the role of medical treatment of distal type aortic dissection

10
Internatronal Journal of Cardtologv, 32 (1991) 231-240 0 1991 Elsevier Science Publishers B.V. 0167-5273/91/$03.50 ADONIS 016752739100176U 231 CARD10 01270 The role of medical treatment of distal type aortic dissection * Kazuhiro Hara I, Tetsu Yamaguchi ‘, Yasuhiko Wanibuchi 2 and Kiyoshi Kurokawa First Department of Internal Medicine, Faculty of Medicine, The Uniuersrty of Tokyo; ’ Center for Cardiovascular Disease, Mitsui Memorrol Hospital. Tokyo. Japan (Received 11 September 1990; accepted 18 January 1991) Hara K, Yamaguchi T, Wanibuchi Y, Kurokawa K. The role of medical treatment of distal type aortic dissection. Int J Cardiol 1991;32:231-240. We analyzed the short-term and long-term outcome of 42 patients with distal type aortic dissection. Twenty-eight patients underwent intensive medical therapy within two weeks after the onset of pain (acute dissection). The remaining 14 patients had chronic dissection. The goals of medical treatment were to control blood pressure and to attain a negative C-reactive protein test result. Hospital survival rate in the patients with acute dissection was %% (27/28). In-hospital complications included changes in mental status, renal dysfunction, bradycardia, orthostatic hypotension, and liver dysfunction, all of which were managed medically. Three of these patients underwent surgical therapy in the chronic phase and were discharged uneventfully. Fifteen (62.5%) of the 24 medically treated patients were discharged with negative C-reactive protein tests. Spontaneous resolution of a dissection was demonstrated by radiological examinations in 8 cases. Five-year survival rates in 24 medically treated patients was 93%. Hospital survival rate in the patients with chronic dissection was 100% (14/14). The rigorous control of blood pressure in the acute phase, and subsequent meticulous evaluation of the dissection by radiological tests and C-reactive protein test provides acceptable short-term and long-term outcomes of patients with acute distal dissection without the need for emergency surgical intervention. Key words: Survival; Event-free survival; Complications: C-reactive protein Introduction Aortic dissection is an uncommon, yet lethal disease. In a collected series of 963 untreated patients. only 8 percent were alive at one year [l]. Correspondence to: K. Hara M.D., Toronto General Hospital, 12 EN-234, 200 Elizabeth Street, Toronto, Ontario. M5G 2C4 Canada. * This research was presented in part at the 52nd meeting of the Japanese Circulation Society. The prognosis of patients with acute distal dissec- tion has improved markedly with advances in medical therapy [2]. Reported in-hospital mortali- ties of medically treated patients have ranged from 10 to 20% [3-111, whereas, until recently, the operative mortalities of such patients have ranged between 25 and 75% [12-171. In recent years, surgical and cardiopulmonary bypass techniques have been improved and more aggressive surgical approaches to the management of acute distal dissection have developed. Oper- ative mortalities for acute distal dissection may be

Upload: kazuhiro-hara

Post on 21-Nov-2016

212 views

Category:

Documents


0 download

TRANSCRIPT

Internatronal Journal of Cardtologv, 32 (1991) 231-240 0 1991 Elsevier Science Publishers B.V. 0167-5273/91/$03.50

ADONIS 016752739100176U

231

CARD10 01270

The role of medical treatment of distal type aortic dissection *

Kazuhiro Hara I, Tetsu Yamaguchi ‘, Yasuhiko Wanibuchi 2 and Kiyoshi Kurokawa ’

’ First Department of Internal Medicine, Faculty of Medicine, The Uniuersrty of Tokyo; ’ Center for Cardiovascular Disease,

Mitsui Memorrol Hospital. Tokyo. Japan

(Received 11 September 1990; accepted 18 January 1991)

Hara K, Yamaguchi T, Wanibuchi Y, Kurokawa K. The role of medical treatment of distal type aortic dissection. Int J Cardiol 1991;32:231-240.

We analyzed the short-term and long-term outcome of 42 patients with distal type aortic dissection. Twenty-eight patients underwent intensive medical therapy within two weeks after the onset of pain (acute dissection). The remaining 14 patients had chronic dissection. The goals of medical treatment were to control blood pressure and to attain a negative C-reactive protein test result.

Hospital survival rate in the patients with acute dissection was %% (27/28). In-hospital complications included changes in mental status, renal dysfunction, bradycardia, orthostatic hypotension, and liver dysfunction, all of which were managed medically. Three of these patients underwent surgical therapy in the chronic phase and were discharged uneventfully. Fifteen (62.5%) of the 24 medically treated patients were discharged with negative C-reactive protein tests. Spontaneous resolution of a dissection was demonstrated by radiological examinations in 8 cases. Five-year survival rates in 24 medically treated patients was 93%. Hospital survival rate in the patients with chronic dissection was 100% (14/14).

