CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 2, March/April 2014
AFRICA
81
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
et al
.
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.
Conclusions
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.
References
1.
Robinson SC, Brucer M. Range of normal blood pressure: a statisti-
cal and clinical study of 11,383 persons.
Arch Intern Med
1939;
64
:
409–444.
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.
Hypertension
2003;
42
: 1206–1252.
3.
Lewinton S, Clarke R, Qizilbash N, Peto R, Collins R. Age-specific
reference of usual blood pressure to vascular mortality: a meta-analysis
of individual data for one million adults in 61 prospective studies.
Lancet
2002;
360
: 1903–1913.
Table 4. Relationship of QTd to LVH 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.
