CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 2, March/April 2020
AFRICA
69
on endoscopy provides macroscopic evidence of oesophagitis
that is graded by internationally accepted criteria.
12
According
to Saltissi
39
and Rosztóczy
et al.,
27
ST changes are more likely
to develop in a diseased oesophagus (e.g. with GORD) due to
pre-sensitisation of pain receptors.
A possible limitation of our study is related to the selection
of GORD subjects, all of whom had grade A oesophagitis. It
is thought that severe oesophagitis associated with ulceration
(grade C onwards), tissue damage and inflammation might
40
have
been a more potent trigger
41
stimulating the viscero-cardiac reflex
resulting in ST changes. Furthermore, it may also be argued that
oesophageal acid instillation is non-physiological, with effects
distinctly different from symptoms experienced in oesophageal
reflux disease. Single, short episodes of acid installation might
not have produced significant ST changes of ischaemia since the
acid infusion in our study was for a duration of five minutes.
Over a 24-hour period, multiple episodes of reflux might occur,
possibly reaching the threshold for triggering ischaemia.
41
Higher
rates of acid-induced chest pain (25 and 68%) have been reported
in studies by Davies
et al.
37
and Tougas
et al.
41
where infusion
was for 10 and 20 minutes, respectively, and associated with a
reduction in the threshold for angina.
There are other limitations that need to be considered in
evaluating the results of this study. The first consideration
relates to the sample size. The study recruited 39 subjects with
ACS, of whom 14 had reversible ischaemia on sestaMIBI.
Since the development of ST changes is more likely to occur in
subjects with reversible ischaemia in comparison to subjects with
completed infarcts (and no residual ischaemia), a larger sample
of subjects with reversible ischaemia would have been more
appropriate. Furthermore, ECG monitoring was only conducted
for a period of one hour after acid instillation.
This study has clinical implications in the approach to subjects
with retrosternal chest pain symptoms. Reliance on the chest pain
characteristics is often difficult in subjects with dual pathology
(GORD plus IHD), often rendering symptoms atypical. In
non-acute subjects, non-invasive testing with sestaMIBI is
helpful for the detection of coronary artery disease and requires
treatment on an individual basis. The development of ST
changes in subjects with recent ACS and a history of GORD is
much more imminent and has immediate prognostic implications
for the management of significant ischaemia and should be
addressed on an individual basis. Such patients need immediate
endoscopy to detect and stage GORD in order to evaluate the
risk of bleeding in subjects receiving antiplatelet therapy.
In subjects with GORD the presence of cardiovascular risk
factors in association with ST changes should alert the clinician
to co-existing coronary artery disease. In the absence of epicardial
coronary disease, the possibility of microvascular disease should
be considered in subjects with the metabolic syndrome and
their risk factors addressed. Proton pump inhibitors should be
considered as part of the treatment
4,22,32,33,42,43
in patients where
myocardial ischaemia co-exists with GORD as they are more
prone to cardiovascular events.
Conclusion
We have shown that at least one-third of our ACS patients had
concomitant GORD, which was probably related to the high
prevalence of obesity in these subjects. While we are unable
to conclude that GORD may serve as a trigger for ischaemia
in subjects with ACS, the high prevalence of the metabolic
syndrome in these subjects suggests the possibility of underlying
microvascular disease.
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