The rigorous control of blood pressure in the acute phase, and subsequent meticulous evaluation of the dissection by radiological tests and C-reactive protein test provides acceptable short-term and long-term outcomes of patients with acute distal dissection without the need for emergency surgical intervention.

Key words: Survival; Event-free survival; Complications: C-reactive protein

Introduction

Aortic dissection is an uncommon, yet lethal disease. In a collected series of 963 untreated

patients. only 8 percent were alive at one year [l].

Correspondence to: K. Hara M.D., Toronto General Hospital, 12 EN-234, 200 Elizabeth Street, Toronto, Ontario.

M5G 2C4 Canada. * This research was presented in part at the 52nd meeting of the Japanese Circulation Society.

The prognosis of patients with acute distal dissec- tion has improved markedly with advances in medical therapy [2]. Reported in-hospital mortali- ties of medically treated patients have ranged from

10 to 20% [3-111, whereas, until recently, the operative mortalities of such patients have ranged between 25 and 75% [12-171.

In recent years, surgical and cardiopulmonary bypass techniques have been improved and more aggressive surgical approaches to the management of acute distal dissection have developed. Oper- ative mortalities for acute distal dissection may be

232

as low as 13-20% and long-term life expectancy for patients discharged after surgical intervention

has been reported as identical to that for a general population matched for age and sex [18-201. It

has, therefore, been proposed that emergency

surgical intervention is the optimal treatment for acute distal dissection.

Is emergency surgical intervention in the acute

phase of distal dissection obligatory? Medical

therapy has been the treatment of choice for pa- tients with this disease admitted to Mitsui Memo-

rial Hospital for these 12 years. We have retro-

spectively analyzed the short-term and long-term results of this approach.

Because no definite medical guidelines except for “blood pressure control” have been reported, a secondary purpose of this review was to develop potential guidelines. which were based on our

experiences to date, for the optimum early and long-term medical treatment of these patients. Be-

cause C-reactive protein is an acute phase protein

which appears only during reactions of tissue in- jury or inflammation [21], we used C-reactive pro-

tein testing as a serological maker of the activity

of acute distal dissection.

Methods

Patients

The case records of forty-two patients (34 or 81% men) with a diagnosis of distal type aortic dissection were reviewed. These comprised all pa- tients admitted to our hospital with this diagnosis between 1976 and 1987. Their ages ranged from 31 to 81 years with a mean age of 58.8 years.

Any dissection involving the ascending aorta was classified as proximal dissection and all other

thoracic dissections were classified as distal dissec- tion [3]. Patients with proximal dissection were excluded from this study. The dissection was con- sidered to be “acute” if time from clinical onset of the dissection to admission to our hospital was less than two weeks and “chronic” if this interval exceeded two weeks [ 181.

Twenty-eight patients (67%) had acute dissec- tion and the remaining 14 had chronic dissection. The time from clinical onset to admission to our

TABLE 1

Chnical characteristics.

Acute Chronic Total (%)

dissection dissection

N

Mean age

Male/female

Referred from

other hospitals

History

hypertension

CVA

OM1

Angina pectoris

CHF

Past AAA

operation

Diabetes mellitus

Gout

28 14 42

51 60 59

24/4 10/4 34/8

19 10 29 (69)

19

1 -. L

0

0

2

1

12 31 (74)

1 l( 2) 2 3( 7) 1 3( 7)

1 I( 2)

1 1( 2) 1 3( 7) 4 5 (12)

C‘VA = cerebrovascular accident; OM1 = old myocardial in-

farction; CHF congestive heart failure; AAA = aneurysm of

abdominal aorta.

hospital in patients with acute dissection ranged

from 0 to 11 days, with a mean of 2.7 days. Ten patients with chronic dissection were admitted within 2 months after the clinical onset. The other

4 patients were admitted 6 months, 18 months, 36 months, and 10 years after the clinical onset. Seventy-four percent of the patients reported a history of prior hypertension. Twenty-nine pa- tients (69%) were referred from other hospitals, where 20 patients had already received antihyper- tensive treatment because of a provisional diagno- sis of aortic dissection (Table 1).

