JAM COLL CARDIOL
1983.1(2).533-40
533
Hypertension and Arterial Aneurysm
JOHN A. SPITTELL, Jr., MD, FACC
Rochester, Minnesota
The rather common coexistence of arterial aneurysm
and systemic hypertension may be attributed to their
respective frequency as clinical findings. The development of hypertension secondary to renal ischemia that
can occur as a complication of certain types of aneurysmal disease is well recognized. Less well appreciated
is the evidence to implicate hypertension as a factor in
the pathogenesis of arterial aneurysms, perhaps in their
progressive enlargement, and even in rupture. Furthermore, after resection of an aneurysm, systemic hypertension adversely influences survival, and it is an im-
Attention is most often directed to the cardiac, renal and
cerebrovascular complications of hypertension so that aneurysmal disease has been relatively neglected even though it
is a legitimate consideration in the spectrum of cardiovascular complications of hypertension. Table I, modified from
a study reported by Roberts (I) in 1975, shows that hypertension was present in 60% of patients with aortic aneurysm
and in 80% of patients with aortic dissection, both incidence
rates being several times greater than that for the general
population of similar age and sex. In this presentation we
consider the relation of arterial aneurysm to hypertension.
The role of hypertension in aortic dissection is examined
separately because the pathogenesis of these two types of
arterial lesion is different.
Arterial Aneurysm
Classification. Aneurysms can be classified in several
different ways, but an etiologic classification is useful in
considering their pathogenesis (Table 2). Hypertension might
participate in the development of several of these etiologic
types of aneurysms.
Pathogenesis. Because the most common aneurysm encountered clinically is atherosclerotic in type, atherosclerotic aneurysm should be considered initially even though
From the Division of Internal Medicine and Cardiovascular Diseases,
Mayo Clime, Rochester, Minnesota.
Address for reprints: John A. Spittcll, Jr., MD, Division of Internal
Medicine and Cardiovascular Diseases, Mayo Clime, Rochester, Mmnesota 55901.
© 1983 by the Amencan College of Cardiology
portant contributing factor in the development of false
aneurysms.
A relation between hypertension and aortic dissection
has received more recognition. Just how systemic hypertension contributes to the occurrence of aortic dissection is not clear, but the effective control of hypertension has the potential for decreasing the incidence of
aortic dissection. The curious clinical association of hypertension with the location of the primary tear in the
proximal part of the descending aorta (type III or type
B) has several plausible explanations.
the mechanism by which atherosclerosis causes weakening
of the arterial wall is unclear (2), nor is it clear that hypertension in the absence of other atherogenic factors causes
atherosclerosis (2). The possible mechanisms include I)
altered endothelial permeability and connective tissue metabolism, 2) pressure augmentation of reflected pulse waves,
and 3) intimal injury (3).
The accelerating effect of hypertension on atherogenesis
has been well demonstrated in hyperlipidemic experimental
animals (4),. it has been postulated that the increased intraluminal pressure augments the driving force behind serum
lipids or alters endothelial permeability to serum components. This is particularly noticeable in the triglyceride and
cholesterylester content as shown in a study of the aorta of
dogs on an atherogenic diet made hypertensive by creating
coarctation (Table 3).
Another aspect of the likely etiologic relation of hypertension to atherosclerosis relates to hemodynamic factors.
Because the arterial pulse wave is reflected as it progresses
distally and augments the primary pulse wave, the pressure
is higher in the abdominal aorta and its distal branches than
in the thoracic aorta, a determinant perhaps in the increased
frequency of atherosclerotic lesions in the abdominal aorta
and lower limb arteries (Fig. I) (3). Clinical experience
supports this and abdominal aortic aneurysms are at least
six times as common as thoracic aortic aneurysms. Even
more interesting is the apparent increase in hypertension as
one considers aneurysms in the proximal and distal arterial
tree (Table 4). It seems reasonable to speculate that hypertension would enhance any hemodynamic influence.
