Marlene

E. Rackson,

MD

Renal Artery Dissection:

#{149} Steven

V. Lossef,

MD

Stenosis Increased

#{149} Thomas

A. Sos,

MD

in Patients Prevalence’

with

The authors retrospectively analyzed the prevalence of renal artery stenosis in 63 consecutive patients with aortic dissection who underwent thoracic and abdominal aortography. Ten patients (16%) had renal artery stenosis, five with atherosclerosis and five with fibromuscular lesions. Risk factors for aortic dissection were Marfan disease in nine patients, bicuspid aortic valve in one, and hypertension in 54 (including seven patients with Marfan syndrome). If the patients with Marfan syndrome and the patient with the bicuspid aortic valve are excluded, renal artery stenosis was present in 10 of 53 patients (19%) when the cause of dissection was presumably hypertension. This finding suggests that renovascular hypertension is a greater risk factor for aortic dissection than is essential hypertension. The success of angiotensin converting enzyme inhibitors and percutaneous transluminal renal angioplasty (PTRA) in controlling renovascular hypertension has been proved. In this series, emergent PTRA successfully controlled the hypertension in one patient with a type B dissection, resulting in an excellent clinical outcome. Angiography should be routinely performed on patients with aortic dissections to evaluate for renal artery stenosis.

to 90% of patients (1-5) with aortic dissections have an antecedent history of hypertension. However, to our knowledge, the proportion of patients with aortic dissection whose hypertension is renovascular in origin has not been previously studied. Medical control of hypertension is the cornerstone of therapy in most patients with type B

Index terms: ta, dissection, cular 80.72 tion, 961.72

Aneurysm, aortic, 981.74 #{149} Aor981 .74 #{149} Hypertension, renovas#{149} Renal arteries, stenosis or obstruc-

angiography

Radiology

1990;

177:555-558

S

EVENTY

aortic

dissection

and

is an

important

adjunct to surgery in patients with type A dissection. In hypertension caused by renal artery stenosis, treatment with percutaneous transluminal renal angioplasty (PTRA) and angiotensin-converting enzyme inhibitors differs from conventional control of hypertension. A relationship between renal artery stenosis and aortic dissection could have an impact on the diagnosis and management of this highly lethal disease. We retrospectively analyzed thoracic and abdominal aortograms in patients with aortic dissection to determine the prevalence of renal artery stenosis.

Aortic

and of these, seven underwent CT before aortography. The studies were reviewed by a panel of three vascular radiologists (ie, the authors). The thoracic aortograms were evaluated for the type of dissection by means of the Stanford classification (6) and for the presence of a pathologic condition predisposing to dissection, such as Marfan disease, bicuspid aortic valve, or coarctation of the aorta. According to the Stanford classification (6), type A dissections are those that involve the ascending aorta, regardless of the site of the initiating intimal tear. Type B dissections are those that originate distal to the origin of the left subclavian artery. On the abdominat aortograms, the renal arteries were evaluated

for the

presence

dissection

involving

the

of patency, renal

artery,

nonvisualization due to filling from the false channel, and stenosis and its cause. A greater than 70% reduction in the transluminal diameter of the renal artery was considered a hemodynamically significant stenosis. The hospital records of patients were reviewed for history of hypertension, presenting blood pressure and renal function, treatment, and clinical outcome. RESULTS

MATERIALS

AND

METHODS

Between 1968 and 1988, 91 patients at the New York Hospital had angiograms that were positive for aortic dissection. From 1968 until 1982, when computed tomographic (CT) scanning began to supplant angiography as the primary diagnostic tool, all patients with aortic dissections who were stable enough to undergo angiograms sixty-three

did were of the

so.

Seventy-four

available

for

of 91 review.