Diagnosis and treatment

Patients considered to have acute dissection

were admitted to our intensive care units and underwent bedside echocardiography and plain CT scan after their condition had been stabilized and their pain relieved. The goal of medical treat- ment was elimination of pain and stabilization of hemodynamic parameters including blood pres- sure control (systolic blood pressure < 120 mmHg) and maintenance of urinary output (hourly output > 20 ml). Indications for aggressive blood pres-

233

sure control were: enlargement of the mediastinum

on the chest X-ray, an intimal flap on the echo- cardiogram, or a hematoma within the aortic wall accompanied by a left pleural effusion on the CT

scan. Symptoms, blood pressure, peripheral pulses, and urinary output were monitored at least four

times per day. Beta-blocker and/or alpha-methyl- dopa were adopted as first line medical therapies. Each attending physician added antihypertensive agents such as trimethaphan, nitroprusside, cal- cium antagonists, angiotensin converting enzyme

inhibitors, and diuretics as needed to control blood

pressure within this range. Sedatives and laxatives

were also added to the regimen. Blood pressure control was less rigid (systolic blood pressure <

140 mmHg) in patients with advanced age (> 70

years) and in patients with a change in their mental status or with renal dysfunction.

The diagnosis of aortic dissection was con-

firmed by angiography or enhanced CT scan within two days of admission [22,23]. Angio- graphic criteria for this diagnosis included an in- timal flap, double lumens, and compressed true lumen with a thickened aortic wall. The specific CT characteristic for diagnosis was a demonstra-

tion of an intimal flap creating a true and false channel. In patients with a crescentic low density area in the descending thoracic aorta on CT scan, the diagnosis of aortic dissection was confirmed

by medial displacement of an intimal calcification

into the aortic lumen in all but five patients, but

supported, in these five patients by concomitant left pleural effusion, and by a positive C-reactive protein test (capillary method) [24]. A titre of more than one plus (i.e. greater than 10 micro- gram/ml in RIA method) was considered to rep-

resent positive C-reactive protein test. Patients were moved to an intermediate ward

when free from pain and when their hemodynamic parameters were satisfactorily stabilized. Symp- toms, results of blood pressure control, and results of C-reactive protein tests were used to develop a protocol for the rehabilitation. Patients underwent

meticulous review with enhanced CT scan or in- travenous digital subtraction angiography before discharge and were discharged after their C-reac- tive protein test results reverted to negative. Be- cause of the positive C-reactive protein test results

on admission, the strategy for 10 patients with chronic dissection, whose clinical onset was within 2 months, was the same as that for the patients

with acute dissection. Surgical therapy was not performed in the acute phase. Indications for surgery in the chronic phase were: persistent or

recurrent pain, rupture, impending rupture, visceral ischemia, or ischemia of the lower limbs.

Follow-up and statistical analysis

Outpatient and inpatient medical records were

reviewed. Both survival and event-free ratio of the

38 discharged patients were analyzed by the para- metric actuarial method of Kaplan and Meier [25].

All late deaths were included in the actuarial calculation of survival, while calculation of event-

free ratio included sudden unexpected deaths, deaths due to an aortic dissection, and dissection-

related operations. The following base-line char- acteristics of the medically treated patients with acute dissection were also analyzed; sex, age, the discharged year (before vs. after 1980) and acuity

of presentation. Patients were followed until death or the last contact with their consulting doctors before April 30, 1989. Mean values were com-

pared using the Bonferroni r-test. Probability val-

ues of 0.05 or less were considered to be statisti- cally significant.

Results

Results of medical treatment in the acute phase of distal dissection

The initial symptom of all 28 patients with acute dissection was pain, which originated in the posterior and interscapular area in 19 (68%) pa- tients. Femoral pulses were absent on presentation in two patients with ischemia of the lower limbs. Laboratory tests revealed jaundice (total bilirubin > 1 mg/dl) in 10 patients and anemia (Hb < 10 g/dl) in three.

Eighteen patients underwent aortography and 5 patients pulmonary angiography. A diagnosis of aortic dissection was made from the angiographic findings in 20 of 23 patients. Communication be- tween the true and false channels was seen in 16

234

of the 20 patients. A CT scan was performed in 22 of 25 patients who were admitted after 1980. The

contrast-enhanced method demonstrated an

opacified false channel in the descending thoracic aorta of 11 patients. The other 11 patients had a

crescentic low density area in the descending thoracic aorta. Ultrasonography demonstrated in- timal flaps in the descending thoracic aorta of 5

patients and in the aortic arch of one patient.

Three of 28 patients with acute distal dissection did not show communication between true and false channels.

Eighteen patients (64%) were admitted to the intensive care units. On admission, systolic blood pressure was 146 + 29 mmHg, mean blood pres-

sure 108 f 23 mmHg, and pulse pressure 60 f 17 mmHg. Seventeen patients had systolic blood pressure of more than 140 mmHg. Propranolol was given in doses of 30-120 mg per day (22

cases) and alpha-methyldopa in doses of 500- 1500 mg per day (13 cases). Trimethaphan (8 cases) and nitroprusside (one case) were also used to control blood pressure.

