Cardiovascular Journal of Africa: Vol 31 No 2 (March/April 2020)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 2, March/April 2020

AFRICA

relieved by rest and nitroglycerin. However, it is documented

that relief with sublingual nitrogycerin is not limited to a pain

of coronary origin,

making it difficult for the clinician to

distinguish between the two conditions when symptoms overlap.

While it may complicate symptomatology in subjects with acute

coronary syndrome,

there is increasing evidence that GORD may

also precipitate cardiovascular events,

particularly since both

conditions share the same nerve plexuses for their innervation.

Theproblemiscompoundedbythefactthatgastro-oesophageal

reflux may occur during exercise and cause exertional chest

pain that mimics angina pectoris. This phenomenon has been

described even during treadmill testing.

Since the prevalence of

cardiac and oesophageal disease increases as patients age, these

ailments may co-exist and interact to precipitate ischaemia. It

has been shown that as many as 50% of patients with cardiac

pain have symptoms of oesophageal disease.

This study showed a 35.1% prevalence of erosive GORD in

patients with recent ACS, which is in keeping with other studies

that have shown prevalence rates varying from 39 to 53%.

21-25

Only one study by Battaglia

et al

. has yielded a much lower

prevalence of 15%, the reasons for which are not clear, possibly

due to a small study sample.

Studies using pH monitoring have documented consistently

similar prevalence rates for GORD in patients with IHD.

22,24,27

a study of 51 patients with coronary artery disease, Rosztóczy

. reported a 45% prevalence of GORD using pH monitoring

and manometry.

Similarly, Svensson

et al

. found a prevalence

of 42% on manometry.

Myocardial perfusion imaging and

oesophageal scintigraphy have also shown a 39% prevalence of

both oesophageal dysfunction and IHD.

Whatever the modality

used to detect GORD, it is apparent that at least one-third of

subjects with IHD have concomitant GORD.

In this study we determined whether GORD could precipitate

ischaemia and used acid instillation during EGD as a surrogate

for acid reflux.

In our study, 20.5% of patients with ACS +

GORD developed ST depression on ECG monitoring shortly

(within five minutes) after acid instillation. Two studies similar

to ours have observed that eight

and 27%

of subjects with

GORD and co-existing IHD developed ST changes after acid

installation. In our study, we documented similar ST changes

in the group with isolated GORD who did not have coronary

disease, as demonstrated on sestaMIBI scanning, and were

therefore unable to conclude that these changes were indicative

of ischaemia.

Lam

et al.

looked at 30 patients with angiographic evidence

of IHD admitted to the CCU with angina.

Their 24-hour

ECG and pH recordings showed that chest pain was preceded

by a drop in pH in only one patient. Based on such findings,

Lam

et al.

and Valori

are also doubtful of the existence of

the link between GORD and ischaemic heart disease. Several

authors have suggested that the development of ST changes and

the documentation of ischaemia in these subjects during acid

installation is probably coincidental,

28-31

whereas other researchers

have postulated the existence of an oesophago-cardiac reflex

resulting in ‘linked angina’

11,17,27

precipitated by acid reflux.

Themechanisms for the development of ST changes in subjects

with GORD and IHD have not been clearly established and are

possibly due to a combination of factors. In Rosztóczy’s study

of 51 patients, ST changes occurred in patients with epicardial

and microvascular disease, as well as in those with a negative

cardiological evaluation. This suggests that the infarct territory is

not a factor in the development of ST changes.

Recently Hui

al.

suggested that oesophageal pain could result in myocardial

ischaemia via an adrenergic stimulus, resulting in increased

myocardial oxygen demand. Alternatively, he postulated that

oesophageal pain could trigger the oesophago-cardiac reflex,

resulting in coronary vasoconstriction and decreased myocardial

oxygen supply.

The explanation for ischaemic ST changes developing in our

subjects with isolated GORD cannot be explained, since these

subjects did not have coronary disease, as demonstrated on

sestaMIBI scans. The possibility that the ECG changes could

have been induced by the procedure itself is unlikely, since no

such ST changes were documented in the normal control group

who did not have GORD or IHD.

Chauhan

et al

. proposed a possible mechanism for ST

changes developing in subjects without IHD on the basis of

microvascular vasoconstriction, as demonstrated by a reduction

in coronary blood flow following acid instillation in subjects with

syndrome X and normal coronary arteries.

They suggested that

these microvascular changes could be mediated via the same

neural reflex or the release of vasoactive substances following

acid installation. Since ST changes on acid installation occurred

in subjects with coronary syndrome X but not in transplant

recipients (denervated hearts), Chauhan and co-workers

concluded that ST changes were due to a viscerocardiac reflex.

A significant finding in our study was the high prevalence

of the metabolic syndrome in the ACS patients, and to some

extent in the isolated GORD subjects, indicating that a few

patients with GORD were also insulin resistant. The association

of microvascular disease with syndrome X and the metabolic

syndrome

might explain the development of ischaemic ST

changes via the oesophago-cardiac reflex, which is thought

to increase microvascular resistance, potentially resulting in

myocardial ischaemia.

Microvascular disease is an established

cause of myocardial ischaemia

33-35

in the absence of epicardial

disease. Although our findings may indicate the presence

of underlying microvascular disease in association with the

metabolic syndrome,

which we documented in both the GORD

and ACS subjects,

a more plausible explanation could be that

the ST changes documented during acid installation were a

false-positive finding, unrelated to the presence of ischaemia,

or a reflex phenomenon that does not necessarily indicate

ischaemia.

11,17,27

An advantage of our study is that oesophageal assessment

was done using fibre-optic endoscopy and only patients with

erosive oesophagitis were selected for the study. A limitation of

earlier studies was that endoscopy was not performed to assess

the oesophageal lesion.

11,37,38

Evidence of erosive oesophagitis

Table 4. Prevalence of ventricular arrhythmias (Lown grade)

Grade

ACS

)

GORD

)

Control

)

-value

(%)

11/39 (28.2)

15/20 (75)

14/22 (64)

(%)

21/39 (53.8)

4/20 (20)

8/22) (36)

(%)

3/39 (7.7)

1/20 (5)

(%)

3/39 (7.7)

0.001

(%)

1/39 (2.6)

0.001

Significant Lown grade arrhythmias. Lown 3 (

0.001) and Lown 4 (

0.001)

were more frequent in ACS compared to GORD subjects and controls after

acid instillation.

ACS, acute coronary syndrome; GORD, gastro-oesopheageal reflux disease.