Cardiovascular Journal of Africa: Vol 31 No 3 (May/June 2020)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 3, May/June 2020 AFRICA 133
Unicel DXC 800 apparatus (Beckman and Coulter, Germany)
(CV% 1.7–3.3%).
The total energy expenditure (TEE) (kcal) in 24 hours was
determined using the Actical® activity monitor (Mini Mitter Co,
Inc, Bend, OR; Montreal, Quebec, Canada).
Statistical analysis
Data were analysed with the TIBCO® StatisticaTM, version 13.3
(Palo Alto, CA, USA). Data are presented as median values
with lower and upper quartiles. Due to the small sample size,
non-parametric statistics were used. The Mann–Whitney U-test
was used to determine significance between the hypertensive
participants with low and high aldosterone levels. Probability
values of p ≤ 0.05 were regarded as significant. Spearman rank
order correlations of aldosterone with the variables were also
determined.
Results
The characteristics of the normotensive and hypertensive black
men with low and high serum aldosterone levels are described
in Table 1. The AA2 ratio, which is currently under evaluation
to be used as a novel marker for primary aldosteronism, was
significantly higher in the hypertensive high-aldosterone group
compared to the hypertensive low-aldosterone group (10.2 vs
3.0; p = 0.003). A lower value of 2.7 for the AA2 ratio was
encountered in the normotensive participants.
The serum potassium (K + ) was significantly lower and the
serum sodium-to-potassium (Na+–K+) ratio significantly higher
in the hypertensive high-aldosterone group compared to the
low-aldosterone group (3.9 vs 4.5, p = 0.016, 34.8 vs 31.8,
p = 0.032 respectively). No differences existed between Ang I,
Ang II, PRA-S and ACE-S in the hypertensive low- and high-
aldosterone groups although levels appeared non-significantly
suppressed in the hypertensive high-aldosterone group (7.6 vs
14.7 pmol/l, p = 0.755; 25.7 vs 44.0 pmol/l, p = 0.277 and 34.9 vs
53.1 pmol/l, p = 0.373, respectively). The medication use is also
shown in Table 1.
In Table 2, potassium in the hypertensive high-aldosterone
men associated negatively and was borderline significant with
aldosterone (Spearman R = –0.496, p = 0.060). The total
peripheral resistance was positively associated with aldosterone
only in the hypertensive low-aldosterone group (Spearman R
= 0.699, p = 0.011). Arterial compliance associated negatively
and was borderline significant (Spearman R = –0.511, p =
0.052), and cortisol associated positively with aldosterone in the
hypertensive high-aldosterone group (Spearman R = 0.500, p =
0.058). Ang I was inversely associated with aldosterone in the
hypertensive low-aldosterone group (Spearman R = –0.606, p =
0.037). Aldosterone, in the hypertensive high-aldosterone group
associated positively and significantly with both Cornell product
(Spearman R = 0.560; p = 0.037) and ACR (Spearman R =
0.589, p = 0.021).
Discussion
The primary aim of this sub-study was to evaluate the role of
aldosterone as contributory factor of hypertension in a black
cohort by making use of the novel AA2 ratio.11 The main
finding of this study was a higher AA2 ratio in the hypertensive
high-aldosterone compared to the hypertensive low-aldosterone
group, suggesting a PA-like condition represented by Ang II,
and independent aldosterone secretion to be a major cause of
hypertension in this subgroup.
The serum K+ concentration was significantly lower in the
hypertensive high-aldosterone group and the serum Na+–K+
ratio was significantly higher compared to the hypertensive
low-aldosterone group. Furthermore, aldosterone was positively
associated with both left ventricular hypertrophy (Cornell
product) and kidney function (ACR) in the hypertensive high-
aldosterone group.
The aldosterone-to-renin ratio (ARR) is the recommended
screening test for PA.15,16 Measurement and interpretation is
challenging when using the ARRbecause several antihypertensive
drugs interfere with the RAAS,15 resulting in an increase in renin
concentration and activity, which subsequently suppresses the
ARR, resulting in false-negative test results. There is a need for
a versatile PA screening assay that does not interfere with anti-
hypertensive treatments and therefore allows a more specific
identification of PA in hypertensive patients on therapy.
Preliminary data have shown that in contrast to the ARR,
the AA2 ratio remains unaffected by angiotensin converting
Table 2. Spearman rank order correlations of aldosterone with
independent variables in hypertensive black men with low (n = 12 )
(≤ 133.2 pmol/l) and high (n = 15) (> 133.2 pmol/l) aldosterone levels
Variables
Hypertensive,
aldosterone
≤ 133.2 pmol/l
Hypertensive,
aldosterone
> 133.2 pmol/l
Spear-
man R p- value
Spear-
man R p-value
BMI (kg/m2 ) 0.007 0.983 –0.014 0.960
Cardiovascular variables
SBP (mmHg) 0.043 0.896 0.337 0.219
DBP (mmHg) 0.380 0.224 0.259 0.350
TPR (mmHg/ml/s) 0.699 0.011 0.400 0.140
Cwk (ml/mmHg) –0.126 0.697 –0.511 0.052
c-pPWV (m/s) –0.074 0.820 0.233 0.546
Biochemical variables
eq Ang I (pmol/l) –0.606 0.037 –0.084 0.767
eq Ang II (pmol/l) –0.510 0.090 0.161 0.566
ACE-S (pmol/l) 0.378 0.226 –0.077 0.785
PRA-S (pmol/l) –0.552 0.063 0.206 0.462
sACTH (pg/ml) –0.207 0.519 0.218 0.435
sCortisol (nmol/l) –0.105 0.746 0.500 0.058
Serum Na+ (mmol/l) 0.287 0.366 –0.204 0.467
Serum K+ (mmol/l) –0.196 0.542 –0.496 0.060
Serum Na+–K+ ratio 0.559 0.059 0.389 0.152
Urinary Na+ (mmol/l) 0.400 0.223 0.390 0.150
Urinary K+ (mmol/l) –0.193 0.549 –0.058 0.839
Urinary Na+–K+ ratio 0.137 0.655 0.478 0.098
End-organ variables
Cornell product (> 244 mV/ms) 0.001 0.999 0.560 0.037
Silent 24-h ST events (n) –0.233 0.491 0.122 0.664
Est creatinine clearance (ml/min) 0.231 0.471 –0.304 0.271
ACR –0.100 0.770 0.589 0.021
BMI: body mass index (kg/m2 ); SBP, DBP: systolic and diastolic blood pressure
(mmHg), respectively; SV: stroke volume (ml); TPR: total peripheral resistance
(mmHg/s/ml); Cwk: Windkessel compliance (ml/mmHg); c-pPWV: carotid-peda-
lis pulse-wave velocity (m/s); Ang I and Ang II: angiotensin I and angiotensin
II (pmol/l); ACE-S: surrogate for angiotensin converting enzyme (AngII/AngI,
pmol/l); PRA-S: surrogate for renin activity (Ang I + Ang II, pmol/l); sACTH:
serum adrenocorticotrophic hormone (pg/ml); ACR: albumin–creatinine ratio;
p-values ≤ 0.05 regarded as significant.