Fig. 1 shows blood pressure control in the acute

phase and at discharge in this group of 20 pa- tients. An overall average of blood pressure in the

acute phase and in the three days prior to dis-

charge was calculated from the data taken at four different times, 0600 a.m., 1000 a.m., 0200 p.m., 0700 p.m., and was shown as mean f SD. In the acute phase, systolic blood pressure, mean blood pressure, and pulse pressure were all significantly reduced to 126 _+ 12 mmHg. 92 + 7 mmHg, and

49 + 10 mmHg, respectively, but there were nine patients who had an average systolic blood pres- sure of more than 130 mmHg. Five patients devel-

oped renal dysfunction, four with mental status change, and four patients were over 70 years of

age. There were no fatalities in these patients with

poor blood pressure control in the acute phase. Table 2 lists early complications of acute distal

dissection. These included pleural effusion and ischemia of lower extremities. Pleural effusion was drained in one patient with severe anemia and was spontaneously absorbed in 9 patients. Orthostatic hypotension, bradycardia, congestive heart failure, and gastrointestinal bleeding occurred in 6 cases (21%) after the medical therapy was commenced.

Ftg. 1. Blood pressure control in the acute phase and at

discharge. Systolic blood pressure (left, hatched bar), mean

blood pressure (left. open bar), and pulse pressure (right. open

bar) in the acute phase and at discharge were significantly

reduced as compared with these on admission (n = 20;

* P < 0.05).

These resolved with medical management. There were no complications in three cases.

Twenty-seven (96%) of 28 patients with acute dissection survived the acute phase. The one pa- tient who died in the acute phase, was a 60-year-old male whose course was complicated by loss of consciousness and azotemia due to acute renal failure. Although hemodialysis and blood pressure control with an angiotensin converting enzyme inhibitor improved pulmonary congestion and he regained consciousness, he died unexpectedly on

TABLE 2

Early complications in 28 patients with acute distal dissection.

Complications No. of cases

None 3

Mental status change 4

Azotemia 1

Renal dysfunction 4

Pleural effusion 11

Ischemia of lower extremities 2

235

the fifth hospital day of a rupture of the aorta,

which was confirmed by autopsy.

Early outcome of the medically treated patients with acute distal dissection

Twenty-four (86%) of the 28 patients with acute dissection were discharged on medical therapy (Table 3). Systolic blood pressure, mean blood pressure, and pulse pressure at discharge were 127 k 13 mmHg, 96 f 9 mmHg, and 51 f 9

mmHg, respectively (Fig. 1). At discharge, there

were 11 patients who had an average systolic

blood pressure of more than 130 mmHg. Although 25 patients showed communication between true

and false channels on admission, this finding was

absent on radiological examinations at discharge

in 8 (32%) of them. As a whole, 11(39%) of 28 patients showed no communication between true and false channels at discharge.

Three patients underwent surgical therapy in

the chronic phase before discharge. One patient underwent transection and insertion of a pros- thetic graft into the thoracic aorta for recurrent

abdominal pain. Axillo-femoral bypass was pro- vided for two patients with ischemia of the lower extremities. There were no operative deaths and

all three patients were discharged. Complications in the chronic phase before dis-

charge included renal dysfunction, bradycardia, orthostatic hypotension, and liver dysfunction. One patient experienced transient paresthesia in

both lower extremities three weeks after the onset of this disease.

C-reactive protein test results were obtained in

27 of the 28 patients with acute distal dissection.

The average maximal titer of C-reactive protein

TABLE 3

Hospital survival.

N Medical Surgical

N Survival N Survival

Acute

dissection 28 25 24 3 3

Chronic

dissection 14 14 14 0 0

TABLE 4

Re-elevation of the titer of C-reactive protein during the

hospitalization.

Patients

(years, sex)

Time from Symptoms/associated

onset of the conditions

disease (weeks)

63. male

73, male

39, male

71, male

60. male

57, male

58, male

66. male

59, female

45, male

70. male -

4

8

5

5.8

5

4

10

transient paresthesia

both legs

back pain/no evidence

of progression of

the dissection

back pain/no evidence

of progression

fever

pneumonia

no symptoms/’

liver dysfunction

low back pain,/

progression of

the dissection

(surgical treatment)

no symptoms,’

progression of

the dissection

acute gout ( X 2)

no symptoms,’

unknown

no symptoms,/

unknown

unknown

(capillary method) during the first two weeks was

4.0 IL 1.4. After an initial decrease, re-elevation of the titer of C-reactive protein during the hospitali- zation was seen in 11 patients. Details of the

clinical course of these patients are presented in Table 4. Back pain or transient paresthesia in both lower extremities preceded the re-elevation of C-

reactive protein titer in 4 patients. One patient

had no symptoms, but radiological examination documented distal progression of the dissection.

