Before the widespread use of coronary stents, restenosis occurred in around one third of lesions dilated by percutaneous transluminal coronary angioplasty (PTCA).1 The actual rates reported in individual case series vary widely depending on patient selection, the definition of restenosis applied, duration of follow up, completeness of angiographic follow up, and whether or not quantitative methods of assessment are used.

Although infrequently resulting in myocardial infarction or death,1 ,2 restenosis is nonetheless an important occurrence since it is associated with the recurrence or deterioration of symptoms and, in some patients, necessitates further attempts at revascularisation.

PTCA does not prevent continued progression of the underlying atherosclerotic disease which may result in further stenoses both at the dilatation site and elsewhere in the coronary arterial system. Furthermore, use of balloon dilatation has been implicated as increasing the risk of early restenosis through both direct and indirect effects. Direct intimal injury at or near the site of dilatation induces fibrocellular proliferation which encourages the deposition of platelets and accelerates formation of atherosclerotic lesions.3 ,4 Balloon dilatation also produces atherogenic effects through the liberation of activated cells and the release of growth promoting factors.5

Cigarette smoking is associated with the development and progression of coronary arterial disease. In their retrospective cohort study Violariset al demonstrate that, on average, current smokers undergo coronary angioplasty three years earlier …