Potential for Myocardial Salvage Utilizing Direct Intracoronary Infusion of Aqueous Oxygen
- Volume 16 - Issue 5 - May, 2004
- Posted on: 8/1/08
- 0 Comments
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Clinical Presentation. A 52-year-old male with a history of tobacco use, hypertension and hypercholesterolemia presented to the emergency room with 6 hours of “chest pressure radiating to the neck and jaw.” Associated dyspnea, diaphoresis and nausea were noted at the time of presentation. Initial electrocardiogram (Figure 1a) demonstrated unequivocal evidence of an inferior myocardial injury pattern. He was triaged to urgent catheterization laboratory intervention.
Diagnostic coronary angiography (Figure 2a) revealed a total occlusion of the right coronary artery (RCA) in its proximal segment. Figure 2B demonstrates the angiographic results following primary stenting of the RCA. Direct intracoronary infusion of aqueous oxygen (TherOx, Irvine, Calif.) as a part of the AMIHOT trial followed percutaneous coronary intervention (PCI) (the patient was randomized as part of the AMIHOT trial after a detailed informed consent). The total duration of direct intracoronary infusion of aqueous oxygen (AO) as mandated by protocol was 90 minutes following PCI.
Following PCI and intracoronary infusion of AO directly in the culprit vessel, amelioration of chest discomfort as well as resolution of electrocardiographic changes were noted. The patient was discharged 2 days later on appropriate antiplatelet therapy.
Two weeks following discharge, myocardial perfusion imaging revealed a minimal defect of the inferior wall. This represented less than 1% of the left ventricle. Gated images demonstrated an end-diastolic volume of 141 ml, an end-systolic volume of 55 ml and an ejection fraction of 61%.
Discussion. Left ventricular systolic function has been demonstrated to be a vital prognostic determinant of survival, irrespective of reperfusion strategy utilized in the setting of acute myocardial infarction.1–7 Reduction of infarct size and preservation of myocardium have both been attributed to early and sustained culprit vessel patency. However, the angiographic appearance of successful restoration of coronary flow has been an inconsistent marker of adequate myocardial reperfusion.8–16
It has also been determined that simply achieving brisk TIMI flow in the culprit vessel may be an inadequate or inconsistent marker for recovery of regional wall motion.17 Reperfusion injury and other pathologic microvascular mechanisms (including distal embolization) are the prime culprits for incomplete recovery of ventricular function in the weeks following an ischemic insult.18–20 It is important to point out that published reports have shown that the deleterious effects related to focal regions of microvascular impairment and ischemia may be attenuated by the local delivery of AO and the resultant achievement of hyperoxemic conditions at the microvascular level.21