Prior to discharge, the C-reactive protein test was negative in 15 (62.5%) of the 24 medically treated patients, equivocal in 3 (12.5%) patients, and positive in 6 (25%) patients. Two elderly pa- tients were discharged, despite positive C-reactive protein test results, because of emotional imbal- ance, and three patients were referred to other hospitals for rehabilitation. The average duration

of positive C-reactive protein test results was 6.5

236

weeks, and the average hospital stay of the medi- cally treated patients was 72 days (range 23-153

days).

Presentation and management of patients with chronic_aortic dissection

The initial symptom of one patient was numb-

ness of the lower limbs, while the remaining 13

patients had a definite history of chest pain or back pain of sudden onset. Angiography demon-

strated a false channel in 10 patients. CT scan

showed a false chamber in 7 patients and a cres- centic low density area in 3 patients. Of the 14 patients with chronic distal dissection, 3 (21%) did

not show communication between the true and false channels.

Early outcome of patients with chronic distal dis- section

All 14 patients were discharged on medical treatment. Systolic blood pressure, mean blood

pressure, and pulse pressure at discharge were

125 + 16 mmHg, 97+ 12 mmHg, and 46+7 mmHg, respectively. There were no differences between acute dissection and chronic dissection in

their systolic blood pressure, mean blood pressure. and pulse pressure at discharge. Persistent com- munication between true and false channels of the aorta on the radiological examination at discharge was documented in 7 patients.

Long-term outcome of all patients after discharge

Mean follow-up of these 41 discharged patients was 5.1 years. The follow-up for 3 patients was not available after one year of discharge. There have been 8 late deaths among 38 patients dis-

charged on medical treatment. The causes of death were a rupture of the aorta in 3 patients, a sudden unexpected death in one, a rupture of the abdomi- nal aortic aneurysm in one, and a cerebrovascular accident in three. Four patients underwent surgi- cal therapy after discharge. Two patients had suc- cessful operations and the remaining two patients suffered operative deaths from emergency surgery for impending rupture of their aneurysms. One of three patients treated surgically during the initial

loo-

90--L__ 80. b

g 70- k

- 60- B*________,

2 50. Q________*_,

g 40- I

* 30. b

20. i &________

IO-

0' 12 3 4 5 6 7 8

Years

Fig. 2. Survival in 38 patients who discharged on medical

treatment. There were significant differences between acute

dissection (0) (n = 24) and chronic dissection (0) (n = 14) in

the actuarial survival rates two years after discharge

(8 P < 0.05).

admission died of a rupture of abdominal aortic aneurysm 6 years after discharge. At the time of

this review, there have been no fatalities among

the six patients who had positive C-reactive pro- tein test results at discharge.

Five-year survival rate was 93% in 24 medically

treated patients with acute dissection (Fig. 2). At two years after discharge the survival rate of the

medically treated patients with acute dissection (100%) was significantly higher than that with chronic dissection (61%) (P < 0.05).

Five-year event-free ratio was 95% in the medi-

cally treated patients (Fig. 3). The event-free ratio also significantly higher in acute dissection

loo? L

90-'--d-;,__ G

80. : ~*___i__-_-_______ii_l *

70. I I 69 0

50. & 40. I I

30. b______A 20.

IO-

0 1 2 3 4 5 6 7 8 9

Years

Fig. 3. Event-free ratto in the same patients as in Fig. 2. The

marks were the same as in Fig. 2. The significant differences of

event-free ratios were noted six years after discharge

(* P -c 0.05).

23-l

(92%) than in chronic dissection (17%) six years after discharge. Causes of death in patients with chronic dissection included cerebrovascular acci- dents in addition to aortic dissection. Acuity of presentation was the significant factor affecting both the survival and the event-free ratio in 38

medically treated patients. Survival rate of the 11 patients with acute dissection who had poor blood

pressure control at discharge was no different from that of the 13 patients whose blood pressure

control was good. Neither sex, age, nor the year of discharge were significant predictors of survival.

Discussion

Choice of therapy for acute distal dissection

There is general agreement that acute proximal dissection with any complication should be treated

surgically whenever possible [26]. There is, how-

ever, still debate about the ideal treatment for acute distal dissection. The concept of immediate

operation for this disease as the treatment of choice was first proposed in a review by Miller et al. in 1979 [18]. In 1983, they reported an oper- ative mortality rate of 13% and a good long-term life expectancy for the discharged patients [19]. As

a result, aggressive surgical management of acute distal dissection has been advocated.

