subjects.

Statistical analysis

The SPSS 17.0 statistical software was used for data analysis. The data obtained were expressed as means and proportions. Statistical significance of variables was tested using the chi-square and Fisher’s exact test for categorical variables and the Student’s t-test for continuous variables. Analysis of variance was used to assess intra-observer variability of height and weight measures of the first 35 subjects.

The strengths of the relationship between QTd and selected continuous variables were assessed with the Pearson’s correlation coefficient. Variables that demonstrated significant relationship to QT dispersion i.e. LVM, LVMI and LVMI-2 in the prehypertensive group were entered as independent variables into a standard (simultaneous) multiple regression model with QTd as the dependent variable. All tests were two-sided and values were considered statistically significant if p < 0.05.


A total of 101 subjects aged between 26 and 86 years were enrolled into the study. The age of the normotensive (n = 57) and prehypertensive group (n = 44) of subjects ranged from 27–86 and 26–78 years, respectively. The ICC for the intra-observer assessment of the measures of height and weight are 0.97 and 0.96, respectively.

Nineteen (43%) of the prehypertensive subjects had both systolic (SBP) and diastolic blood pressure (DBP) within the prehypertensive range. This subpopulation of the prehypertensives with a mean age of 53.37 ± 10.96 years consisted of four male and 15 female subjects. Their mean QTd of 39.21 ± 13.46 ms was similar to QTd of the rest of the cohort (n > 0.05).

The clinical characteristics of the study group are presented in Table 1. There were no differences in the age, gender and anthropometric measurements of the two groups. The prehypertensive group however had significantly higher BP indices.

The electrocardiographic measures of the two groups are presented in Table 2. The heart rate, QTc, QTc and ECG LVH status of the two groups were similar.

Table 3 shows the echocardiographic measurements of the groups. The prehypertensive group had significantly higher IVSTd, LVM, LVMI-1 and LVMI-2 values.

The relationships of QTd to LVH determined by ECG and echocardiography are presented in Table 4. QTd was independent of LVH status, not only in the whole cohort, but also in the two groups.

QTd correlated significantly with LVM (r = 0.58, p = 0.003), LVMI (r = 0.55, p = 0.006) and LVMI-2 (r = 0.49, p = 0.016) in the prehypertensive subjects. Several other variables were tested in both groups but did not correlate with QTd (p > 0.05): age, weight, height, BMI, SBP, DBP, pulse pressure (PP), heart rate, QTc, LVIDd, LVIDs, IVSTd, LVPWd, RWT and ejection fraction (EF). None of the independent variables (LVM, LVMI and LVMI-2 in the prehypertensive group) in the simultaneous regression model with QTd as the dependent variable made statistically significant contributions to the equation (computed R2 = 34%, adjusted R2 = 24%). The beta-values and the levels of significance were 0.50 and 0.31 for LVM, 0.04 and 0.96 for LVMI and 0.14 and 0.96 for LVMI-2.


PHT is an intermediate stage between normal BP and hypertension. The mechanisms of excess CV risk/end-organ damage associated with PHT are presumed to be the same as that of hypertension. This suggests that CV risk and end-organ damage in PHT, together with their surrogates such as QTd and LVH, are also intermediate.

Increased QTd is a marker of increased myocardial electrical instability, which has been associated with hypertension.11,13,14 This study showed similar QTd values in normal and PHT subjects. This is at variance with the report by Dogru et al.28 of higher QT dispersion in prehypertensives when compared with normotensive individuals.

Racial differences may contribute to this discrepancy. Studies have suggested significant differences in the cardiac structure and function of subjects of African descent compared with non-negroid subjects.29,30 This was further demonstrated in a study by Zhu et al. of white and black PHT subjects,31 which suggested that cardiovascular characteristics of prehypertension appear to be race dependent.

