new AHA blood pressure measurement guidelines
Details:
Tools
to measure hypertension:
--Oscillometric
office devices: relies on non-invasive waveforms detected by these devices,
which reflect mean arterial BP (when oscillations are maximal), and through
software calculates the SBP and DBP; these devices minimize some of the human
error in measuring blood pressure, as found in direct human auscultation. Also,
these devices are more accurate than previous ones in patients with arrhythmias
(eg atrial fibrillation)
--
Automated office blood pressure (AOBP): these are fully automated
oscillometric devices capable of taking multiple readings without an observer
being present (preferably 3 or more readings)
-- elevated AOBP has a graded increased risk for fatal and nonfatal CVD events
in those not taking antihypertensives, from an SBP range of 110-119, until >
160 mmHg, and from DBP from 60-69 until >90 mmHg
-- in adults taking antihypertensives, unattended AOBP in the range of 110-119
mmHg is associated with lower CVD events
--
24 hour ambulatory blood pressure monitors (ABPM):
-- blood pressure phenotypes:
-- white-coat hypertension (clinic-based BP hypertensive but
out-of-office BP not so, in patients not on medications) and white-coat effect
(white-coat hypertension in those on medications): prevalence 15-30%, up to
30-40% in patients on multiple antihypertensives with SBP> 140 or DBP> 90
mmHg in the clinic. Most studies, but not all, have shown that white-coat
hypertension by itself incurs no or minimal excess cardiovascular risk (and in
the studies which did show increased risk, most of that risk was explained by
the presence of other cardiac risk factors). And, secondary analysis of the
Syst-Eur trial found that active treatment of the white-coat effect did not
lower CVD event rates
--
[one article I felt to be pretty compelling for this was in 556 patients with
resistant hypertension as determined in the office (3 antihypertensives at
maximum dose but still hypertensive) followed 4.8 years, and found that ABPM
predicted cardiovasc events, controlling for the office-based BP as well as
traditional risk factors, and that 40% of those with clinic-based “resistant
hypertension” did not even have hypertension on ABPM (see htn
refractory salles arch int med 2008 in dropbox, or Salles
GF. Arch
Intern Med. 2008;168(21):2340-2346 )]
-- repeat ABPM or home-based monitoring should
be considered annually for untreated patients with white-coat hypertension,
since they have a higher rate of transition to sustained hypertension
-- masked hypertension (BP in the clinic was normal,
but hypertensive outside): most definitions include daytime or 24-hour ABPM to
determine, though in Europe they recommend only the 24-hr ABPM. Masked
hypertension can apply to patients not on meds or on them (“masked
effect”). The clinical risk of masked htn is similar to those with
uncontrolled sustained hypertension, both in the in-office and out-of-office settings
--present in 15-30% of the general
adult population with BP <140/90 in the office
--If “nocturnal hypertension” is
included (see below), the Jackson Heart Study found that 50% of black
participants had masked hypertension
--a high proportion of patients whose
office-based BP is within 20/10mmHg have masked hypertension
--masked htn is more common In those
with diabetes, CKD, and OSA
--Nocturnal hypertension (htn
only at night), estimated in >20% of white and 40% of black populations; and
higher in those with diabetes and CKD.
--one report found that evening dosing of BP
meds resulted in decreased nocturnal BP and cardiovascular outcomes (see htn
night meds dec cvd chronobiointl2010 in dropbox, or Hermia RC.
Chronobiology Intl 2010; 27(8): 1629): in this study 2156 hypertensive people
on meds were randomized to ingest all BP meds in am, vs taking at least one at
night. those getting bedtime meds had lower mean sleep-time BP, higher
sleep-time relative BP decline, reduced non-dipping (34% vs 62%) and better
24-hr ABPM control. After 5.6 years, they had 68 vs 187 cardiovascular events (61%
reduction). They also comment that night-time calcium channel blockers
decrease edema (!!)