According to recent reports, one-year survival

rates of medically treated patients with acute dis- tal dissection range from 75% to 90% [6-111. With

our strategy of medical management, the hospital mortality rate was 4% and the five-year survival

rate was 93%. Our results are therefore compara- ble to those achieved by aggressive surgical ther-

apy. Some limitations of an exclusively medical ap-

proach to treatment of acute distal dissection in- clude drug-related morbidity and side effects, late

attrition rates, contraindications to drug therapy, lack of compliance on the part of the patients, and the eventual need for late surgical intervention [19]. However, our study showed that these limita- tions were rarely factors in patient management in the acute phase and could be overcome without difficulty. Early complications in our patients in- cluded changes in mental status, renal dysfunc-

tion, and pleural effusion. Although these compli-

cations hampered strict blood pressure control, they did not mandate emergency surgery in the acute phase.

Although our experience is that medical ther- apy is an effective strategy for the management of

dissection, it can be argued that surgical therapy would be inevitably required in some cases be-

cause of the progression of this disease. Other authors expressed a concern that any delay in

surgical treatment may have an adverse effect on outcome [18,27]. Two patients in our series under-

went emergency surgery for impending rupture of the aortic aneurysms, but did not survive their

operations. It is therefore important that even the

patients who were treated successfully at the acute

phase be surveyed carefully at the chronic phase. We suggest that surgical treatment should be per-

formed urgently when impending rupture is sus- pected, whether by changes in the patients’ clinical

status or changes in their aorta on CT scan, digital

subtraction angiography, or magnetic resonance imaging [28-301.

From our analysis we concluded that strict medical treatment in an acute phase, elaborate examination of the aorta by CT scan and angio- graphy at discharge, and urgent surgical interven-

tions, if needed’ in the chronic phase, permit acceptable survival and event-free ratio from this disease. Emergency surgical intervention does not

appear to be an essential component of the

management for patients who presented in the acute phase of their dissection.

Doroghazi reported that late survival after dis-

charge from the hospital was similar for patients with all types of dissection and modes of therapy and that the lo-year actuarial survival of patients discharged from a hospital was approximately 60 percent [6]. In our study, late survival of the patients with chronic dissection was less than that

of patients with acute dissection. Patients with chronic dissection also suffered from cerebrovas- cular accidents in addition to aortic dissection. Because there were no differences between acute and chronic dissections in clinical characteristics listed at Table 1 nor in blood pressure control at

discharge, higher incidence of dissection-related events in chronic dissection might come from dif-

238

ferences in the incidence of “no communication between true and false channels” (acute dissection

[39%] vs. chronic dissection [21%]) 14,311. Because spontaneous closure of the dissection was docu-

mented in 32% of the patients with acute dissec-

tion during their hospitalization, one interpreta-

tion of these results is that strict medical therapy

in the acute phase may facilitate closing or healing of the false channel of the aorta and may be an

important component of the therapeutic approach to patients with acute distal dissection [32].

Cooke has described the angiographic and

pathological features of penetrating aortic ulcer. In such patients medical therapy leads to recur- rence of symptoms that requires surgical interven- tion [33]. In our study, the 33 patients who under-

went angiography did not show these features of penetrating aortic ulcer. It is possible that one or

more of the 8 patients where dissection was di- agnosed by CT scans may have had a penetrating aortic ulcer, but none of these patients have suffered recurrence of aortic dissection. Therefore.

it is unlikely that any of our subjects had penetrat-

ing aortic ulcers.

Medical treatment of distal type aortic dissection

The general aims of current medical treatment

for aortic dissection are to control pain, lower blood pressure and reduce the velocity of ventricu- lar contraction [34,35]. It is not yet clear which factor contributes most to progression of aortic dissection. Some authors have reported that aortic dissections can occur or be exacerbated by hexa- methonium or nitroprusside therapy [36]. Because these drugs have a direct positive inotropic effect on the myocardium and increase the force of ventricular ejection, a reduction in systolic blood pressure alone appears insufficient to control pro-

gression of the dissection. Beta-blockers, alpha- methyldopa, and trimethaphan have therefore been recommended as drugs of choice [37].

We used beta-blockers or alpha-methyldopa to decrease the ejection velocity of the left ventricle in all patients except one with serious complica- tions. Though blood pressure control in the acute phase did not meet our initial goal (systolic blood pressure < 120 mmHg) in a11 patients, the hospital

mortality and morbidity of our patients were very low. Our results suggest that pharmacological re-

duction of systolic blood pressure and pulse pres- sure is the cornerstone of medical treatment.

