Deleterious Effects of a Systemic Lytic State on Reperfused Myocardium

Abstract

Our observations indicate that the responses of ischemic myocardium to reperfusion are influenced by factors beyond those effects attributable to ischemia and reperfusion per se. Pharmacological lysis of coronary thrombi results in alterations characteristic of reperfusion injury and associated with impaired functional recovery. Such changes are also evident, although to a lesser extent, when reperfusion of northrombotic occlusions is induced by mechanical recanalization in the presence of a systemic lytic state but not in its absence. However, such effects were not seen with direct mechanical recanalization of thrombotically occluded vessels. In aggregate, these findings indicate that induction of a systemic lytic state, together with products released by lysis of intracoronary thrombi, generates an inurious milieu that exerts adverse effects on reperfused myocardium.

Angioplasty Strategies in ST-Segment–Elevation Myocardial Infarction

“…22,23 By treating the underlying fissured plaque, primary PCI also reduces recurrent ischemia and reinfarction compared with both fibrin-specific and -nonspecific agents. 13 Moreover, reperfusion injury and hemorrhagic transformation of a bland infarction, which occurs after fibrinolytic therapy but rarely after primary PCI, 24,25 also may result in increased myonecrosis and the mechanical complications of transmural infarction. 26 Finally, despite exclusion of patients at high risk for major bleeding and neurological events in the randomized comparative trials, log-rank p for trend = 0.0003 2.8% Figure 2.…”

Angioplasty Strategies in ST-Segment–Elevation Myocardial Infarction

“…As a result, only an incremental 25% of patients benefitted by restoration of TIMI grade 3 flow with fibrinolysis before intervention, although all patients were exposed to the potentially deleterious effects of fibrinolysis and performance of PCI in a lytic state, including increased femoral access site and intracranial bleeding, reperfusion injury, and hemorrhage into the wall of the plaque and myocardium with infarct extension and possibly myocardial rupture. [35][36][37] Fibrinolytic therapy also enhances platelet activation, 38 likely increasing recurrent ischemia and reinfarction. Many patients also presented beyond 2 to 3 hours after infarct onset (the period during which additional myocardium is most likely to be salvaged by early reperfusion), 39 and the amount of myocardium at risk in patients with nonanterior infarction may not have been sufficient to justify the risks of fibrinolysis.…”