The subjects in our study may have had lower BP values, i.e. closer to normotension than those in the above study, with a consequent blunting of the expected difference in the QTd values of the subjects, with normal BP and PHT. Data have suggested a wide variation in the QTd of normal individuals (BP < 140/90 mmHg), hence it has been difficult to define what constitutes a normal QTd.11 This variation may reduce the ability of QTd to discriminate between prehypertension and normotension, with a consequent similarity observed in the QTd values of prehypertensive and normotensive subjects in this study.

LVH, a compensatory mechanism for ventricular overload, is an independent risk factor for CV morbidity and mortality in normotensive and hypertensive individuals.32,33 The present study showed higher indices of LVH, i.e. IVSTd, LVM and LVMI in the PHT subjects. Manios 34 and Drukteinis et al..35 documented similar findings of higher LVM in prehypertensives than in normotensives, even after adjusting for co-variates. Conversely, Zhu et al.31 reported similar LVM values in normotensive and hypertensive subjects. Differences in study population and the methodology of BP measurement (use of ambulatory or office BP and different protocols) may have accounted for this variation.

The normotensive and prehypertensive groups in the present study were however similar in terms of ECG LVH status. This may be attributed to the low sensitivity of ECG criteria in detecting LVH, therefore limiting their ability to measure milder changes in LVM expected in prehypertension.36,37 The report of Ang and Lang,38 that the sensitivities of ECG LVH criteria are substantially lower when tested in the general population than in a high-risk population, such as hypertensive patients, gives further credence to this view. Both ECG LVH and echocardiographic LVH as prognostic factors for CVD may reflect different pathological processes and thereby influence prognosis in different ways.38

The demonstration of similar QTd in normotensive and prehypertensive subjects, together with a concomitantly higher LVM in PHT seen in our data suggests that left ventricular structural remodelling precedes electrical remodelling in a continuum of cardiovascular changes induced by increasing BP in prehypertension. This probably confers a higher sensitivity to LVM measurement over ECG parameters, such as QTd and LVH measurement in the detection of prehypertensive changes in the myocardium.

The relatively small study population and the recording of the ECG at a speed of 25 mm/s, which is the usual speed of ECG recordings in clinical practice, were limitations in this study. QT interval measurements are more reproducible at faster paper speed recordings.11 Moreover, the cross-sectional design of this study precludes the establishment of a cause–effect relationship between prehypertension and increased LVM. This relationship, including the likelihood of reverse causality between LVM and prehypertension, will be better addressed by a prospective study. However, the findings of this study can serve as a basis for further studies on the effects of prehypertension in adult black Nigerians.


The findings of similar ECG parameters (QTd and ECG LVH) in prehypertensive and normotensive subjects suggest a limitation in the usefulness of ECG for CV risk stratification in prehypertension. Conversely, echocardiography may be a good screening tool for the detection of prehypertensive changes in the heart. However, this may not be feasible in resource-poor countries such as Nigeria.