There are no definite guidelines as to the re-

habilitation of medically treated patients with

aortic dissection. Our approach has been to stabi-

lize hemodynamic parameters, evaluate the sever- ity of their disease radiologically, determine time

of discharge by using C-reactive protein test re- sults as a reference and provide our patients with guidelines for activity and discharge.

The importance of accurate radiological evalua- tion of the aorta has been stressed by many authors

[26]. We would emphasize the importance of evaluating the healing of the injured aortic wall serologically in addition to performing the mor- phological evaluations.

Although the usefulness of C-reactive protein testing in evaluating the severity of aortic dissec-

tion has not been described previously. a raised C-reactive protein level provides unequivocal evi- dence of an active tissue-damaging process [38-

40]. For example, the magnitude of the C-reactive protein elevation reflects the extent of tissue in- jury in acute myocardial infarction [41,42]. We

therefore proposed that C-reactive protein could be used as a maker of tissue injury and healing of the aorta in the patients with acute aortic dissec- tion. Interpretation of the C-reactive protein titer

should take into account any concurrent disorders that may also produce tissue injury or necrosis. For example, infection and acute gout also raised the titer of C-reactive protein over the observation period in this study. Our results lead us to propose that basing the patient’s rehabilitation programme on results of the C-reactive protein test may avoid

further tissue injury and recurrence of aortic dis- section.

We believe that our overall approach should result in the very good short-term and long-term

survival of medically treated patients with acute distal dissection.

Acknowledgements

The authors thank the staff, the residents, and the nurses of the Center for Cardiovascular Dis-

239

eases, Mitsui Memorial Hospital, Tokyo. The

authors also thank J.S. Floras, MD PhD, and Nobuharu Akatsuka, MD for their critical review of the manuscripts and useful suggestions. The authors are indebted to Ms Mary Anne Beddows

for her secretarial support.

1

2

3

4

5

6

I

8

9

10

11

References

Anagnostopoulos CE. Prabhakar MJS. Kittle DF. Aortic

dissections and dissecting aneurysms. Am J Cardiol

1972:30:263-273.

Wheat MW Jr. Acute dissecting aneurysms of the aorta:

diagnosis and treatment-1979. Am Heart J 1980;99:373-

387.

Daily PO. Trueblood HW, Stinson EB. WuerfIein RD.

Shumway NE. Management of acute aortic dissections.

Ann Thorac Surg 1970;10:237-246.

McFarland J. Wirleson JT. Dinsmore RE et al. The medical

treatment of dissecting aortic aneurysms. N Engl J Med

1972;286:115-119.

Vecht RJ. Besterman EMM, Bromley LL, Eastcott HHG.

Acute dissection of the aorta: Long-term review and

management. Lancet 1980;1:109-111.

Doroghazi PM, Slater EE, DeSanctis RW et al. Long-term

survival of patients with treated aortic dissection. J Am

Co11 Cardiol 1984:3:1026-1034.

Bergholm U. Hall&i A. Dissecting aneurysm of the de-

scending thoracic aorta. Stand J Thor Cardiovasc Surg

1984;18:45547.

Masuda Y, Yamada Y, Morooka N. Watanabe S, Inagaki

Y. Evaluation of medical treatment of aortic dissecting

aneurysms. J Jap Co11 Angiol 1986;26:509-512.

Amemiya K, Taira A. Matsuo K. Treatment and prognosis

of aortic dissection. J Jap Co11 Angiol 1986;26:513-517.

Fradet G. Jarnieson WRE, Janusz MT et al. Aortic dissec-

tion. A six-year experience with 117 patients. Am J Surg

1988:155:697-700.

Gustavsson CC. Gustafson A. Albrechtsson U. Larusdottir

H, Stahl E. Olin C. Diagnosis and management of acute

aortic dissection, clinical and radiological follow-up. Acta

Med Stand 1988:223:247-253.

12 Dalen JE. Alpert JS, Cohn LH. Black H, Collins JJ. Dissec-

tion of the thoracic aorta. Medical or surgical therapy? Am

J Cardiol 1974:34:803-808.

13 Strong WW. Moggio RA, Stansel HC Jr. Acute aortic

dissection. Twelve-year medical and surgical experience. J

Thorac Cardiovasc Surg 1974;68:815-821.

14 Parker FB. Neville JF Jr.. Hanson EL. Mohiuddin S, Webb

WR. Management of acute aortic dissection. Ann Thor

Surg 1975;19:436-442.

15 Reul GJ, Cooley DA, Hallman CL, Reddy SB, Kyger ER,

Wukasch DC. Dissecting aneurysm of the descending aorta.

Arch Surg 1975;110:632-640.

16

17

18

19

20

21

22

Appelbaum A, Karp RB, Kirklin JW. Ascending vs. de-

scending aortic dissections. Ann Surg 1976:183:296-300.

