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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 2, March/April 2017
122
AFRICA
In this study, we tried to determine whether proximal
anastomosis performed on the ascending aorta in patients who
had undergone CPB and isolated CABG surgery had any effect
on the mean increase in aortic diameter during the early and
mid-term postoperative period. Arteriotomy on dilated aortae
for proximal anastomosis of saphenous vein grafts to the aorta
leads to disruption of the elastic structure and connective tissue
integrity of the aorta. How this affects the dilatation of the aorta
is unknown. This study aimed at answering that question.
In our study, we found that annual increases in all segments
of the aorta were statistically significantly different in both
groups. In patients who had undergone proximal anastomosis
of the ascending aorta, increases in the diameter of the
sinotubular junction and ascending aorta at one and three years
postoperatively were significantly greater than in patients who
had not undergone a proximal anastomosis. We believe that
this strengthens our hypothesis, which asserted that surgical
manipulation on a dilated ascending aorta increases the speed
of aortic expansion.
An aortic diameter exceeding normal limits, based on the
patient’s age and body surface area, is termed aortic dilatation,
and if it increases more than 50% of normal, it is termed aortic
aneurysm.
4
Aneurysm of the ascending aorta is a frequently
seen clinical condition. Haemodynamic force, degradation of
the configured extracellular matrix, familial predisposition and
transmural inflammation have been demonstrated as aetiological
factors for this disease.
5
Aortic wall strain acts in direct proportion with aortic
diameter and pressure, while it is in inverse proportion with aortic
wall thickness, in compliance with Laplace’s law [wall strain
=
pressure
×
radius (r)/2
×
wall thickness (h)].
6
The wall of the
enlarged aorta has a risk of rupture. Recent studies have reported
that aneurysms with a diameter less than 50 mm have a 2%
annual risk of rupture.
6
However, as reported in various studies,
for aneurysms with a diameter of 60 mm, annual risk of rupture
and mortality increases up to 11.8 and 6.9%, respectively. The
probability of their combined risk has been reported at 14.1%.
7
In patients with aneurysms of the ascending aorta who
will undergo valvular surgery, dilatations of less than 50 cm,
unexplained dilatations of
≥
55 mm, patients with Marfan
syndrome and bicuspid aortic dilatations of
≥
50 mm, and for
smaller dilatations with an annual growth rate of 10 mm, surgery
is recommended.
8
In our patients, the aortic diameter was 40–45
mm (mean 41.5
±
1.4 mm) without any connective tissue disease
as aetiological factor, so we did not consider any indication for
surgery in our patients.
Postoperative dilatation rate is important because of the
risks of dilatation and rupture. Expansion rate of the ascending
aorta with a diameter of 40 mm following aortic valve surgery
has been reported as 0.5–2.4 mm/year (mean 0.45 mm/year).
9,10
However Andrus
et al
. found an expansion rate after aortic valve
replacement (AVR) of –0.1 mm/year. This suggests that AVR
changes the natural course of aortic dilatation.
11
Keane
et al
. reported that ascending aortae of patients with
bicuspid valves are more frequently prone to dilatation.
9
In their
series of 14 cases, Yasuda
et al
. followed their patients for 10 years
and reported an annual aortic expansion rate of 0.08 mm/year.
In their studies using CT angiography and echocardiography for
evaluation, they indicated that an increase in the aortic diameter
of 0.2–0.3 mm within 10 years was not statistically significant.
In our study, postoperative (group 2) dilatation in cases with
tricuspid aortic valves had an annual dilatation rate of 1 mm/
year (Table 2). We believe that this dilatation rate was related to
risk factors independent of surgery and valvular pathology.
Natsuaki
et al
. reported that patients who underwent
mechanical valve implantation carried a higher risk of aortic
dissection and rupture when compared with those who
had received biological valves.
12
This contradicts the belief
that biological valves leave behind greater residual gradient
and undergo faster degeneration in sepsis and infection as
endocarditis. In our patients during the three years of follow up,
we did not observe aortic dissection and rapid development of
aneurysmatic dilatation (Fig. 1). However, cases with post-CABG
dissection have occasionally been reported in the literature.
13
Mortality rates in cases of surgery of the ascending aorta have
been reported to range between 1.7 and 17.1% and in re-operated
cases, between 6 and 32%.
14,15
The surgical procedures used and
aetiological factors are known determinants of mortality.
13
In their series, Atik
et al
. detected aortic dilatations in three
(17%) patients following coronary artery surgery.
14
Songur
et
al
. reported aortic dilatation in 50 cases within nine years of
cardiac surgery; eleven (22%) of these cases with aortic dilatation
developed after CABG. In these cases, average diameter of
the ascending aorta after the first and second operation was
indicated as 4.1 and 5.5 cm, respectively.
16
Aortic manipulation
(proximal anastomosis line, cannulation, suture lines, cross-
clamping injury) and aortic valve pathologies have been held
responsible for the development of these dilatations. No case–
control studies where aortic valves were evaluated following
proximal anastomosis have been performed.
In our cases, we detected a dilatation rate of 3.04mmover three
years (7.1%) at the level of the tubular segment of the ascending
aorta. In the patients who underwent proximal anastomosis,
aortic dilatation was more severe (median 3.7 mm per three
years; 8.7%) but the intergroup difference was not statistically
significantly different (
p
=
0.059). In the first postoperative year,
the intergroup difference was significantly different at the level
of the tubular aorta (
p
=
0.02). Dilatation of all segments of the
ascending aorta over time was statistically significantly different
in both groups (
p
=
0.001; Table 2). Intergroup difference in the
tubular ascending aorta in the first year could have been related
to the proximal anastomosis. However when the magnitude of
standard deviation and width of confidence intervals are taken
into consideration, a confounding effect of aetiological factors
(connective tissue disease) should not be overlooked (Fig. 1).
The causative effects of risk factors such as diabetes mellitus,
hypercholesterolaemia, age, hypertension, smoking and alcohol
abuse on atherosclerosis are well recognised.
17
Narrowings or
occlusions occur in the vasa vasorum of the atherosclerotic
aorta, which result in an increase in the levels of elastase enzyme,
a decrease in the levels of anti-protease enzyme and degradation
of the elastin. Consequently, aneurysmatic dilatations develop
on the weakened vascular wall.
18,19
Matsuyama
et al
. detected
a higher number of patients with PAD, TIA, stroke, current
and past smoking history and COPD among those who had
developed aortic dilatation following AVR.
20
However, they
reported a lower incidence of aortic dilatation in patients who
used beta-blockers and those with calcified aortae.
21
In our patients, the presence of COPD, smoking, stroke and
beta-blocker use did not differ between the groups (
p
>
0.05)