VOLUME 9 NUMBER 3 • SEPTEMBER 2012
105
SA JOURNAL OF DIABETES & VASCULAR DISEASE
REVIEW
risk of experiencing events was increased in diabetes (HR: 1.29,
95%
CI: 1.05–1.58) and in patients with underlying co-morbidities
such as coronary artery disease, peripheral vascular disease and renal
dysfunction.
The reader also needs to be cognisant of the important limitations of
reported BPs in clinical trials, as outlined by Fischer
et al.
In a systematic
review of 1 372 trial reports, there was inconsistency in reporting BP
and no study has reported target control in individuals.
9
In addition,
the limitations of office BP must be clearly stated. The closer the BP is
to target, the greater the uncertainty of the ‘actual’ mean BP, taking
into account the natural variability of BP, white coating and masking.
White coating is increasingly exaggerated in older people.
All practitioners, in assessing BP control in diabetics, older indivi-
duals and other high-risk patients should make use of ambulatory
and home BP monitoring in addition to office measurements to
avoid the pitfalls of both over- and under-treatment of high-risk
patients. For example, if an office BP is recorded at 170/100 mmHg,
and the white-coat or masking effect is 20/10 mmHg, in both
instances the patient requires intensification of treatment as the
‘
actual’ mean BP for the white coater would be 150/90 mmHg and
for the masker 190/110 mmHg. However if the office BP is recorded
at 140/90 mmHg and the white-coat or masking effect is 20/10
mmHg, there is considerable uncertainty. The ‘actual’ mean BP
would be 120/80 mmHg for the white coater and 160/100 mmHg
for the masker, resulting in completely different clinical decisions
regarding the hypertensive management. It is estimated that
up to 30% of hypertensives will display white-coat or masking
effects.
However, there is a pattern emerging from these studies where
stroke shows no J point at current target BP levels but there is a
nadir for coronary artery disease and CV death, particularly at a
systolic BP of 130 mmHg and diastolic BP of 67 mmHg. This is
especially so in high-risk, elderly subjects, which includes diabetics.
In the author’s opinion, based on current data, the systolic target
should be 130 mmHg (but not below) to balance the competing
risks of stroke reduction and increased CV events. In addition, a low
diastolic BP < 70 mmHg should be avoided. Greater use of ABPM
and home monitoring is advocated to assist in the assessment.
Definition of hypertension
The SEMDSA guidelines use the definition of hypertension if BP
remains > 140/80 mmHg instead of the traditional definition >
140/90
mmHg. This is a small detail but there should be consistency
of definition.
Choice of antihypertensive therapy and initiation
of treatment
There are two areas of disagreement here. With regard to the
choice of initial diuretic with normal renal function, the SEMDSA
guideline recommends a thiazide while SAHS recommends either
a thiazide or indapamide. Low-dose hydrochlorothiazide is a weak
antihypertensive in monotherapy and has no outcome data at this
dose.
10
Indapamide on the other hand has been clearly shown in the
HYVET study to reduce events as first-line therapy.
11
In the author’s
opinion, if monotherapy with a diuretic is selected then it should
be indapamide. However, in combination therapy, these differences
are much less important.
The second important point is that the SAHS guideline
recommends combination therapy
de novo
if the BP is > 20/10
mmHg above goal. This recommendation is based on two important
points. Firstly the average response to any antihypertensive agent is
about 10/5 mmHg and 20/10 mmHg for two drugs in combination
treatment. Secondly sequential monotherapy has been shown
to delay control of BP, but even when combination therapy is
instituted, there is ‘failure to catch up’ with patients given initial
combination therapy.
12
Hypertension treatment algorithm
The hypertension algorithm of the SEMDSA and SAHS guidelines
are broadly in agreement, but SEMDSA’s is overly complicated.
The SEMDSA guideline makes an important distinction regarding
calcium channel blockers (CCBs). Non-dihydropyridine (DHP) CCBs
are advocated in combination with ACE inhibitors in the presence
of albuminuria, whereas for patients without albuminuria, a DHP
CCB is advocated. In contrast the SAHS guideline recommends
CCBs as part on mono- or combination therapy without reference
to the non-DHP or DHP subclass.
The recommendation for using non-DHP CCBs for proteinuria
is based on small studies done by Bakris
et al.
13
In the much larger
Benedict study, verapamil was not shown to prevent new-onset
microalbuminuria or the progression of microalbuminuria in patients
with type 2 diabetes, whereas the ACE inhibitor trandolopril was
clearly effective.
14,15
In general, BP control in addition to ACE
inhibitors is the most effective strategy to reduce proteinuria and,
in the author’s opinion, the antihypertensive should be selected on
the basis of tolerability and ability to control BP.
Conclusions
Both the SEMDSA and SAHS guidelines provide important guidance
for treatment of hypertension in diabetes. In their broad perspective
they are very similar and perhaps we should not be distracted by the
small differences. After all, if we achieved a target BP of < 140/90
mmHg in the majority our patients with diabetes and hypertension,
this would be a giant step forward. Perhaps in the future, the two
guidelines could be harmonised to avoid these small differences.
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