In

74 patients, abdominal aortograms were obtained. These 63 patients form the basis of this report. Eighteen of the 63 patients in this study underwent angiography in 1982 or later,

Of 63 patients with aortic dissections, 32 had type A and 31 had type B dissections. Nine patients had Marfan disease and one had a bicuspid aortic valve; all of these patients had type A dissections. No patient was pregnant. No patient had aortic coarctation. Fifty-four of the patients (86%) had an antecedent history of high blood pressure, including seven of the patients with Marfan disease. Excluding the nine patients with Marfan disease and the one patient with bicuspid aortic valve, 47 of 53 (89%) had hypertension. The distribution and character of renal

1 From the Department of Radiology, The New York Hospital-Cornell University Medical College, New York. From the 1989 RSNA scientific assembly. Received December 28, 1989; revision requested February 14. 1990; revision received May 22; accepted May 30. Addre reprint requests to M.E.R., Department of Radiology, Beth Israel Medical Center, 16th St and First Aye, New York, NY 10003. C RSNA, 1990

artery

involvement

in Table 1. Ten of hemodynamically

Abbreviation: minal

renal

patients

PTRA angioplasty.

=

are

shown

had evidence significant renal

percutaneous

translu-

555

artery

stenosis a history

had

(Table 2), and of hypertension.

all

10 Five

clonidine, and hydrochlorothiazide, with normal blood pressure mm Hg). Patient 10.-A 59-year-old

patients had fibromuscular disease (Fig 1), and five had atherosclerotic lesions (Fig 2) of the renal arteries. Eight of the 10 had type B dissections, and two had type A dissections. None of the patients with Marfan syndrome nor the patient with

the

bicuspid

aortic

valve

had

aortic

renal

artery

dissection

stenosis

was

Illustrative

thiazide,

of

in

10 of 53 (19%).

Cases

thiazide. At the time of admission was being treated with propranolol, 40 mg orally daily. Blood pressure

B dissection

distal

to the

to

aortic

the

extending left

he at

from

subclavian

bifurcation.

intensive

care

the

then

a 2-week

period

unit,

patient

the

enzyme resulted

lent

blood

lowing

of the

charged

The

on a regimen

supplemented

556 #{149} Radiology

with

pain. Admission blood pres150/110 mm Hg, and a chest showed a widened mediThe blood urea nitrogen 19 mg/dL (6.8 mmol/L), creatinine level was 1.1 mg/

was inhibiin excelal-

of patient

was

of captopril propranolol,

B aortic

dissection.

dis-

series

of 63 patients,

Table

1

Renal Artery Patients with

we de-

factor

for dissection

than

is

essential hypertension. Hypertension is the most important etiologic factor leading to aortic dissection. In multiple series, the prevalence of hypertension in aortic dissection varies from 70% to 90% (15). The prevalence of hypertension in this series was 86% overall and 89% excluding the patients with Marfan syndrome and bicuspid aortic valve.

However,

the

relationship

of reno-

vascular hypertension to aortic dissection is not known. In this series the prevalence of significant renal artery stenosis that presumably caused

Involvement in 63 Aortic Dissection Renal Artery No.

Finding

Not

seen:

fills

Left

Patients

6 2

8 4

10 4

7 46

12 36

17 52

2

3

3

from

false channel Normal Suboptimal for evaluation

renovascular Furthermore, bicuspid

hypertension was 16%. Marfan syndrome and aortic valve are both wellcauses

of

absence

fore, with

of

Right

Stenosis Dissection

the

scribe an association between preexistent renal artery stenosis and aortic dissection. Although the development of renovascular hypertension after an aortic dissection that compromises the renal artery is a known entity, we postulate that renovascular hypertension may predispose the patient to aortic dissection and be more

of a risk

aortogram. lumen and appearance Left rePatient

-

Right renal artery fills from true demonstrates a “string of beads” characteristic of medial fibroplasia. nal artery fills from false lumen. died in the operating room.