1. Robinson SC,Brucer M,Range of normal blood pressure: a statistical and clinical study of 11,383 persons.Arch Intern MedYear: 193964409444
2. Chobanian AV,Bakris GL,Black HR,Cushman WC,Green LA,Izzo JL Jr,et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.HypertensionYear: 2003421206125214656957
3. Lewinton S,Clarke R,Qizilbash N,Peto R,Collins R,Age-specific reference of usual blood pressureto vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies.LancetYear: 20023601903191312493255
4. Vasan RS,Larson MG,Leip EP,Kannel WB,Levy D,Assessment of frequency of progression to hypertension in non hypertensive participants in the Framingham Heart Study: a cohort study.LancetYear: 20013581682168611728544
5. Vasan RS,Beiser A,Seshadri S,Larson MG,Kannel WB,D’Agostino RB,et al. Residual lifetime risk for developing hypertension in middleaged women and men: The Framingham Heart Study.J Am Med AssocYear: 2002287810031010
6. Gupta P,Nagarajau SP,Gupta A,Chikkalingaiah KBM,Prehypertension – time to act.Saudi J Kidney Dis TransplYear: 201223222323322382212
7. Agyemang C,Owusu-Dubus E,Prehypertension in the Ashanti region of Ghana, West Africa: an opportunity for early prevention of clinical hypertension.Public HealthYear: 2008122192417825331
8. Wang Y,Wang QJ,The prevalence of prehypertension and hypertension among US adults according to the new joint national committee guidelines: new challenges of the old problem.Arch Intern MedYear: 2004164192126213415505126
9. Isezuo SA,Sabir AA,Ohwovoriole AE,Fasanmade OA,Prevalence, associated factors and relationship between prehypertension and hypertension: a study of two ethnic African populations in Northern Nigeria.J Hum HypertensYear: 20112522423020555358
10. Mainous AG,Everett CJ,Liszka H,King DE,Egan BM,Prehypertension and mortality in a nationally representative cohort.Am J CardiolYear: 200494121496150015589003
11. Sahu P,Lim PO,Rana BS,Struthers AD,QT dispersion in medicine; electrophysiological Holy grail or fool’s gold.Q J MedYear: 200093425431
12. Mangoni AA,Kinirons MT,Swift CG,Jackson SH,Impact of age on QT interval and QT dispersion in healthy subjects: a regression analysis.Age AgeingYear: 20033232633112720621
13. Abdal-Barr MG,Safwat M,Nammas W,Would corrected QT dispersion predict left ventricular hypertrophy in hypertensive patients?Blood PressYear: 201221424925422428608
14. Ale OK,Ajuluchukwu JN,Oke DA,Mbakwem AC,QT Dispersion in Hypertensive Nigerians with and without Left Ventricular Hypertrophy.West Afr J MedYear: 2013321576123613296
15. Bednar MM,Harrigan EP,Anziano RJ,Camm AJ,Ruskin JN,The QT interval.Prog Cardiovasc DisYear: 2001435 Suppl 114511269621
16. Micozzi MS,Albanes D,Jones DY,Chumlea WC,Correlations of body mass indices with weight stature, and body mass composition in men and women in NHANES I and II.Am J Clin NutrYear: 1986447257313788825
17. Bazett HC,An analysis of the time relations of electrocardiograms.HeartYear: 19207353370
18. Mirvis DM,Goldberger AL. Electrocardiography.Bonov RO,Mann DL,Zipes DB,Libby P. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine.9th edn. Elsevier Sanders. Year: 2012126167
19. Djordjevic D,Deljanin Ilic M,Tasic I,Nearly two decades of QTc dispersion in cardiology.Med BiolYear: 20071430107111
20. Malik M,Batcharov VN,Measurement, interpretation, and clinical potential of QT dispersion.J Am Coll CardiolYear: 2000361749176611092641
21. Araoye MA,Left ventricular hypertrophy by electrocardiogram: A code system applicable to Negroes.Nig Postgrad Med JYear: 199639297
22. Araoye MA,Letter to the Editor: LVH by ECG.Nig Postgrad Med JYear: 19994189
23. Sokolow M,Lyon TP,The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limbs leads.Am Heart JYear: 19493716118618107386
24. Dada A,Adebiyi AA,Aje A,Oladapo OO,Falase AO,Comparison of Araoye’s criteria with standard electrocardiographic criteria for diagnosis of left ventricular hypertrophy in Nigerian hypertensives.West Afr J MedYear: 200625317918517191415
25. Sahn DJ,De Maria A,Kisslo J,Weyman A,The Committee on M-mode Standardization of the American Society of Echocardiography: Recommendations regarding quantitation in M-mode echocardiography. Results of a survey of echocardiographic measurementsCirculationYear: 19785810721083709763
26. Levy D,Anderson KM,Savage DD,Kannel WB,Christiansen JC,Castelli WB,Echocardiographically detected left ventricular hypertrophy: Prevalence and Risk Factors. The Framingham Heart Study.Ann Intern MedYear: 198810817132962527
27. De Simone G,Daniels SR,Devereux RB,Meyer RA,Roman MJ,deDivitiis 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 CardiolYear: 199220125112601401629
28. Dogru MT,Guneri M,Tireli E,Sahin O,Celik T,Iyisoy A,QT interval and dispersion differences between normal and prehypertensive patients: effects of autonomic and left ventricular functional changes.Anadolu Kardiyol DergYear: 200991152219196568
29. Mayet J,Shahi M,Foale RA,et al. Racial differences in cardiac structure and function in essential hypertension.Br Med JYear: 1994101110148068083
30. Chapman JN,Mayet J,Chang CL,Foale RA,Thom SA,Poulter NR,Ethnic differences in the identification of left ventricular hypertrophy in the hypertensive patient.Am J HypertensYear: 19991243744210342780
31. Zhu H,Yan W,Ge D,Treiber FA,Harshfield GA,Kapuku G,et al. Cardiovascular characteristics in American youth with prehypertension.Am J HypertensYear: 200720101051105717903687
32. Schmieder RE,End organ damage in hypertension.Dtsch Arztebl IntYear: 20101074986687321191547
33. Brown DW,Giles WH,Croft JB,Left ventricular hypertrophy as a predictor of coronary heart disease mortality and the effect of hypertension.Am Heart JYear: 200014084885611099987
34. 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.StrokeYear: 2009401515151819164793
35. Drukteinis JS,Roman MJ,Fabsitz RR,Lee ET,Best LG,Russell M,et al. Cardiac and systematic hemodynamic characteristics of hypertension and prehypertension in adolescents and young adults – The Strong Heart Study.CirculationYear: 200711522122717210838
36. Bacharova L,Electrocardiography – Left ventricular mass discrepancies in left ventricular hypertrophy: electrocardiography imperfection or beyond perfection.J ElectrocardiolYear: 20094259359619608195
37. Reicheck N,Devereax RB,Left ventricular hypertrophy: relationship of anatomic, echocardiographic and electrocardiographic findings.CirculationYear: 198163139113986452972
38. Ang DSC,Lang CC,The prognostic value of the ECG in hypertension: Where are we now?J Human HypertensYear: 200822746046718432258

