Intravascular ultrasound observations of @entity731 formation and @entity256 in @entity1 with XXXX .

@entity1 @entity6 @entity146 @entity731 @entity73 @entity1373 @entity256 @entity5707 @entity453 @entity850
@entity453 is more @entity146 in @entity6 @entity1 than in nondiabetics; they have more diffuse disease, higher mortality rates and worse clinical outcomes after coronary interventions. Intravascular ultrasound (IVUS) produces transmural tomographic images of the coronary arteries in vivo. Recent IVUS studies have provided new insights into the mechanisms of @entity850 formation and @entity256 in both nondiabetic and @entity6 @entity1 . Arterial @entity5707 is defined as a change in arterial area. During @entity731 , an increase in arterial area usually accompanies plaque accumulation to delay lumen compromise. @entity850 formation is related to: (a) the rate of plaque accumulation versus the rate of positive @entity5707 ; and (b) the limits and ultimate failure of positive @entity5707 . However, there is a marked variability in @entity5707 . IVUS studies have suggested that @entity5707 may be impaired in some @entity6 @entity1 during @entity731 . Following non-stent catheter-based interventions, serial (post-intervention and follow-up) IVUS studies have shown that the change in lumen area correlates better with the change in arterial area ( @entity5707 ) than with the change in plaque area (neointimal @entity1373 ). In some @entity1 , a positive @entity5707 response mitigates against the increase in plaque area to limit late lumen loss and @entity256 . Neointimal @entity1373 is exaggerated in @entity6 @entity1 . Despite this, there is a reduced frequency of positive @entity5707 , potentially similar to the @entity73 in some @entity6 @entity1 during @entity731 . Failed or inadequate arterial @entity5707 may contribute to the pathogenesis and natural history of @entity453 in @entity6 @entity1 .
