New Insights into ACS Derived from Intracoronary Imaging

Over the last decade the increased use of intravascular ultrasonography (IVUS) and optical coherence tomography (OCT) has led insight in the multiple mechanisms of acute coronary instability. Whereas the traditional view of the pathophysiologic substrate of acute coronary syndromes was of an acute rupture of a thin fibrous cap covering non-hemodynamically significant lesion resulting in thrombus formation it now appears that there are at least four possible mechanisms: plaque rupture, plaque erosion, calcified nodule, all causing acute thrombus formation and spontaneous coronary artery dissection (SCAD).

On the basis of multiple invasive imaging studies, it has been shown that lesions associated with future instability have a greater plaque burden, a higher remodeling index, and increased intramural lipid deposition compared to stable lesions. While thinner fibrous caps are more common in lesions causing ACS than those in the setting of stable angina, cap thickness in the setting of ACS often exceeds 70 μm, and is occasionally as thick as 150 μm. Depending on the intravascular imaging study the incidence of plaque rupture causing an acute coronary syndrome ranges 35-65%, plaque erosion 25-47%, calcified nodule up to 9.6% and SCAD less than 1.6%. ACS caused by plaque erosion or calcified nodules can be treated conservatively while the treatment of SCAD should initially be conservative.