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Among the possible causes listed by Dr Chandrasekaran and Dr Kurbaan (August 2002, JRSM1) for the enigmatic condition of myocardial infarction with angiographically normal coronary arteries are atheroma, hypercoagulable state, emboli, endothelial dysfunction, dissection and inflammation. The observations of Bogren2, as well as ours3, indicate that functional coronary artery disease in the presence of seemingly normal coronary arteries may also be caused by abnormal stiffness of the aortic wall (syndrome X). To understand the mechanism, one has to recall the fact that the lion's share of coronary flow occurs during diastole and this flow equals the ‘back-flow’ from the aortic arch, which is entirely dependent on aortic wall compliance. In other words, during systole the aorta expands proportionally with the pressure and with the elasticity of its wall, and in diastole the flow reverses and the compliant aorta ‘pays back’ the amount of blood that it stored. As aortic compliance decreases because of fibrosis or for other reasons, so does the aortic back-flow. In severe cases, aortic wall stiffness could lead to coronary underperfusion and myocardial ischaemia.