An aor-

DISCUSSION In this

angio-

pressure,

discontinuation

nitroprusside.

ena-

known

in the

experimental

tensin I converting tor, captopnil. This control

and

was admitwith acute and posteri-

tery. The patient’s blood pressure could be controlled only with high doses of intravenous sodium nitroprusside that could not be tapered. Three days after the aortogram was obtained, PTRA of the left renal artery was successfully performed (Fig 2). There was a mild residual stenosis but no pressure gradient after dilation. After the angioplasty the patient was easily weaned off the nitroprusside and given oral medication. Upon discharge, while he was taking labetalol, 400 mg twice a day, his blood pressure was 1 10/80 mm Hg.

renal

medically and required high doses of intravenous sodium nitroprusside (5 ig/kg/min) supplemented by combinations of clonidine, propranolol, hydrochlorothiazide, trimethaphan camsylate, prazosin, and guanethidine. Despite use of multiple oral antihypertensive medications, the intravenous nitroprusside could not be

given

daily,

artery

Both

ac, superior mesentenic, and right common iliac arteries filled from the false lumen. The patient was treated

After

once

togram confirmed this finding and revealed a 70% stenosis of the left renal artery, which filled from the true lumen, and a normal right renal ar-

arteries had beaded appearances characteristic of medial fibromuscular dysplasia. The right renal artery was supplied by the true lumen and the left by the false lumen. The celi-

tapered.

or chest sure was radiograph astinum. level was and the

of a type

admission was 200/ 1 10 mm Hg. An abdominal bruit was present, and the right lower extremity pulses were absent. The blood urea nitrogen level was 14 mg/dL (5.0 mmol/L) and the creatinine level was 0.8 mg/dL (71 imol/L). Aortography demonstrated

a type

25 mg

dL (97 imol/L) and was unchanged during his hospital course. A dynamic CT scan of the chest was suggestive

Patient 3.-A 39-year-old white man with a 20-year history of hypertension was admitted to New York Hospital in December 1978 after 3 days of severe back pain and acute onset of right lower-extremity claudication. His hypertension had previously been refractory to guanethidine, methyldopa, and hydrochioro-

just

man

a 2-year history of hypertension controlled with hydrochloro-

lopnil, 10 mg once daily, ted to New York Hospital onset of tearing anterior

associ-

ated renal artery stenosis. Excluding the nine patients with Marfan syndrome and the patient with the bicuspid aortic valve, the prevalence significant

with poorly

(120/80

aortic

dissection

in

of hypertension.

if we exclude the Marfan syndrome

patient with bicuspid then the prevalence stenosis in hypertensive

There-

nine and

patients the one

aortic valve, of renal artery patients

with dissection would be even greater (ie, 10 of 53, or 19%). This is higher than

the

estimated

ovascular

al population tension, which tion between

and

prevalence

hypertension

aortic

of subjects is 5% (7). renal artery

dissection

has

important consequences nosis and treatment thal disease.

Degeneration

of ren-

in the

gener-

with hyperAn associastenosis

potentially

for the diagof this highly le-

of the

aortic

media

has classically been associated with aortic dissections, although it is found in the normal aging process

well.

Hirst

a factor

aortic

and

Gore

or condition

dissection

(8) suggest

as

that

predisposing

also

needs

to

to be

present, and the most important of these is hypertension. The other most frequent predisposing factors

are

Marfan

syndrome,

which November

is a 1990

Figure There sion;

2. Patient 10. (a) Thoracic aortogram. is a severe stenosis of the proximal left marked improvement in blood pressure

Table 2 Patients with Patient! Age!Sex

Renal

Stenosis

Artery

Dissection Type

l!69!F

There is an renal artery. was noted.

and Aortic

Right Renal Artery

Blood

Artery

aorta. (b) pressure

Abdominal gradient

aortogram. across the

(mm

Pressure Hg)

Blood Nitrogen

Urea (mg/dL)*

Creatinine (mg/dL)t

Treatment

B

N

Ath

200/100

49(17.5)

3.3(292)

Sung

B

Ath

Ath

156/100

32(11.4)

2.0(177)

Med

Paraplegic

3!39!M 4!40!M

B A

FMD Ath

FMD Ath

202/110 90/40

14 (5.0) 47(16.8)

0.8 (71) 2.5(221)

Med Med

Survived Died

170/110

11(3.9)

