THE ROLE OF HYPERTENSION

Edward DO. Freis, M.D.

T HAS BEEN STATED, on good authority,

for many years, that hypertension is
a symptom only, an insignificant mani-
festation of an underlying vascular dis-
ease which proceeds inexorably regard-
less of the level of blood pressure.
Therefore, reduction of blood pressure,
according to these authorities, is not a
rational procedure because the vascular
damage proceeds nevertheless. Such a
nihilistic attitude was quite permissible
20 years ago when there were no effec-
tive methods for reducing and control-
ling hypertension. The whole question
was academic anyway, and if physicians
could be dissuaded from giving worth-
less and presumably dangerous medica-
tions, so much the better.

Today, however, the situation is con-
siderably different. We now have anti-
hypertensive agents, or combinations. of

these, which are able to reduce and
maintain the blood pressure often into
the normotensive range. For example,
in a large-scale cooperative study on
antihypertensive drugs in the Veterans
Administration, the results, as yet un-
published, indicate that a nontoxic com-
bination of available drugs has reduced
the average diastolic blood pressure of
a large group of mild and moderate
hypertensive patients to below 90 milli-
meters Hg-—~that is, into the normal
range.

This was accomplished without sig-
nificant discomfort to the patient and
by simple rule of thumb methods of
dosage and administration. The study,
rigidly controlled by double blind
placebo technics, leaves no doubt that
methods for controlling the blood pres-
sure at least in the less severe cases, have

MARCH, 1960.

assume a new importance,

come of age and are available to any
physician who cares to use them... This
advance makes the question of the sig-
nificance of the high blood pressure itself
We must
seriously seek an answer now as to
whether the presence of a high pressure
in the arterial tree is of itself harmful
or of no consequence. I have tried to
find factual evidence for the opinion
that the level of blood pressure is of no
consequence. [| could find very little.

Usually the opinion was expressed
without any factual data to support it,
or else it was based on a small personal
experience of one physician or one small
clinic. In the latter, no attempt was
made to differentiate between casual and
basal blood pressure; and we now know
that a fair number of hypertensive pa-
tients may be quite labile, exhibiting
much higher blood pressures when the
doctor records them in his office or in
the clinic than at other times. Failure
to differentiate these labile patients from
the less labile leads to hopeless confu-
sion when one attempts to correlate blood
pressure and longevity, particularly if
the series is small.

The life insurance companies some
years ago compiled their data on the
relationship between the level of blood
pressure at the time of the initial insur-
ance examination and subsequent life
expectancy. This was a cooperative study
involving 20 of the largest insurance
companies of North America, and it in-
cluded hundreds of thousands of indi-
viduals.

The results of that study show that
in regard to systolic blood pressure there
is a smooth curve correlation between

W
the level of systolic blood pressure and
the subsequent life expectancy—which,
incidentally, pays no attention to the so-
called borderline or normality of 140
millimeters of mercury.

With regard to diastolic pressure there
also is such a relationship, which pro-
ceeds down to about 88 millimeters of
mercury. Thereafter the data suggest
that patients below that level have a
different condition and have a much bet-
ter life expectancy.

Since hypertension is a slowly pro-
gressing disease in most individuals, it
is not yet possible to say with finality
that reduction of blood pressure with
antihypertensive agents prolongs life. It
will be five, ten, or even more years be-
fore that evidence is in. The previous
speaker said we have plenty of time, but
T do not think we have so much time.

There is one form of hypertension
where the rate of progression is so rapid
that even short-term studies under five
years can disclose significant differences.

That condition is malignant hyperten-
sion. In an untreated series of 146 pa-
tients the survival at the end of one
year was 20 per cent and at the end of
three years was 9 per cent. In our own
series of 64 cases of treated hyperten-
sion, there was a 65 per cent survival at
the end of one year and about 48 per
cent at the end of three years. The ex-
perience of other investigators, both in
this country and in Great Britain, has
been similar; namely, that reduction of
blood pressure has prolonged life sig-
nificantly even in this most severe type
of hypertension where vascular damage
is already far advanced.

