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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 2, March/April 2017
AFRICA
79
was performed with the RIMA on the right coronary artery
(RCA) in one patient, and in another using a radial artery graft.
All except two patients were operated on electively (these
patients had coronary artery dissection at postpartum, and
acute myocardial infarction, and they had emergency surgery).
According to the EUROscore, two patients were evaluated as
moderate risk, and the others were low risk. Two patients with
low ventricular function were placed in the intensive care unit
(ICU) under inotropic support.
Patients were followed up routinely, and the extubation time
was 7.4
±
3.2 hours. Duration of ICU and hospital stay was 1.4
±
0.9 and 5.6
±
2.1 days, respectively. The medical treatment of
two patients who were diagnosed with Takayasu’s arteritis and
had severe extensive peripheral vasculopathy was continued
as scheduled. Pre-operatively scheduled antihypertensive,
antihyperlipidaemic and antidiabetic medical treatments were
continued after surgery. Routine anticoagulant (acetylsalicyclic
acid 150 mg/day) treatment was added on the first postoperative
day. There were no hospital mortalities.
All patients were contacted using the contact information in
their medical files, and all of the contacted patients were alive.
All except one patient reported that they had no limitations in
physical activities, or socio-economic and emotional aspects,
and their quality of life was no different from that of the normal
population. One patient said he was not actively working
because he had respiratory distress and low functional capacity.
During control coronary angiography (CAG), one patient
with dyspnoea, low functional capacity and moderate risk, who
was operated on in April 2003, was diagnosed with obstructed
saphenous vein grafts in December 2004, and it was observed
that LIMA flow was slow and weak. Another patient, who had
bypass surgery on the LAD and RCA in 2004, had coronary
angiography performed in 2010 and a preliminary diagnosis
of non-ST-segment MI. Angiography revealed that the grafts
were patent, however there was critical stenosis in the circumflex
artery (Cx), which had not undergone bypass surgery before.
Angioplasty was performed on the Cx.
In another patient, a stent was implanted in January 2006,
and LAD bypass was performed in June 2006 after stent stenosis.
In the control CAG in October 2006, we observed that the
LIMA was open. Control CAG in 2009 of an unsymptomatic
patient who had had triple-vessel bypass in 2003 revealed that
the grafts were patent.
Control CAG in 2007 of another patient with single-vessel
bypass in 2003 revealed a patent graft. A patient with single-
vessel bypass in 2004 also had a patent graft in 2009. Other
patients who reported having no problems did not present to any
hospital. Seven out of 20 followed-up patients said that they were
still smoking the same number of cigarettes.
We found five homozygous and 11 heterozygous mutations
in
MTHFR
, which predisposes individuals to CAD or deep-vein
thrombosis (DVT). Eight patients were found to have a
GpIIIa
gene polymorphism, which is associated with increased risk of MI.
Fifteen patients had a polymorphism in the promoter region of the
PAI-1
gene, which is a major inhibitor of the fibrinolytic system.
Discussion
Coronary artery disease is generally defined as a disease of
advanced age because of its prevalence in older individuals.
However it may also be encountered less frequently in younger
people. Since they are active members of the national economy, it
is clear that these young individuals should be treated in the most
effective way. Successful treatment should involve uncomplicated
and safe surgery, resulting in patient survival.
4
Currently, criteria
for successful treatment include not only patient survival but also
duration of recovery and returning to an active life without any
problems, as well the economic aspects of appropriate treatment
options.
4
Risk factors such as smoking and hyperlipidaemia are more
commonly observed among young adults with severe coronary
artery disease, whereas diseases such as hypertension and
diabetes are more frequently observed in the elderly population.
5,6
Cessation of smoking and improving dyslipidaemia may play
a significant role in decreasing disease prevalence in early
adulthood.
5,6
CAD requiring CABG is common in middle-aged or elderly
populations. In the current era, primary prevention includes
identifying the genetic risk as well as optimising the modifiable
risk factors. This is critical in this young population group before
target-organ damage occurs.
7
Selecting appropriate conduits for long-lasting graft patency is
another important issue in these patients. The use of other arterial
grafts such as the radial artery was proven to be superior to venous
grafts for long-termpatency, especially on the left coronary system.
8
We observed some remarkably good early results in our series.
Unfortunately, a more disappointing panorama can be observed
when analysing their long-term evolution. Arteriosclerosis is a
progressive disease and many patients in our series suffered its
consequences during their follow up, as recurrent heart ischaemia,
or major peripheral vascular complications, or both.
Genetic studies of CAD and MI are lagging behind genetic
studies of other cardiovascular disorders. The major reason for
the limited success in this field of genetics is that CAD and MI
are complex diseases, believed to be caused by many genetic
and environmental factors, and the interaction between these
factors.
9
Appropriate treatment and prevention of these diseases
is difficult because they are multifactorial.
Many risk factors have been identified for CAD and MI,
including smoking, advanced age, male gender, diabetes mellitus,
high systolic blood pressure, personal history of angina pectoris,
family history of CAD or MI, high-fat diet, infectious agents,
obesity, increased plasma total and low-density lipoprotein
(LDL) cholesterol levels, increased plasma triglyceride levels, and
decreased plasma high-density lipoprotein (HDL) cholesterol
levels.
10-12
Among these factors, family history is one of the
most significant independent risk factors for CAD and MI.
13
This supports the hypothesis that genetic factors contribute to
the development of CAD and MI, and we therefore used three
genetic diagnostic tests to find a relationship between genetic
make-up and heart disease.
Rare genetic defects that cause extremely high plasma
homocysteine levels also cause CAD.
14,15
It was therefore
hypothesised that, even within the normal range of plasma
homocysteine concentrations, higher levels may appreciably
increase CAD risk.
15
The enzyme methylene tetrahydrofolate
reductase, encoded by the
MTHFR
gene, uses folate to
metabolise and thereby remove homocysteine.
16
The
MTHFR
C677T polymorphism is common (T-allele frequency 15–45%) in
many populations and reduces enzyme efficiency.