Mills SE, Teja K. Crosby IK, Sturgill BC. Aortic dissection.

Surgical and nonsurgical treatments compared. Am J Surg

1979:137:240-243.

Miller DC, Stinson EB, Oyer PE et al. Operative treatment

of aortic dissections: experience with 125 patients over a

sixteen year period. J Thorac Cardiovasc Surg 1979:78:

365-382.

Miller DC. Surgical management of aortic dissections. In:

Doroghazi RM and Salter EE, eds. Aortic dissection. New

York: McGraw-Hill Inc., 1983:193-243.

Stephen DB. Killen DA, Reed WA. Operative experience

with 50 thoracic aortic dissections. Southern Med J 1982;

75:1467-1470.

Pepys MB. C-reactive protein fifty years on. Lancet

1981;1:653-657.

Smith DC. Jang GC. Radiological diagnosis of aortic dis-

section. In: Doroghazi PM and Slater EE. eds. Aortic

dissection. New York: McGraw-Hill Inc., 1983;71-132.

23 Egan TJ. Neiman HL. Malave SR, Sander JH. Computed

tomography in the diagnosis of aortic aneurysm dissection

or traumatic injury. Radiology 1980;136:141- 146.

24 Yamada T, Tada S, Harada J. Aortic dissection without

intimal rupture: diagnosis with MR imaging and CT. Radi-

ology 1988;168:347-332.

25 Kaplan EL, Meier P. Nonparametric estimation of incom-

plete observations. Am Stat Sot 1958;10:457-459.

26 DeSanctis RW. Doroghazi PM. Austin WC, Buckley MJ.

Aortic dissection. New Engl J Med 1987;317:1060-1067.

27 Ruberti U, Odero A, Arpesani A et al. Acute aortic dissec-

tion. J Cardiovasc Surg 1988;29:70-79.

28 Godwin JD, Turloy K, Herfkens RJ, Lipton MJ. Computed

tomography for follow-up of chronic aortic dissections.

Radio1 1981;139:655-660.

29 Geisinger MA, Risius B, O’Donnell JA et al. Thoracic

aortic dissections: Magnetic resonance imaging. Radiology

1985;155:407-412.

30 Guthaner DF. Brody WR, Miller DC. Intravenous aorto-

graphy after aortic dissection repair. Am J Roentgen01

1981;137:1019-1022.

31

32

33

34

35

36

Dinsmore RE, Willerson JT, Buckley MJ. Dissecting

aneurysm of the aorta. Angiographic features affecting

prognosis. Radiology 1972;105:567-572.

Hoshino T. Ohmae M, Sakai A. Spontaneous resolution of

a dissection of the descending aorta after medical treatment

with a beta blocker and a calcium antagonist. Br Heart J

1987:58:82-84.

Cooke JP, Kazmier FJ, Orszulak TA. The penetrating aortic

ulcer: pathologic manifestations. diagnosis and manage-

ment. Mayo Clin Proc 1988;63:718-725.

Prokop EK. Palmer RF, Wheat MW Jr. Hemodynamic

forces in dissecting aneurysms. Circ Res 1970;27:121-127.

Carney WI Jr. Rheinlander HF. Cleveland RJ. Control of

acute aortic dissection. Surg 1975;78:114-120.

Moran JF, Derkac WM. Conkle DM. Pharmacologic con-

240

trol of acute aortic dissection in hypertensive dogs. Surgical

Forum 1978;29:231-234.

37 Wheat MW Jr. Intensive drug therapy. In: Doroghazi RM

and Slater EE. eds. Aortic dissection. New York: Mac-

Craw-Hill Inc.. 1983;1655191.

38 Kushner I, Broder ML, Karp D. Control of the acute phase

response. J Clin Invest 1978:61:235-242.

39 Gewurz H, Meld C. Siegel J. Friedel B. C-reacttve protein

and the acute phase response. In: Stollerman CH. ed.

Advances in internal medicine. Vol 27. Chicago: Year Book

Medical Publishers Inc., 1982:345-372.

40 Hedland P. Clinical and experimental studies on C-reactive

protein (acute phase protein). Acta Med Stand (Suppl)

1961:Suppl 361:1-70.

41 DeBeer FC, Hind CRK. Fox KM, Allan RM, Maseri A,

Pepys MB. Measurement of serum C-reactive protein con-

centration in myocardial ischemia and infarction. Br Heart

J 1982:47:239-243.

42 Pietilf K. Harmoinen A, Piiyhiinen L, Koshinen M. Hetk-

kila J. Ruosteenoja R. Intravenous streptokinase treatment

and serum C-reactive protein in patients with acute

myocardial infarction. Br Heart J 7987:58:225-229.