0735-1097/83/020533-8$03 00
534
1 AM Cal l CAR DIal
SPIITEl l
1983,1(2) 533-40
Table 1. Frequen cy of S ystemic Hyperten si on in Variou s
C ard iovascular C onditions (the hypertensive di sease s)
Table 2 . Et iologic T ypes of Arterial Aneurysm s
I . Arteriosclerotic
2. Infectious
Syphilitic
Mycotic
3. Traumatic
Penetrating arterial trauma
Blunt arterial trauma
Chronic compression
(post-stenotic dilation)
Deceleration
4. Arteritides
5, Congenital
Arterial wall defects
Hereditary disorders
Marfan's syndrome
Ehler-Danlos syndrome
Percent With
Hypertension*
Condition
Sudden death
Angina pectoris
Acute myocardial infarction
Complications of acute
myocardial Infarction
Aneurysm of aorta
Fusiform, saccular or cylindric
Dissecting
Atherothrombotic obstruction
of abdominal aorta
or of its branches
Cerebrovascular accident (stroke)
Atherothrombotic cerebral
infarction
Intracerebral hemorrhage
Charcot-Bouchard aneury sm
Renal failure
50
50
50
70
60
80
70
50
> 90
> 90
> 90
Rupture. Quite closely related to our concern about the
growth rate of aneury sms is interest in rupture of aneurysms.
The greate st investigative activity in the area of factors
related to rupture of aneurysms deals with intracranial saccular aneurysms. Althou gh there is controversy concerning
the influence of hypertension on their rupture , Ferguson ( 14)
in an excellent revie w of the physical factors concluded that
the likelihood of rupture is proport ional to the stress on the
wall (Fig. 2) . One variable in the law of Laplace is pressure ,
and becau se wall stress is related to the product of the inner
radius and the pressure , it stands to reason that the intraaneur ysmal pressure will be greater than in adjacent arterial
segments of normal caliber. Because wall thickne ss and
aneurysm size enter into the equation, it is not surprising
that some studies have not shown a direct relation between
systemic hypertension and intracranial aneurysm rupture while
other studies have indicated such a relation (15,16).
There are very few data on the relation of hypertension
to aortic or peripheral arterial aneurysm rupture, but a
recentl y completed 30 year study of thoracic aneurysm (17)
has shown that every patient in whom rupture of the aneurysm occurred had long-standing hyperten sion. Clearly, we
need furthe r study on this important point , but until we have
"Blood pressure = systo lic > 140 or diastolic > 90 mm Hg. Limned to persons
less than 66 years of age .
(Modified with permission from Robert s WC [ I] )
A third consideration is the evidence that hypertension
induces intimal changes and myoint imal thickening in the
arteries of experimental animal s ( lO, l l) . Added to these
relation s is the well known loss of elastic tissue and increased collagen with aging , which may both result from
and favor hypertension (12) .
Once fo rmed, an aneurysm tends to gradually enlarge,
a sequence that is not surprising when the law of Laplace
is remembered. Studies of the rate of enlargement of aneurysms (5) are limited. Bernstein et al. (13) followed the
growth rate of abdominal aortic aneury sms in 49 poor risk
patients, utilizing B-mode ultrasound tracings. They found
that small aneurysms grow an average of 0.4 em per year ,
but dramatic increases in size occurred unexpectedly in some
patients ( 13). However, correlation trials and further investigation of the influence of hypertension on the growth
rate of aneurysms are urgentl y needed to clarify this point.
Table
3. A ort ic Arch Lipid Values* (dogs)
C
TG
CE
TNL
Normal Diet
Normal arch
Coarcted arch
3.66 :t 027
5.08 :t 0.32
1.0\ :t 0.09
1.13 :t 0.32
1.17 == 0.39
0.70:t 0 11
6.27 == 0 76
7.20 :t 062
Atherogenic Diet
Normal arch
Coarcted arch
8.20 :t 2.87
11.0 :t 3.48
I 55 :t 0.98
14.04 == 0.79
3.32 :t 1.82
24.57 :t 12.35
13.47 :t 0.99
51.49 :t 18.\ 7
'Values are expressed as mg/g dry weight extrac ted vessel ± standard errors Total neutral lipids (TNl ) are fract ionated into cholesterol (C) . triglyceride s (TG) and
cholesteryles ters (CE)
(Modified with penn ission from Fuchs l e A. Hagen P. l arson RM [4] )
J AM CaLL CARDIaL
1983;1(2):533-40
HYPERTENSION AND ARTERIAL ANEURYSM
(J --
535
PR
2t
= wall stress
P = pressure
(j
R
t
I
=radius
=wall thickness
I
Figure 2. Variables influencing aneurysmal wall stress. (Reprinted from
Ferguson GG [14], with permission.)
Abdominol
Figure 1. Changes in mean and pulse pressures and in blood flow in
different parts of the arterial tree. reI. = relative. (Modified with permission from Folkow B, Neil E. The pressure. In: Circulation. New York,
London, Toronto: Oxford University Press, 1971:57-72.)
such data, aggressive therapy to control any systemic hypertension in the patient with a known aneurysm appears
indicated.
