Intracoronary and Noninvasive Imaging for Prediction of Distal Embolization and Periprocedural Myocardial Infarction During Native Coronary Artery Percutaneous Intervention

Abstract

T he incidence of periprocedural myocardial infarction (MI) after percutaneous coronary intervention (PCI) ranges from 2% to 50%, depending on the clinical presentation, type of procedure, choice of biomarker (creatine kinase [CK]-MB or troponin), and the threshold used to qualify the diagnosis. 1 Because of this heterogeneity of definition, the prognostic implications of periprocedural MI are controversial. However, several studies have demonstrated that periprocedural MI is associated with worse in-hospital, short-term, and long-term clinical outcomes, including death, recurrent MI, and need for revascularization. [3][4][5] Various mechanisms can lead to periprocedural MI, such as side branch occlusion or vessel spasm; however, distal embolization of atheroma or thrombus seems to be a dominant cause. 6 In a cardiac MRI (cMRI) study of patients undergoing complex native coronary PCI, elevated troponin levels post-PCI correlated with new myocardial enhancement because of side branch occlusion in 43% of cases and in the apical myocardium distal to the stent in 57% of cases, as would be expected with distal embolization. 7Numerous studies have documented the occurrence of distal embolization during both elective and urgent PCI and have characterized its histopathologic substrate. In an analysis of catheter-retrieved materials from human studies of patients undergoing PCI for acute coronary syndrome (ACS), 8 those with no-reflow had significantly higher amounts of visible atheroma and microscopic components such as platelet-fibrin complexes, cholesterol crystals, and macrophages. 8 In another study of 37 lesions in 35 patients undergoing elective PCI, microscopic particles were captured by embolic protection devices (EPDs) in 28 (75.6%) lesions.9 Thrombotic components (fibrin strand-entrapped platelets, leukocytes, and red cells) accounted for the majority (≈75%) of captured debris, whereas plaque components (fibrous tissue, calcium spots, acellular amorphous material, macrophages, foam cells, and cholesterol clefts) accounted for the minority (≈25%).9 Similar findings were demonstrated among 33 patients undergoing either native or saphenous vein graft PCI.10 Supporting these in vivo findings, in a postmortem analysis of patients who died of ischemic heart disease, many had evidence of coronary microemboli, composed of cholesterol crystals, hyaline, and platelet aggregates. 11Clinically, distal embolization can result in asymptomatic biomarker elevation or symptomatic ischemia; angiographically, it can present as visually undetectable silent embolization, macroembolization resulting in epicardial coronary obstruction, or severe microvascular obstruction resulting in no-reflow.Coronary angiography has limited capacity to assess the risk for distal macro-or microembolization. The development of advanced intracoronary imaging techniques and noninvasive imaging techniques, such as coronary computed tomography angiography (CCTA) and cMRI, provides an opportunity for detailed analysis of plaque composition, which can pot...

Coronary plaque morphology on multi-modality imagining and periprocedural myocardial infarction after percutaneous coronary intervention

“…Patel et al has performed similar review regarding the comparison on coronary imaging for prediction of PMI, and raised several discussions about procedural safety and merit, modification of PCI strategy [47]. Intracoronary imaging is generally a safe procedure, and may allow PCI optimization to reduce the risk of PMI from causes other than distal embolization, such as side branch occlusion or incomplete lesion coverage.…”

“…Statins are regarded as an important agent for the prevention of PMI. Takano et al [47] demonstrated that low-dose rosuvastatin was sufficient for patients who are already taking statins. A meta-analysis of Wang et al [48] demonstrated that in 24 RCTs with a total of 5526 patients, high-dose statin pretreatment was associated with 59% relative reduction in PMI (odds ratio [OR]: 0.41; 95% confidence interval [CI]: 0.34–0.49; P  < 0.00001) and 39% relative reduction in MACE (OR: 0.61; 95% CI: 0.45–0.83; P  < 0.002).…”

How to Detect and Treat Coronary Fibroatheromas

“…Potential clinical strategies to mitigate this risk include vasodilator administration (nicardipine is the authors' preferred medication due to longer half-life and modest hypotensive effect), aggressive anticoagulation (with addition of a glycoprotein IIb/IIIa inhibitor, which is usually given as bolus only without post-PCI infusion), attempts for plaque "vaporization" (e.g., by using laser), and deployment of an embolic protection device (usually a filter that can capture both embolized plaque and/or thrombus) (12). Although these steps are logical, their Third, fibroatheroma detection within a lesion treated with PCI may allow for optimal stent selection (13).…”

How to differentiate the etiology of LV dysfunction as to whether it is “ischemic cardiomyopathy” or “dilated non-ischemic cardiomyopathy”? Invasive coronary and myocardial assessment is the approach of first choice

“…9,10 To gain insight into whether the non-obstructive plaque results from repetitive silent ruptures, displays features of plaque rupture, erosion, thin-cap fibroatheromas, chronic occlusion with spontaneous recanalization, and the extent of vascular remodeling, virtual histology intravascular ultrasound, near-infrared spectroscopy, or optical coherence tomography can be deployed. [11][12][13] If there is no evidence of hemodynamically significant epicardial stenoses by FFR or ominous signs of acute intravascular pathology on intracoronary imaging in the presence of angiographically moderate CAD, we would next recommend measuring coronary flow reserve (CFR) to assess the of combination epicardial and microvascular flow in aggregate. If the CFR is \2, the patient has combined epicardial and microvascular dysfunction, with the FFR value providing information of the relative contribution of epicardial stenosis to the total ischemia.…”