5!55!F

B

N

FMD

B

FMD

FC

7!56!M

B

FMD

FMD

8!66!F 9!68!M 10,’59,’M

A B B

FMD N N

FC Ath Ath

= atherosclerosis, = surgical. in parentheses

are

in parentheses

are in micromoles

Note.-Ath

palpable,

Surg

Numbers

*

I Numbers

FC

fills

from

in millimoles

per

an

intimal

tear

followed

by

a hematoma that establishes a cleavage plane in the aortic media (2,9). It is the propagation of the dissecting hematoma that is responsible for severe and potentially lethal complications such as penicardial tamponade, myocardial

plegia, emia.

infarction,

stroke,

and visceral The two main

factors

responsible

hematoma and the

para-

and limb ischhemodynamic for

extending

systole

(10),

which

pressure

in the

the

ment

of aortic

dissections

increases

aorta.

Treatinvolves

intensive medical therapy, whether or not the aorta is surgically repaired. In the acute setting, type A dissections

(11,12). treated Volume

are

treated

surgically

if possible

Type B dissections medically at first 177 #{149} Number

2

channel,

liter

of urea.

Med

Survived

0.8 (71)

Sung

Died

120,174

25(8.9)

1.5(133)

Med

Survived

160/80 158/90 150/110

10 (3.6) 18(6.4) 19(6.8)

0.6 (53) 1.1(97) 1.1(97)

Sung Med PTRA

Survived Survived Survived

FMD

fibromuscular

dysplasia,

Med

there is continued pain, uncontrolled hypertension, acute aortic insufficiency, or signs of arterial compromise by extension of the hematoma. If one of these conditions occurs, surgery is indicated. Medical therapy of dissections, both acute and chronic, is directed at the hemodynamic forces responsible for propagating the hematoma, namely, myocardial contractility and systemic blood pressure. This therapy

are systemic hypertension rate of rise of pressure dur-

pulse

NA

13 (4.6)

70!palp

false

Died

medical,

N

normal,

NA

-

not

available,

paip

per liter.

congenital disorder of connective tissue; pregnancy; congenital bicuspid valve; and aortic coanctation. The initiating event in a dissection is usually

le-

Outcome

2,’681M

6!50!F

ing

no

Dissection

Left Renal

intimal tear (arrow) in the descending thoracic (c) After PTRA, there is residual stenosis but

are usually (13) unless

usually

includes

the

propranolol, and sodium side, a potent vasodilator. lol has a negative inotropic that decreases myocardial ity

and

therefore

decreases

beta

blocker

nitroprusPropranoeffect contractilthe

pulsa-

tile force of blood flow in the aorta. Sodium nitroprusside is a smoothmuscle relaxant that rapidly lowers blood pressure and reduces cardiac preload by decreasing venous return. Experience with angiotensin converting enzyme inhibitors in the setting of dissection is limited, but they are

of theoretical value in patients with renal artery compromise. Dissection extending into the renal arteries that compromises renal blood flow has long been suspected of contributing a renovascular component to the hypertension, especially when it is uncontrollable. Preferential dissection involving the left renal artery has been recognized angiographically (14) and was also noted in our series (Table 1). In 1970, Siegelman et al (14) described six patients with blood pressures greater than 210/110 mm Hg and more than 50% occlusion of the left renal artery caused by dissection. Renal vein renm measurements were not obtamed, although a renovascular basis for the hypertension was postulated. Rose et al (15) described one patient with severe hypertension due to extension of the hematoma into the renal artery, with an elevated renin level, who was successfully treated by means of embolization of the reRadiology

#{149} 557

nal artery with gelatin sponge. Noda et al (16) described a patient with uncontrollable hypertension after a type B dissection that caused occlusion of the left renal artery. Peripheral plasma renin activity was elevated, and the blood pressure responded to infusion of saralasin, the angiotensin II antagonist (17). Clearly, directing therapy specifically toward the renovascular component of the hypertension was efficacious in the two cases described in this series. Patient 3, with fibromuscular disease of the renal arteries, could be tapered off intravenous