Prognosis. What is the effect of hypertension on the
prognosis for patients whose aneurysm has been repaired,
and is there a potential for benefit by aggressive hypotensive
therapy? Regarding survival after operation, Crawford et
a1. (18) in their excellent follow-up study of 920 patients
operated on for abdominal aortic aneurysm found that hypertension along with heart disease and advanced age accounted for 95% of the deaths that occurred within 30 days
of surgery. They found that in the long term, the effects of
hypertension on survival were almost the same as the effects
of other associated diseases (Fig. 3), including heart disease,
and although the likelihood of an opportunity to improve
the outlook for patients with hypertension appears to exist,
the opportunity is often not well appreciated.
Another aspect of the course of the patient whose aneurysm has been repaired is the effect of blood pressure on
the reconstructed arterial system. The most common com-
plication is of course, graft occlusion, but the second most
common complication is false aneurysm formation. In a
study of their arterial reconstructions, Szilagyi et a1. (19)
found hypertension in 68.3% of patients who developed a
false aneurysm, but in only 21.3% of patients without a
false aneurysm; they regarded hypertension as a principal
etiologic factor in 56 of their 205 patients with a false
aneurysm. In a careful review of the subject, Satiani (20)
concluded that multiple factors, including hypertension, are
probably involved in false aneurysm formation. Despite the
attention given to this subject, and the apparent role of
hypertension, there seems to be less emphasis on the importance of controlling any associated hypertension after
aneurysm resection and arterial repair than these follow-up
studies indicate is needed.
Conclusion. In summary, hypertension is common in
patients with aneurysm (Table 5). It probably plays a role
in aneurysm formation either directly or indirectly, or both.
Whether hypertension accelerates aneurysm growth rates is
not clear and further studies are needed. There is evidence
to suggest that hypertension plays a role in aneurysm rupture. After aneurysm resection, hypertension adversely influences survival and is an important contributing factor in
the development of false aneurysm.
Table 4. Incidence of Hypertension in Reported Series of Aneurysms
Location of
Aneurysm
First
Author, Year
No. of
Cases
Incidence of
Hypertension (%)
Thoracic aorta
Abdominal aorta
Joyce, 1964 (5)
Walker, 1972 (6)
Roberts, ~ 1975 (I)
Brown, 1981 (7)
Hines, 1953 (8)
Wychuhs, 1970 (9)
107
104
47
63
60
50
59
67
Popliteal artery
*Necropsy senes.
422
69
152
J AM CaLL CARDIaL
1983.1(2) 533-40
536
SPITTELL
100
90
80
70
u.J
60
c.:>
«:
>-
z
Figure 3. Effect of hypertension on survival after resection of abdominal aortic aneurysm. F = no disease, P =
hypertensive: S = associated nonhypertensive disease.
(Reprinted with perrmvsion from Crawford ES, et al. [181 )
50
u.J
u
40
'"
u.J
o,
30
20
10
00
10
15
20
25
SURVIVAL TIME IN YEARS
Aortic Dissection
The relation of aortic dissection to hypertension has received considerably more attention, however, than has the
role of arterial aneurysm to hypertension. Burchell (21) was
among the first to call attention to this association in 1955
when he observed that "if Marfan's syndrome and pregnancy are excluded it is proper to teach that aortic dissection
is always associated with hypertension .... " Further, he
observed that the higher the blood pressure the greater the
likelihood of aortic dissection.
Pathogenesis. In the last 25 years, there have been significant developments bearing on the relation of hypertension to aortic dissection. Studies in experimental aortic dissection in turkeys and results of treatment of aortic dissection
in human subjects with agents that both lower blood pressure
and reduce the rate of pressure change (dP/dt max) have
shown that such agents are effective in arresting further
dissection and preventing rupture of acute aortic dissections.
The considerable work in this area has clarified several
issues (22-24).
There has been a reexamination of the etiology of aortic
dissection, formerly thought to be due to cystic medial necrosis, and most investigators now believe that this is not
the underlying cause (25). Rather, it appears that the changes
seen in the media of the aorta result from injury induced
by hemodynamic forces and their subsequent repair (25,26).
Table 5. Hypertension and Aneurysms
I.
2
3.
4.
5.
6.