[TableWrap ID: T1] Table 1  Clinical characteristics of the study population
Characteristic Total population n = 101 Mean ± 2SD n (%) Normotensive group n = 57 Mean ± 2SD n (%) Prehypertensive group n = 44 Mean ± 2SD n (%) p-value
Age 59.96 ± 13.54 50.74 ± 13.89 55.84 ± 12.65 0.06
Gender 0.94
Male 34 (33.7) 19 (33.3) 15 (34.1)
Female 67 (66.3) 38 (66.7) 29 (65.9)
Weight (kg) 69.10 ± 13.10 68.02 ± 12.32 70.50 ± 14.05 0.20
Height (m) 1.63 ± 0.08 1.63 ± 0.07 1.62 ± 0.10 0.44
BMI (kg/m2) 26.17 ± 4.72 25.61 ± 4.63 26.89 ± 4.78 0.18
BMI class 0.35
Normal 45 (44.6) 29 (50.9) 16 (36.4)
Overweight 35 (35.6) 18 (31.6) 18 (40.9)
Obese 20 (19.8) 10 (17.5) 10 (22.7)
SBP (mmHg) 118.27 ± 19.50 112.39 ± 6.24 125.89 ± 7.34 < 0.001
DBP (mmHg) 73.70 ± 7.43 71.05 ± 6.60 77.14 ± 7.10 < 0.001
MAP (mmHg) 88.56 ± 6.98 84.83 ± 5.61 93.39 ± 5.48 < 0.001
PP (mmHg) 44.56 ± 9.04 41.33 ± 6.86 48.75 ± 9.83 < 0.001

BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; MAP, mean arterial blood pressure; PP, pulse pressure.

