• Interventional cardiology
• coronary artery disease
• coronary physiology
• lipids
• genetics
• atherosclerosis
• lipoproteins
• lipid drugs
• drug trials
• lipids in atherosclerosis

Stent malapposition (SM), also referred to as incomplete stent apposition, is defined by the separation of at least one stent strut from the intimal surface of the arterial wall with evidence of blood behind the strut, without involvement of side branches.1 SM can be quantified by measuring the number of malapposed struts, the arc subtended by the malapposed struts, the distance between the malapposed struts and the vessel wall, and the area, length and volume of the gap between the stent and the vessel wall.^w1 This phenomenon, commonly identified by intravascular ultrasound (IVUS) imaging studies, may be detected early, at the time of stent implantation (and classified as acute) or later, at follow-up (therefore classified as late). Late stent malapposition can be further classified, in terms of pathogenesis, into two broad categories: late persistent SM, when an inadequately apposed stent (during the initial intervention) remains incompletely apposed at follow-up; and the late acquired stent malapposition (LASM) when it is documented despite the appropriate apposition of the stent during the index procedure. The different types of stent malapposition are graphically explained in figure 1A,B. It is evident that differentiating between the two different forms of late SM requires intravascular imaging both at stent implantation and at follow-up.2

LASM represents a well recognised problem in interventional cardiology that became more prominent in the era of drug eluting stents (DES) (reported incidence 10–25% compared to about 4–6% after bare metal stent (BMS) implantation, in native coronary arteries).3 ,4 ^{w2 w3} Its clinical significance, that will …