A common association
A factor in pathogenesis
? effect on growth rate
May predispose to rupture
Shortens survival after resection
Contributes to development of false aneurysms
Exactly how hypertension, which is present in more than
60% of cases, contributes to aortic dissection is not clear.
Roberts (27) believes that hypertension has a direct weakening effect on the aortic media and, although a common
denominator in aortic dissection, it is probably not the sole
cause of aortic dissection. Another possible mechanism is
the adverse effect of hypertension on the vasa vasorum,
which could lead to faulty nutrition of the media (28). It
does appear that a reduction of elevated blood pressure has
the potential to decrease the incidence of aortic dissection.
Extension or rupture. Although the exact cause of aortic dissection is unknown, the relation of pulse wave characteristics to extension of existing dissections and their rupture has been clarified experimentally and supported by clinical
experience. In their studies of a Tygon model of an aorta
and of dog aortas, Prokop et al. (29) found that no disTable 6. Pharmacologic Treatment for Acute Aortic Dissection
Hypertensive Patients
I Trimethaphan intravenously to maintain a systolic
blood pressure in the range of 110 mm Hg (or
lowest level that maintains a un nary output of 25 to
30 ml/h) until oral drugs are controlling blood
pressure
OR
sodium mtroprusside Intravenously can be used In
place of trimethaphan but should be accompanied by
propranolol
2. Propranolol, I mg intravenously every 4 to 6 hours
PLUS
or 20 to 40 mg orally every 6 hours
AND if additional blood pressure control is needed
3. Reserpine, I to 2 mg intramuscularly every 4 to 6
hours or 0 25 mg orally twice daily
AND/OR
4 Guanethidine, 25 mg orally once or twice daily
Normotensive Patients
I. Propranolol, I mg Intramuscularly every 4 to 6
hours or 20 to 40 mg orally every 6 hours
HYPERTENSION AND ARTERIAL ANEURYSM
J AM CaLL CARDIOL
537
1983;1(2):533-40
Table 7. Incidence of Hypertension in Aortic Dissection
Incidence of Hypertension (%)
First Author, Year
No. of
Cases
Actual
Hirst, 1958 (30)
Lindsay, 1967 (31)
Slater, 1976 (32)
Leonard, 1979 (33)
Dalen, 1980 (34)
463
62
124
171
69
63
8\
65
65
61
section occurred with nonpulsatile flow at pressures up to
400 mm Hg, but that pulsatile flow produced rapid dissection
with a maximal systolic pressure of 120 mm Hg. Of interest,
the dissecting dog aorta also either ruptured externally or
reentered the aortic lumen. These investigators concluded
that pulse wave characteristics, and in particular dP/dt max,
are important in the propagation of an existing dissection.
Clinically, most centers currently utilize a drug regimen in
the initial management of the patient with aortic dissection,
with the goal of reducing dP/dt max and at the same time
lowering any hypertension that is present (Table 6).
Hypertension and type III dissections. Closer examination of the blood pressure findings in the several series
Figure 4. Classification of aortic dissection. Type I, primary tear in ascending aorta and dissection involving aortic arch and distal aorta for a
variable distance; type II, dissection involving only ascending aorta; type
III, primary tear in subclavian artery and extending distally for a variable
distance. Others classify aortic dissection into only two types, those involving the ascending aorta (types I and II above) and those originating
in the descending aorta (type III above). (Modified with permission from
DeBakey ME, Henly WS, Cooley DA, et at. Surgical management of
dissectmg aneurysms of the aorta. J Thorac Cardiovasc Surg \965;49: 13048.)
Site of Intimal Tear (%)
Actual and
Presumed
Proximal
Distal
15
9
70
30
65
56
83
55
92
82
77
of cases shown in Table 7 reveals a much greater incidence
of hypertension in the type III (Fig. 4) dissection in which
the intimal tear is in the distal arch, usually just beyond the
origin of the left subclavian artery. This curious clinical
association and clue to type III dissection might be explained
in one of several ways. First, some patients with existing
systemic hypertension may have a propensity related to some
unrecognized hemodynamic stress to develop an intimal tear
just beyond the left subclavian artery, just as the patient
with Marfan's syndrome, classic coarctation or a bicuspid
aortic valve most commonly has a type I dissection involving
the ascending aorta. A second possibility is that proposed
by Fox et al. (35) in their study of the significance of acute
hypertension in traumatic aortic rupture (Table 8). Earlier
workers had proposed aortic luminal constriction by the
hematoma as the basis of the hypertension proximal to the
site of rupture, but such a mechanism would presume hypotension distal to the aortic rupture and such is not the
usual case. More recent work indicates the existence of
sympathetic afferent nerve fibers in the area of the aortic
isthmus, capable of causing a reflex systemic hypertension
in response to a stretching stimulus as occurs when the aortic
media and intima are ruptured. A third possible mechanism
is occlusion of one or both renal arteries by the aortic dissection with resultant hypertension due to renal ischemia.