--Nondipping (<10% decline in
nocturnal BP) and reverse-dipping (sleep BP higher than daytime):
normally night-time BP is lower than daytime, probably
from decreased sympathetic nervous system activity.
Found in 10-30% of white and up to 65% of black populations
--associated with increased risk of cardiovascular
target-organ damage
--Morning BP surge, normal phenomenon in early AM (cortisol
surge): associated with increased risk of stroke and MI. Exaggerated increase
of morning surge on ABPM may be asssociated with more cardiovasc events
--when to consider ABPM: assessing white-coat or
masked htn; monitoring BP med efficacy for these; assessing for nocturnal htn;
evaluation of postural, postprandial, and drug-induced hypotension, and
assessing for autonomic dysfunction. also to confirm prior ABPM findings when
they are borderline (and nondipping BP, isolated nocturnal BP and isolated
daytime hypertension have pretty poor reproducibility)
--Home BP monitoring (HBPM),
instructing the patient to check their blood pressure at home, resting quietly,
with a cuff that has been validated as being accurate [i ask the patient to
bring in the cuff, simulataneously check their cuff with them doing it on
one arm while i check the other; then vice versa]. the poor cousin of ABPM, but almost as good by
several studies [which do not have a consistent methodology. some discard the
first measurement and only look at one a few minutes later]. good for
white-coat and masked hypertension. not useful for the nocturnal variants.
also, not as many studies as ABPM, so not the preferred modality. a variant of
this is pharmacy BPs [but good to advise the patient to sit quietly in the
pharmacy for a few minutes before taking the blood pressure]. HBPM should be
followed with ABPM if any concern about results
-- Targets for blood pressure control, per AHA/ACC 2017
guidelines:
-- clinic-based blood pressure: 130/80
-- ABPM: 24 hour 125/75; daytime 130/80;
nighttime 110/65
--HBPM: 130/80
Commentary
-- blood pressure should still initially be taken in both arms, because persistent
differences in SBP > 10 mmHg are relatively common, potentially related to
coarctation of the aorta or upper extremity arterial obstruction. [and, there
are studies showing that differences of >15mmHg is an indicator or increased
vascular disease risk and death]
--per the new AHA hypertension guidelines, the basic goal for
office-based blood pressure is 130/80 (see http://gmodestmedblogs.blogspot.com/2017/11/new-aha-hypertension-guidelines.html ,
which translates to 46% of the US adult population having hypertension. per
their definitions:
-- normal blood pressure is SBP <120 and DBP
<80 mmHg
-- elevated blood pressure is SBP 120-129 and
DBP <80 mmHg
-- stage I hypertension is SBP 130-139 or DBP
80-89 mmHg
-- stage II hypertension is SBP >140, or DBP
>90 mmHg
--surprisingly, these new guidelines on BP methods come just a
week after a systematic review/meta-analysis of AOBP measurements and basically
come to the same conclusions about AOBP. For review and more commentary on
AOBP, see http://gmodestmedblogs.blogspot.com/2019/02/automated-office-bp-as-good-as-abpm.html .
-- a concern, also raised in this past blog, is the self-evident
inadequacy of AOBP in picking up nocturnal hypertension or those identified as
non-dippers by the 24 hour ABPM, both of which seem to be related to increased
cardiovascular events
-- one baseline issue with all hypertension measurements is that
accuracy depends on standardized techniques and appropriate observer training.
