CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 6, November/December 2020
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AFRICA
this was more effective than ACE inhibitor-plus-thiazide
combination, although potassium needs to be monitored due
to risk of hypokalaemia. However, thiazide-like diuretics may
not be widely available, in which case a thiazide diuretic would
be used.
Importantly, the ISH guidelines stress the importance of
controlling the BP, regardless of what drugs are available for use.
They have provided alternatives to the standard first-line agents.
They have also made it clear that, while it is optimal to use SPC,
free combinations can be used in settings where SPC are limited.
It is optimal to use agents with longer half-lives that require
once-daily dosing. They recommend the use of single agents for
BP control in the setting of frail elderly patients only or in the
setting of stage 1 hypertension, where lifestyle measures have not
improved the BP to target. The long half-life of amlodipine may
make it the drug of choice in this setting, making it the preferred
choice over a diuretic.
If BP is not controlled, the initial combination must have the
dose optimised before adding a diuretic. This is an important
difference to other major guidelines. Beta-blockers are only used
for treatment of hypertension associated with specific cardiac
conditions such as heart failure, ischaemic heart disease and
atrial fibrillation.
The ISH guidelines have stressed the importance of ensuring
good adherence, as have other international guidelines. They
have highlighted means to improve adherence to antihypertensive
therapy, both essential and optimal. It is essential that adherence
to antihypertensive therapy is improved in whatever ways are
available. While it is ideal to be able to monitor adherence,
the methods available may not be feasible and have many
limitations. However, where possible, it is recommended to
monitor adherence using the best tools available/feasible in the
particular setting.
Resistant hypertension
Resistant hypertension should be suspected if office BP is >
140/90 mmHg on treatment with at least three antihypertensives
(in maximal or maximally tolerated doses), including a diuretic.
It is essential to exclude pseudo-resistance (white-coat effect,
non-adherence to treatment, incorrect BP measurements,
errors in antihypertensive therapy) and substance-induced
hypertension, such as non-steroidal anti-inflammatories
(NSAIDs) as contributors. Health behaviours and lifestyle also
need to be optimised.
If truly resistant, low-dose spironolactone is recommended,
especially if K
+
is < 4.5 mmol/l and eGFR is > 45 ml/min. If
this fails, then referral to a specialist or the investigation of
secondary causes is recommended under the optimal approach.
Under the essential approach, addition of other antihypertensive
medication is recommended and a screen for secondary causes
with a history, examination and basic tests, for example, thyroid-
stimulating hormone, electrolytes, creatinine and eGFR, and
dipstick urine.
Ethnic differences
In populations of African descent, hypertension and HMOD
occur at younger ages. There is greater resistance to treatment,
more nocturnal hypertension, and increased risk of kidney
disease, stroke, heart failure and mortality.
20
This may be
related to physiological differences in the renin–angiotensin–
aldosterone system, altered renal sodium handling, CV reactivity
and early vascular aging. These are important considerations
when treating patients from SSA. Studies done in SSA suggest
amiloride is a useful agent in controlling BP in patients with
resistant hypertension,
21
but amiloride is not mentioned in the
ISH guideline.
Hypertensive emergencies/urgencies
Hypertensive emergency is a severely elevated BP associated
with acute HMOD and requires immediate BP lowering,
usually with intravenous therapy. Urgency refers to severely
elevated BP without acute HMOD and can be managed with
oral antihypertensive agents. In SSA these complications of
hypertension are relatively common, but an evidence-based
approach to management is lacking.
The essential requirements are a clinical examination,
evaluation of HMOD, including fundoscopy, and the following
investigations: haemoglobin, platelets, creatinine, sodium,
potassium, lactate dehydrogenase, haptoglobin, urinalysis for
protein, urine sediment and ECG. In SSA, access to ECG
and urinary sediment is limited, and measurement of lactate
dehydrogenase and haptoglobin is unnecessary. A simple dipstick
and creatinine will alert the clinician to kidney damage, which is
the most common complication of a hypertensive emergency.
Hypertensive emergencies require immediate BP lowering to
prevent or limit further HMOD, but unfortunately there is sparse
evidence to guide management, and recommendations are largely
consensus based. The time to lower BP and the magnitude of BP
reduction depends on the clinical context, but in general a 25%
immediate reduction is recommended. Large drops in BP can
precipitate stroke due to loss of cerebral autoregulation.
The ISH guidelines recommend intravenous labetalol and
nicardipine, which are generally safe to use in all hypertensive
emergencies. However, intravenous labetalol has limited
availability in SSA and nicardipine is not listed on the WHO
essential drugs list and in 2010 was only available in Cameroon
and Senegal.
22
Nitroglycerine is an option, however, access to
high-care and intensive-care units is very limited. In the absence
of the above, an oral long-acting CCB
23
or oral labetolol is
probably the safest choice and a loop diuretic is an option in the
setting of pulmonary oedema. All patients should be followed up
and should achieve optimal BP control.
Hypertension and co-morbidities
A detailed analysis of this section is beyond the scope of the
review. In addition to BP control under optimal and essential
recommendations, effective treatment of the other risk factors to
reduce the residual cardiovascular risk is essential. Low-density
lipoprotein (LDL) cholesterol should be reduced according to
risk profile: (1) > 50% and < 1.8 mmol/l in hypertension and
cardiovascular disease (CVD), chronic kidney disease, diabetes
mellitus or no CVD and high risk; (2) > 50% and < 2.6 mmol/l in
high-risk patients; (3) < 3 mmol/l in moderate-risk patients. The
fasting serum glucose levels should be reduced below 7 mmol/l or
glycated haemoglobin (HbA
1c
) below 7%. Serum urate should be
maintained below 0.387 mmol/l, and < 0.357 mmol/l in patients