Let us turn now to a consideration
of the relationship between hypertension
and atherosclerosis. The high incidence
of strokes due to cerebral atherosclerosis
and thrombosis and hemorrhage is so
common in hypertensive patients that it
needs no further documentation. It is
less well appreciated that coronary
atherosclerosis and myocardial infarction

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are more prevalent in the hypertensive
than in the normotensive population. In
one study of over one thousand cases
of myocardial infarction it was found
that the incidence of coronary occlusion
was five times more common in hyper-
tensive than in normotensive men, and
twenty times more common in hyperten-
sive as contrasted to normotensive
women. In the carefully evaluated data
from the Framingham study, hyperten-
sion was found to correlate significantly
with the incidence of coronary artery
disease.

Obviously some factors are operative
in the hypertensive patient which tend
to accelerate and promote the develop-
ment of atherosclerosis. Hypertension
may not cause atherosclerosis but it
provides a fertile soil for the develop-
ment of atherosclerosis. This factor, ac-
celerating atherosclerosis, could be the
elevation of blood pressure per se, or
some other unknown and mysterious fac-
tor which operates entirely independently
of the blood pressure.

Evidence on this question can be de-
duced from some interesting experiments
of nature. There are certain types of
congenital heart disease such as patent
ductus arteriosus with right to left shunt,
or large interventricular septal defects
where the pulmonary arterial pressure
more than quadruples its normal value.

’ Occasionally these patients survive to

early adult life; and when they do they
are commonly found at autopsy to have
extensive atherosclerosis not of the sys-
temic arteries, but of the pulmonary
arterial tree.

Now, if the hypertension itself is of
no consequence, 1s it not strange that
when hypertension exists in the systemic
circulation atherosclerosis is accelerated
there and spares the pulmonary vessels?
But when hypertension is limited to the
pulmonary circulation, atherosclerosis
develops in the pulmonary arteries but
spares the systemic vessels. It seems that
one can fit the facts much better by

VOL. 50, NO. 3, A.J.P.H.
postulating that it is the elevated blood
pressure per se which accelerates the
formation of atherosclerotic plaques.

Another critical experiment of nature
is exemplified in the hypertension pro-
duced by coarctation of the aorta. Here,
because of the constriction in the de-
scending thoracic aorta, hypertension is
present in the upper half of the body,
but below the constriction the blood pres-
sure is usually normal. Thus, if it is
the elevation of blood pressure which
accelerates atherosclerosis, one would ex-
pect to find more plaque formation
above the coarctation in the region of
elevated blood pressure than below it in
the region of normal blood pressure.
And indeed there is evidence to sub-
stantiate this expectation.

Time does not permit me to go into
the large and growing body of evidence
which suggests that high blood pressure
is bad for all arterial blood vessels, not
only in facilitating the development of
atherosclerosis, but also of arterioloscle-

HYPERTENSION

rosis and necrosis. The evidence also is
good that hypertension imposes a heavy
load on the heart leading first to hyper-
trophy and then to dilation and failure.

If this indeed be true, that it is the
elevation of blood pressure which is the
major cause of the cardiovascular dam-
age in hypertension (and my reading of
the available evidence indicates more
strongly that it is than that it is not),
and since reduction of blood pressure
can now be readily achieved in most
patients, then the problem of blood pres-
sure control has become an important
issue in preventive medicine. No anti-
hypertensive drug can dissolve a fibrous
and calcified atherosclerotic plaque once
it has been formed. The principal value
of such drugs is prophylactic.

For this reason it might be well for
those interested in public health and
preventive medicine to consider seriously
the problem of early hypertension, par-
ticularly in young and middle-aged
adults.

Dr. Freis is senior medical investigator, Mt. Alto Veterans Administration

Hospital; Washington, D. C.

MARCH, 1960

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