I read with interest the Letter to the Editor titled “Inflammation, systemic lupus erythematosus and the Kounis mast cell activation-associated syndrome” from Nicholas G Kounis. In it, the author suggests a possible pathophysiological mechanism related to coronary vasospasm due to mast cell activation as the main reason for acute coronary syndrome in patients with systemic lupus erythematosus.

I would by no means dismiss this as a possible factor, and indeed the literature describes thrombophilias as an associated mechanism that should always be borne in mind. However, I consider that the author, in attempting to demystify the subject, runs the risk of simplifying a disease that is complex, highly prevalent and an important risk factor for cardiovascular disease.

The author appears to go against all the efforts by researchers to clarify the main cause of acute myocardial infarction in young patients with lupus. All recently published studies draw the same conclusion, that these patients’ coronary arteries show diffuse early atherosclerosis.1–6 Chronic systemic inflammation is probably the main cause of the atherosclerotic process, and mast cells may well be involved. However, once again I stress that we should not associate this with vasospasm and put forward a pathophysiological theory as the absolute truth, especially when it is contradicted by the findings of cine coronary angiography in all relevant studies.1–6 In conclusion, I believe that further studies are still needed in this area. But until proven otherwise, early atherosclerosis is the best-established process in this disease and rigorous control of conventional risk factors such as systemic hypertension, dyslipidemia, smoking and diabetes is essential, together with appropriate control of the systemic inflammatory disease.