Regardless of the cause of the hypertension and irrespective of whether surgical management of aortic dissection is undertaken, careful control of any hypertension is an
integral part of good management in both the short and long
term because hypertension clearly worsens the prognosis of
the patient with aortic dissection (40). Ideally, the antihypertensive regimen should include one or more of the drugs
Table 8. Traumatic Rupture of the Aorta and Hypertension
First Author,
Year
No. of
Cases
Incidence of Acute
Hypertension (%)
Kirsch, 1970 (36)
Symbas, 1973 (37)
Fleming, 1974 (38)
Tumey, 1976 (39)
Fox, \979 (35)
12
104
50
31
50
72
43
10
31
7
538
J AM cou, CARDIOl
SPITrELL
1983;1(2):533--40
Figure 5. Retrograde aortogram demonstrating occlusion of the left renal
artery by aortic dissection extending into the abdominal aorta
which also decrease dP/dt max, though the relation of this
pharmacologic action to an improved long-term prognosi s
has not been shown.
Aneurysmal Disease as a Cause of
Renal Hypertension
There is another aspect to the issue of hypertension and
aneurysm, already alluded to-namely, the complication of
renal ischemia secondary to the aneurysmal disease or dissection. Mo st investigators have concluded that saccular
renal artery aneury sm without evidence of renal artery stenosis or lateralizing renal vein renin s probabl y does not
cause hypertension. The frequent relation of renal artery
aneury sm to hypertension seems to be more than coincidental , however, unles s one is willing to explain it on the
basis of preselection of patients for hypertension (4 1). An
occasional patient with renal artery aneury sm may develop
acute accelerated hypertension and, on investigation that
includes aortography, prove to have renal infarction as a
result of thromboembolism from the mural thrombus in the
renal artery aneury sm. This complication , though rare. must
be kept in mind because nephrectomy in such patient s might
result in relief of their hypertension.
As mentioned earlier, aortic dissection can compromise
the circulation to one or both kidne ys and produce severe
and uncontrollable hypertension (Fig. 5). This. of course,
is one of the indications for prompt surgical treatment of
aortic dissection regardless of type.
The third type of renal ischemia that occurs with aneurysmal disease is atheromatous embolization of the renal
arterioles from the mural thrombu s in an abdominal aortic
aneury sm (Fig . 6). Typ ically, patients with this condition
can be recognized by their clinical feature s-that is, livedo
reticularis, blue toes (Fig . 7A), hypertension and renal insufficiency-ali due to arteriolar embolization (Fig. 7B) by
atheromatous debris (42). The renal circulation is involved
even though the aneurysm may be infrarenal becau se of the
anterograde-retrograde flow in the arterial system. The only
effect ive treatment of patients with atheroembolism is resection of the source of emboli, and at times this is hazardous
becau se of the compromised renal function .
Conclusion. Although definitive studies on the subject
are few, collection of data from multiple types of investigation s clearly shows that the intimate relation s of hypertension and aneurysmal disease are mult iple and important.
Many gaps exist , however, in our knowled ge of this association and important opportunities for needed investigation s are numerou s. Both arterial aneurysms and dissection should be thought of in the same context as the card iac,
cerebr al and renal complications of hypertension-perhaps
prevent able and certainly deserving of aggressiv e blood
pressure control.
Figure 6. Arteriosclerotic aneurysm of abdominal aorta contaimng laminated thrombus thick enough to produce a lumen of about normal caliber.
(Reprinted with permission from Spittell JA Jr. Aortic and peripheral
arterial aneurysms. Cardiovasc Clin 1971;3:114-25.)
J AM COLL CARDIOL
1983 .1(2\:533 -40
HYPERTENSION AND ARTERIAL ANEURYSM
Figure7. Atheroembolism from abdominal aort ic aneurysm. A, livedo reticularis
and multiple blue toes . B , cholesterol
embolization (multiple clefts) of arteriole
in biopsy sample of area of livedo reticularis. (Reprinted with permission from
Spinell JA Jr (42).)
.,
. s.-
539
..
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