Reocclusion: The flip side of coronary thrombolysis

Abstract

Since the introduction of thrombolytic therapy for acute myocardial infarction, the incidence of coronary artery reocclusion has been intensively studied. Also, the prediction and diagnosis of reocclusion by angiographic and clinical variables, as well its invasive and pharmacologic prevention, have gained much attention. By angiographic definition, reocclusion requires three angiographic observations: one with an occluded artery, one with a reperfused artery and a third for the assessment of subsequent occlusion (true reocclusion). Since the introduction of early intravenous reperfusion therapy, most studies use only two angiograms: one with a patent and one with a nonpatent infarct-related artery. A search for all published reocclusion studies revealed 61 studies (6,061 patients) with at least two angiograms. The median time interval between the first angiogram after thrombolysis and the second was 16 days (range 0.1 to 365). Reocclusion was observed in 666 (11%) of 6,061 cases. Interestingly, the 28 true reocclusion studies showed an incidence of reocclusion of 16 +/- 10% (mean +/- SD), and the 33 studies with only two angiograms 10 +/- 8% (p=0.04), suggesting that proven initial occlusion of the infarct-related artery is a risk factor for reocclusion after successful thrombolysis. The other predictors for reocclusion are probably severity of residual stenosis of the infarct-related artery after thrombolysis and perhaps the flow state after lysis. Reocclusion is most frequently seen in the early weeks after thrombolysis. The clinical course in patients with reocclusion is more complicated than in those without this complication. Left ventricular contractile recovery after thrombolysis is hampered by reocclusion. Routine invasive strategies have not been proven effective against reocclusion. In the prevention of reocclusion, both antiplatelet and antithrombin strategies have been tested, including hirudin and hirulog, but the safety of these agents in thrombolysis is still questionable. Thus, reocclusion after thrombolysis is an early phenomenon and is more frequent after proven initial occlusion of the infarct-related artery. Reocclusion can be predicted by angiography after thrombolysis. Because reocclusion is detrimental, strategies to prevent it should be developed and carried out after thrombolytic therapy for acute myocardial infarction as soon as they are deemed safe.

The smoker’s paradox after successful fibrinolysis: reduced risk of reocclusion but no improved long-term cardiac outcome

“…The reduced risk was observed consistently across many different subgroups and occurred independent of antithrombotic regimen and culprit stenosis severity, a known strong predictor of reocclusion in this setting [27][28][29]. The majority of reocclusions have been shown to occur without clinical reinfarction [12][13][14]. In our study reocclusion occurred without clinical reinfarction in almost 80% of cases, while 46% of patients with reocclusion did not experience recurrent ischemic events.…”

“…Given the strong relationship between reocclusion and outcome after successful fibrinolysis [12][13][14], previous studies addressed the risk of reocclusion in smokers in search for potential mechanisms explaining their favorable outcome. Results of these studies have been conflicting.…”

“…After successful fibrinolysis, outcome is strongly related to reocclusion of the infarct artery, which portends an increased risk of death, reinfarction and revascularization [12][13][14]. Notably, most reocclusions occur without clinical reinfarction [12][13][14].…”

“…Notably, most reocclusions occur without clinical reinfarction [12][13][14]. Even in these cases, reocclusion has adverse impact on recovery of left ventricular function [15].…”

Efficacy and safety of tenecteplase in combination with the low-molecular-weight heparin enoxaparin or unfractionated heparin in the prehospital setting: the assessment of the safety and efficacy of a new thrombolytic regimen (ASSENT) 3 plus randomized trial in acute myocardial infarction

“…13 Despite the development of a series of new fibrinolytic agents 14 -16 for the treatment of STEMI, there has been little improvement in survival rate over the past decade, which is perhaps partly related to limited improvement in coronary perfusion, continued occurrence of reinfarction, and bleeding complications. 17,18 The new single-bolus fibrinolytic drug tenecteplase has facilitated the treatment of acute myocardial infarction, with efficacy equivalent to alteplase for 30-day and 1-year mortality and with the added benefit of less systemic bleeding. 16 Because of its simplicity, the bolus regimen is an attractive choice for the prehospital setting.…”