CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 2, March/April 2017
118
AFRICA
The effect of proximal anastomosis on the expansion
rate of a dilated ascending aorta in coronary artery
bypass surgery: a prospective study
Ahmet Yavuz Balcı, Unsal Vural, Rezan Aksoy, MD Fatih Özdemir, Seçkin Satılmı
ş
, Mehmet Kızılay,
Mutlu
Ş
enocak, Huseyin
Ş
a
ş
kın,
İ
lyas Kayacıo
ğ
lu,
İ
brahim Yekeler
Abstract
Background:
This study was designed to determine the
short- and long-term effects of proximal aortic anastomosis,
performed during isolated coronary artery bypass grafting
(CABG) in patients with dilatation of the ascending aorta
who did not require surgical intervention.
Methods:
The study was performed on 192 (38 female and
160 male patients; mean age, 62.1
±
9.2 years; range, 42–80
years) patients with dilatation of the ascending aorta who
underwent CABG surgery between 1 June 2006 and 31 May
2014. In group 1 (
n
=
114), the saphenous vein and left inter-
nal mammarian artery grafts were used, and proximal anas-
tomosis was performed on the ascending aorta. In group 2 (
n
=
78), left and right internal mammarian artery grafts were
used, and proximal aortic anastomosis was not performed.
Pre-operatively and in the first and third years postoperative-
ly, the ascending aortic diameter was measured and recorded
using transthoracic echocardiography at four different regions
(annulus, sinus of Valsalva, sinotubular junction and tubular
aorta).
Results:
A statistically significant difference was found
between the groups for the number of grafts used and the
duration of aortic cross-clamping and cardiopulmonary
bypass. No significant intergroup difference was seen for the
mean diameter of the ascending aorta (
p
>
0.05). Annual
changes in the aortic diameter were found to be extremely
significantly different in both groups (
p
=
0.0001). Mean
values of the aortic diameter at the level of the sinotubular
junction and tubular ascending aorta, mean aortic diameters
(
p
=
0.002 and
p
=
0.0001, respectively), annual increase in
diameter (
p
=
0.0001 and
p
=
0.0001, respectively), and mean
annual difference in diameter (
p
=
0.0001 and
p
=
0.0001,
respectively) at one and three years postoperatively were
statistically significantly different between the groups.
Conclusion:
In patients with ascending aortic dilatation who
did not require surgical intervention and who had proximal
anastomosis of the ascending aorta and underwent only
CABG, we detected statistically significant increases in the
diameter of the sinotubular junction and tubular aorta up to
three years postoperatively.
Keywords:
coronary artery bypass grafting, aortic dilatation,
proximal anastomosis
Submitted 23/11/15, accepted 10/7/16
Published online 22/8/16
Cardiovasc J Afr
2017;
28
: 118–124
www.cvja.co.zaDOI: 10.5830/CVJA-2016-071
Aortic dilatation is a clinical entity with many aetiological
factors, which can be seen singly or in association with other
cardiac pathologies. Generally, anuloaortic ectasia, Marfan
syndrome, atherosclerotic aortic degeneration, aortic dissection
and bicuspid aortic valve disease accompany aortic dilatation.
1
Despite novel approaches in surgical and endovascular
treatment procedures for aneurysms, the same degree of
advancement has not been achieved with regard to the molecular
and cellular mechanisms that trigger its pathogenesis and
progression. Genetic factors and inflammatory responses
are recognised as important aspects in the development of
aneurysms. Fedak
et al.
reported the fundamental role of matrix
metalloproteinases (MMP) in the structural integrity of the
aorta.
2
In some studies, loss of elastin and collagen of the aortic
wall has been demonstrated to induce the development of
aneurysms. Loss of elastin and collagen is caused by an increase
in the activity of matrix proteinases (elastase and collagenase)
or a decrease in the activity of anti-proteases [mellaproteinase
tissue inhibitor (TIMP)] and alpha-1-antitrypsin.
2
Increase in
the levels of intercellular adhesion molecules induces migration
of macrophages to this region, with the resultant increase in
the production of MMP2 and MMP9, fragmentation of elastin
and triggering of aneurysm formation. Macrophages degrade
elastin by activating tumour necrosis factor and interleukin-1.
The production of elastin and collagen may also be impaired
Department of Cardiovascular Surgery, Dr Siyami Ersek
Cardiovascular Surgery and Thoracic Hospital, Istanbul,
Turkey
Ahmet Yavuz Balcı, MD
Unsal Vural, MD,
unsalvural@gmail.comMD Fatih Özdemir MD
Mehmet Kızılay MD
Mutlu
Ş
enocak MD
İ
lyas Kayacıo
ğ
lu MD, PhD
İ
brahim Yekeler, MD
Department of Cardiovascular Surgery, Ko
ş
uyolu Training
and Research Hospital, Istanbul, Turkey
Rezan Aksoy, MD
Department of Cardiology, Acibadem University, Istanbul,
Turkey
Seçkin Satılmı
ş
, MD
Department of Cardiovascular Surgery, Derince Training
and Research Hospital, Istanbul, Turkey
Huseyin
Ş
a
ş
kın, MD