[TableWrap ID: T2] Table 2  ECG measurements according to BP group.
Characteristic Total population n = 101 Mean ± 2SD n (%) Normotensive group n = 57 Mean ± 2SD n (%) Prehypertensive group n = 44 Mean ± 2SD n (%) p-value
Heart rate (beats/min) 73.35 ± 10.94 72.11 ± 9.53 74.95 ± 12.47 0.38
QRS (ms) 79.96 ± 3.51 79.54 ± 3.46 80.50 ± 3.53 0.18
QTd (ms) 38.72 ± 11.34 38.96 ± 11.06 38.41 ± 11.81 0.81
QTc (ms) 417.92 ± 23.63 415.58 ± 23.25 420.95 ± 24.04 0.26
Sokolow–Lyon 8 (7.9) 4 (7.0) 4 (9.1) 0.73
Araoye’s code 10 (9.9) 4 (7.0) 6 (13.6) 0.33

QTd, corrected QT interval; QTd, QT dispersion, QRS, QRS duration, LVH, left ventricular hypertrophy.

[TableWrap ID: T3] Table 3  Echocardiographic measurements according to BP groups
Characteristic Total population n = 60 Mean ± 2SD n (%) Normotensive group n = 36 Mean ± 2SD n (%) Prehypertensive group n = 24 Mean ± 2SD n (%) p-value
LVIDd (cm) 4.52 ± 0.44 4.50 ± 0.41 4.55 ± 0.49 0.64
LVIDs (cm) 2.90 ± 0.43 2.93 ± 0.41 2.84 ± 0.46 0.43
IVSTd (cm) 1.05 ± 0.21 1.00 ± 0.20 1.15 ± 0.21 0.01
LVPWd (cm) 0.88 ± 0.14 0.88 ± 0.15 0.91 ± 0.13 0.29
RWT (cm) 0.40 ± 0.09 0.39 ± 0.09 0.41 ± 0.09 0.57
LVM (g) 153.03 ± 35.91 144.54 ± 35.55 165.75 ± 33.21 0.024
LVMI-1(g/m2) 84.93 ± 18.64 80.45 ± 18.65 91.65 ± 16.84 0.021
LVMI-2 (g/m2.7) 50.49 ± 12.02 47.51 ± 12.00 54.96 ± 10.84 0.017
EF (%) 72.72 ± 8.73 71.44 ± 8.57 74.65 ± 8.80 0.17
Echo LVH 2(3.33) 1(1.67) 1(1.67) 1.00

LVM, left ventricular mass; LVMI, left ventricular mass index; LVH, left ventricular hypertrophy; LVIDd, left ventricular internal diameter in diastole; LVIDs, left ventricular internal diameter in systole; IVSTd, interventricular septal thickness in diastole; PWTd, left ventricular posterior wall thickness in diastole.

[TableWrap ID: T4] Table 4  Relationship of QTd to LV H status.
LVH classification LVH status Total population QTd (ms) p-value Normotensive group QTd (ms) p-value Prehypertensive group QTd (ms) p-value
Sokolow–Lyon No LVH 38.77 ± 11.31 0.88 39.11 ± 11.10 0.72 38.33 ± 11.72 0.88
LVH 38.13 ± 12.39 37.00 ± 11.94 39.25 ± 14.57
Araoye No LVH 38.78 ± 10.78 0.88 39.36 ± 10.89 0.33 39.97 ± 10.67 0.54
LVH 38.20 ± 16.44 33.75 ± 13.77 41.17 ± 18.61
LVMI No LVH 39.72 ± 10.24 0.97 40.60 ± 10.70 0.96 38.39 ± 9.58 0.87
LVH 40.00 ± 0.00 40.00 ± 0.00 40.00 ± 0.00

QTd, QT dispersion; LVH, left ventricular hypertrophy; LVMI, left ventricular mass index.

Article Categories:
  • Cardiovascular Topics

Keywords: prehypertension, left ventricular hypertrophy, left ventricular mass, QT dispersion, adult black Nigerian.

Previous Document:  Intra-uterine growth restriction as a risk factor for hypertension in children six to 10 years old.
Next Document:  Optimal utilisation of sulphonylureas in resource-constrained settings.