Culprit Lesion Atherothrombectomy During Acute Myocardial Infarction

Abstract

A 70-year-old man presented to the emergency department with chest discomfort, hypotension, and bradycardia. The initial ECG revealed an ST-segment elevation inferoposterior myocardial infarction (MI). The patient was treated with aspirin, atropine, dopamine, unfractionated heparin, and eptifibatide, and was then referred for emergent cardiac catheterization. After temporary pacemaker placement, coronary angiography revealed a subtotal occlusion of the midright coronary artery (RCA) that was associated with a large intracoronary thrombus (Figure 1, left) and TIMI-2 flow. To minimize the possibility of coronary atherothromboembolism and the no-reflow phenomenon, a decision was made to perform a culprit lesion atherothrombectomy using an Export catheter (Medtronic) over a FilterWire distal protection device (Boston Scientific). Two sequential aspirations were performed, resulting in a marked resolution of the thrombus and reduction of the lesion length (Figure 1, middle). Coronary stenting produced a good angiographic result without evidence of the no-reflow phenomenon (Figure 1, right). The catheter aspirate demonstrated 3 visible specimens 3 to 6 mm in diameter. A small amount of debris was noted within the distal protection device. Histopathological analysis of the aspirate revealed a fibrin-rich thrombus along with cholesterol crystals, indicative of a ruptured lipid-rich plaque (Figure 2). The aspirate also demonstrated cellular inflammation, as evidenced by lipid-laden macrophages and a dense neutrophilic infiltrate surrounding the cholesterol crystals. Consistent with a lack of atherothromboembolism, the patient's predischarge echocardiogram revealed a normal ejection fraction of 62% without wall motion abnormalities. This report demonstrates interventional extraction of an acute coronary plaque rupture, the primary event underlying acute myocardial infarction.

Vascular Repair by Grafting Based on Magnetic Nanoparticles

“…Although the desired effect was not achieved, this may also be due to the selection of candidate drugs. In addition, myocardial infarction caused by coronary plaque rupture can also cause severe inflammation and even heart failure [ 126 , 127 , 128 ]. Zhang et al [ 129 ] studied in a rat myocardial infarction model, using an in vitro epicardial magnet to accumulate MNPs that bind to the human VEGF gene encoded by an adenovirus vector in the ischemic area.…”