nitroprusside

days, when his medical successfully

only

captopril regimen. treated

after

14

was added to Patient 10 was by

means

of

PTRA for uncontrollable hypertension in the postdissection period. The underlying mechanism linking renal artery stenosis with aortic dissection is unknown. Prolonged severe hypertension from refractory renovascular hypertension may lead to mechanical injury to the aorta. Direct deleterious vasoactive effects on the wall of large arteries by a hyperreninemic state have been implicated by Brunner et al (18). Dzau and Safar implicated direct effects of angiotensin II on the walls of large arteries as a cause of decreased compliance in hypertension (19). Renal vein renin determinations and peripheral renin levels are not routinely obtained in patients with aortic dissections but would be helpful in demonstrating the renovascular source of hypertension in these patients. Although a renal artery stenosis in a hypertensive patient is suggestive of renovascular hypertension, the two are not necessarily related. If blood pressure cannot be controlled by means of the usual intensive medical therapy, the presence of renovascular hypertension and renal artery compromise should be considered. PTRA and/or the addition of angiotensin converting enzyme inhibitors would then be useful for therapy of the renovascular component of the hypertension. The efficacy of PTRA is well recognized

(20,21). PTRA management gency

abdominal

aortic

surgery

ventional

radiologic

arterial

9.

compromise.

hypertension should be aggressively looked for and treated when present in the setting of aortic dissection. Although aortography remains the standard of reference for diagnosing aortic dissection, the accuracy and ease of CT has reduced the role of aortography (2224). Every patient should undergo abdominal aortography for evaluation of the renal arteries. Aortography should be part of the diagnostic algorithm and need not be performed on an emergency basis. Once the diagnosis of dissection has been established, depending on the patient’s clinical course and treatment priorities, aortography, with PTRA when appropriate, should be performed once the patient has been stabilized or after repair of the ascending aorta. U

Hirst AE, Gore I. The etiology thology of aortic dissection. In:

Med

Prokop

1987;

pa-

Doroghazi

3i7;i060-1068.

EK, Wheat

Hydrodynamic

11.

and

RM, Slater EE, eds. Aortic dissection. New York: McGraw-Hill, 1983; 13-54. DeSanctis RW, Doroghazi RM, Austen WG, Buckley MJ. Aortic dissection. N EnglJ

10.

procedures

should be performed with the utmost caution in the setting of dissection. PTRA should be performed only by experienced practitioners, taking care to avoid catheterizing the false channel or performing any manipulation that might extend the dissection and cause further Renovascular

8.

in a

patient with renal artery stenosis and uncontrollable high blood pressure after a dissection. However, inter-

MW

Jr, Palmer

forces

RF.

in dissecting

aneu-

rysms. Circ Res 1970; 27:121-127. Crawford ES, Svensson LG, Coselli fir HJ, Hess KR. Aortic dissection dissecting aortic aneurysms. Ann

JS, 54and Surg

1988; 208:254-273.

12.

13.

DeBakey ME, Cooley DA, Creech 0 Jr. Surgical considerations of dissecting aneurysms of the aorta. Ann Surg 1955; 142:586-612. Wheat MW Jr. Palmer RF, Bartley TD, Seelman RC. Treatment of dissecting an-

eurysms 14.

15.

16.

of the aorta without

hypertension

aneurysm. 17.

Japan

1972;

Brunner

by

Heart

dissecting

J 1981;

aortic

122:281-

rone, Med

177:1203-1205.

HR.

sential

19.

J

286. Turker RK, Hall MM, Yamamoto M, Sweet CS, Bumpus FM. A new, long-lasting competitive inhibitor of angiotensin. Sdence

18.

surgery.

Thorac Cardiovasc Surg 1965; 50:364-373. Siegelman 55, Sprayregen S, Strasberg Z, Attai LA, Robinson C. Aortic dissection and the left renal artery. Radiology 1970; 95:73-78. Rose EA, McNicholas KW, Bethea MC, Casarella WJ, Bregman D. Renovascular hypertension following surgical repair of dissection aneurysm of the thoracic aorta. Surgery 1978; 83:235-237. Noda Y, Sukiyama K, Omae T. Renin dependent

Laragh

JH,

hypertension:

heart

Baer

renin

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November

1990