Although acute myocardial infarction has been shown to be associated with the use of specific COX 2 inhibitors, its association with non-specific COX inhibitors is less apparent.2
Traditional NSAIDs, including diclofenac sodium, are among the most commonly prescribed analgesics over the counter. Diclofenac sodium is a non-selective COX inhibitor which acts by inhibiting both COX 1 and COX 2, resulting in anti-inflammation, analgesia and antipyresis.3
Previous reports have demonstrated the increased risk of myocardial infarction with the use of conventional NSAIDs including diclofenac sodium compared with non-users.3,4
As diclofenac is similar to celecoxib (a COX 2 inhibitor) in terms of COX 2 blocking effects, it could theoretically increase the risk of thrombotic events like other COX 2 inhibitors.
Our patient developed an anaphylactic reaction as well as an acute inferior myocardial infarction following ingestion of diclofenac sodium. Unfortunately, he developed an allergic reaction to aspirin too, which indicates his sensitivity to NSAIDs as a whole. Hypersensitivity to NSAIDs is frequently a result of a non-immunological mechanism, particularly in the presence of asthma.5,6
In our patient, this can be explained to some extent by the absence of eosinophilia, which is frequently present in allergic inflammation such as in Kounis syndrome.7
It is our opinion that the anaphylactic reaction caused coronary vasoconstriction. However, the visualisation of atheroma on intravascular ultrasound and thrombus at angiography raises the possibility of concomitant plaque rupture. Hence, myocardial infarction may have developed as a consequence of both allergic reaction and the prothrombotic effect of cyclo-oxygenase inhibition.
There are several case reports on adverse reactions to diclofenac sodium and coronary events reported in the literature. Mori et al
reported a case of allergic vasospastic angina due to diclofenac sodium, although neither myocardial necrosis nor abnormal coronary arteries were demonstrated.8
In the case reported by Gluvic and colleagues, a patient developed acute myocardial infarction secondary to hypersensitivity reaction to intravenous diclofenac,9
but there was a lack of angiography to visualise any coronary abnormalities. Sim recently reported a patient with myocardial infarction triggered by an allergic reaction to an NSAID,10
but coronary thrombus was not identified angiographically. In contrast to these case reports, our patient demonstrated a complete spectrum of myocardial infarction together with angiographically proven coronary thrombus as a result of pre-existing atheroma combined with the adverse drug reaction.
- Our case suggests the possible risk of cardiovascular thrombotic events associated with the use of conventional COX inhibitors.
- Coronary thrombus may develop as a result of exaggerated thrombotic response to ruptured atherosclerotic plaque which may be precipitated by NSAIDs.
- In selected cases, anticoagulation with a vitamin K antagonist may be a reasonable alternative when there is failure of other modalities to remove the thrombus.