For example, a study in medical students found remarkably poor adherence to the
accepted guidelines for taking routine office-based blood pressure (see http://gmodestmedblogs.blogspot.com/2017/09/the-most-important-hypertension-blog.html )
--
I am a bit leery of the numbers of people from the studies with the different
blood pressure phenotypes. They all seem to be associated quite high
percentages: do 30% of the patients with BP<140/90 really have masked
hypertension, and up to 30% have white coat hypertension, and 30% are nondippers, and….?? A bit hard to believe
--Blood pressure variability: there have been a few studies
looking at blood pressure variability and clinical outcomes (see http://gmodestmedblogs.blogspot.com/2016/09/blood-pressure-variability-increases.html for
a pretty recent meta-analysis. And, amlodipine is probably the best med to
decrease BP variability (see htn bp variability amlodipine htn2017 in dropbox, or DOI: 10.1161/HYPERTENSIONAHA.117.10087). An
older Lancet study found that decreasing blood pressure variation in a patient
led to decreased stroke, noting that strokes happen early in the morning, and
that most other antihypertensives do not have good 24-hour blood pressure
control; and calcium-channel blockers (most used being amlodipine) had much
less blood pressure variability than other classes of BP meds (see htn
variability and stroke lancet 2010 in dropbox, or Webb AJS. Lancet
2010; 375: 906).
-- evening
dosing of meds: there are several reports of increased stroke in the studies of patients on
ACE-I, which does have a short half-life and increasing early AM BPs, suggesting that evening dosing may be
better
--a major concern here with blood pressure
variability as determined by differences in blood pressure in an individual
over time is that HCTZ does lead to good day-time blood pressures, as we find
in the office, but has the worst BP variability during over a 24-hour period (ie, the ABPM is much higher for HCTZ than for any other drugs,
though the office-based BP is about the same as for other antihypertensives, including calcium-channel blockers). Though HCTZ is the
most commonly prescribed antihypertensive.... see http://gmodestmedblogs.blogspot.com/2016/04/chlorthalidone-is-better-than-hctz-for.html for
details, including the advantage of chlorthalidone vs HCTZ (there has
been concern that there is more hypokalemia with chlorthalidone, though on a
mg-per-mg dose it is about the same. one issue is that in the US chlorthalidone
is only available as a 25 mg pill. when i sent around this blog, a physician
responded that he was able to cut the pill in quarters and did just fine with
1/4 pill per day...)
so, a few points of interest:
--these recommendations continue the 8 year transition (begun in
the UK in 2011) to use non-office based BP measurements as primary, especially
ABPM and HBPM, but now extended to the newer AOBP devices (ABPM continuing to
be the goldish standard, though as noted above, for certain findings their
results are not so reproducible)
--it is still not so transparent as to who should get ABPM. it is
clear from several studies that about 30% of patients with stage 1 hypertension
(perhaps more with new BP guidelines) do NOT have hypertension on ABPM, and may
be subjected to medicalization and meds, both with their potential adverse
consequences. so, perhaps those with BP in that gray area are good candidates
for ABPM or AOBP. the whole issue of masked htn is really unclear (to me). they
comment that those within 20/10 from goal (ie, 110/70) have the highest
likelihood. but that's really huge numbers of people. i think a better
algorithm is for people with near-goal hypertension to check a home-based BP
with a validated machine
--i really support using amlodipine as first-line drug, since it
is pretty well tolerated (and perhaps edema is less with evening dosing), and
it decreases blood pressure variability the most. HCTZ should not really
be used as a single agent (one gets reassuring blood pressures in the office,
but the 24-hour ABPMs are abysmal, as noted above). if using ACE
inhibitors, giving them at night is an intriguing possibility, though
medication adherence at night is harder for some people.
--a blog from a few years ago reviewed a couple of enlightening studies: one showing the people with higher night-time BP had
increased risk of diabetes; the other that night-time BP meds led to lower risk
of diabetes (see http://gmodestmedblogs.blogspot.com/2015/09/take-blood-pressure-meds-at-night-to.html )
--as per the blog last week, AOBP may be a much easier way to get
a pretty accurate BP (see http://gmodestmedblogs.blogspot.com/2019/02/automated-office-bp-as-good-as-abpm.html ).
it can be done in little time in the clinic (especially if the clinician has 2
rooms: sees a patient in one room; and a medical assistant puts the next
patient in the other room, dims the lights, perhaps have some calming music,
puts the AOBP machine on the patient, leaves the room. And when the
clinician goes to see that patient, they get a much
more accurate BP reading on which to make major therapeutic decisions
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