Seeing is Believing: iFR and OCT in Acute Coronary Syndrome
Presenter
Dr. Dorothy Jung, MD, Penn State Health Milton S. Hershey Medical Center, Hershey, PA
Dr. Dorothy Jung, MD, Aaron Lee, MD, FSCAI and Chad Zack, M.D., Penn State Health Milton S. Hershey Medical Center, Hershey, PA
Title
Seeing is Believing: iFR and OCT in Acute Coronary Syndrome
Introduction
A 61 year old gentleman presented with typical angina. He was found to have an elevated troponin and dynamic EKG changes concerning for ischemia. A culprit lesion was not readily apparent on coronary angiography; the patient had an occluded RCA which appeared chronic and 60% stenosis of the mid-LAD which was insignificant by iFR (0.96). Intracoronary imaging was utilized which revealed plaque rupture and non-occlusive soft plaque in the mid-LAD. The lesion was successfully treated with a drug-eluting stent and post-dilated with excellent result.
Clinical Case
A 61 year old gentleman with a remote history of ulcerative colitis s/p proctocolectomy and venous thromboembolism in the setting of COVID infection presented to the ED with several hours of typical angina. EKG on presentation showed sinus rhythm and t-wave inversions in III, avF as well as transient 1-mm ST elevations in V1-V4. Troponin-T peaked at 0.135 ng/ml. Coronary angiography did not demonstrate a clear culprit lesion: there was total occlusion of the proximal RCA that appeared chronic as well as moderate stenosis (60%) of the mid-LAD. Physiologic assessment was performed of the mid-LAD stenosis and was found to be non-ischemic (iFR 0.96). Attempts at traversing the stenosis in the RCA with a coronary wire were unsuccessful; this, in addition to the presence of left-to-right collaterals, led us to believe that the RCA was likely not the culprit lesion. We decided to re-evaluate the LAD stenosis, recognizing that iFR/FFR may not be accurate in the culprit vessel in the setting of acute coronary syndrome. OCT was performed which demonstrated fibrous cap disruption and plaque cavity, suggestive of plaque rupture in the mid-LAD, without evidence of significant intraluminal thrombus. It was determined this was likely the culprit vessel. The lesion was treated with an Onyx Frontier 3.5 x 26 mm drug eluting stent and post-dilated with a Euphora non-compliant 4.5 x 12 mm balloon with excellent angiographic result. The patient was discharged the following day on dual-antiplatelet therapy. At three months post-intervention, the patient was enrolled in cardiac rehabilitation and had returned to his daily activities, including recreational hockey.
Discussion
This case highlights the limitations of iFR/FFR in an acute plaque event where the culprit vessel is not obvious angiographically. In acute coronary syndrome, iFR/FFR results may be above the ischemic threshold in the culprit vessel, as in this case where plaque rupture and intimal disruption were demonstrated on OCT but the luminal area of the vessel was largely preserved. Furthermore, pooled analysis of DEFINE-FLAIR and iFR-SWEDEHEART demonstrated that, compared to patients with stable angina, patients with ACS who had PCI deferred based on negative FFR/iFR values experienced higher incidence of MACE. Intracoronary imaging allows for localization and characterization of lesions which, in an acute plaque event, may not be readily apparent on angiographic and physiologic evaluation.