At 3 months after successful thrombolysis, reocclusion occurred in about 30% of patients, regardless of the use of antithrombotics. Compared with placebo, aspirin significantly reduces reinfarction rate and revascularization rate, improves event-free survival, and better preserves left ventricular function. The efficacy of Coumadin on these end points appears less than that of aspirin. The still-high reocclusion rate emphasizes the need for better antithrombotic therapy in these patients.
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.
BACKGROUND After successful thrombolysis for acute myocardial infarction, reocclusion is observed in about 30% of patients after 3 months and usually occurs without reinfarction. We studied the impact of reocclusion without reinfarction on global and regional left ventricular function and on remodeling during that period. METHODS AND RESULTS The patients for this analysis constituted a subset of those enrolled in the APRICOT-trial, which was designed to study the efficacy of antithrombotics on the prevention of reocclusion. Patients were selected who had a left anterior descending- or right coronary artery-related myocardial infarction, had an angiographically patent infarct-related vessel when studied < 48 hours after intravenous thrombolysis, and underwent repeat cardiac catheterization at 3 months. Paired contrast ventriculograms of quality sufficient to analyze regional wall motion, global ejection fraction, and ventricular volumes were analyzed in 129 patients. Enzymatic infarct size and baseline left ventricular function as well as other baseline characteristics were similar in patients with (n = 34) and without (n = 95) reocclusion. Ejection fraction improved in anterior infarction without reocclusion from 47 +/- 10% to 54 +/- 13% (P = .0001) but not with reocclusion (baseline, 48 +/- 13%; 3 months, 48 +/- 16%). No improvement was seen in inferior infarction with or without reocclusion. Persistent patency allowed preservation of end-systolic volume index (ESVI) at 3 months (37 +/- 14 mL/m2) to baseline level (38 +/- 13 mL/m2), with a better chance for improvement of > 10 mL/m2 without reocclusion in those with baseline values > 40 mL/m2. After reocclusion, in contrast, ESVI increased from 37 +/- 14 to 43 +/- 20 mL/m2 (P = .08). Comparable mean changes of ESVI in response to persistent patency or reocclusion were seen in anterior versus inferior infarction. Recovery of infarct zone contractility was impaired by reocclusion, both in terms of abnormality of segment shortening and expressed in the number of segments showing abnormal wall motion. In anterior but not in inferior infarction, infarct zone contractility was better with good collaterals to the reoccluded artery compared with poor collaterals. CONCLUSIONS After successful thrombolysis for acute myocardial infarction, reocclusion without reinfarction withholds salvaged myocardium from regaining contractility. This has deleterious consequences for regional and global left ventricular function and for remodeling. To further optimize prognosis in patients after thrombolysis, future research should focus on the prevention of reocclusion and should evaluate revascularization therapy in patients with reocclusion.
This analysis shows the adverse influence of reocclusion on long-term clinical outcome in relation to reinfarction and need for revascularization. To further optimize prognosis after thrombolysis, prevention of reocclusion should become a main priority. Future research should focus on the criteria and timing of elective revascularization procedures in the prevention of coronary reocclusion.
Introduction: Permanent transvenous pacemaker therapy is an essential management option in patients with symptomatic bradyarrhythmias, but harbors a concomitant risk of serious complications. As most complications are lead-or pocket-related, intracardiac leadless pacemaker therapy has the potential to positively impact patient outcome. Since the first leadless pacemaker implant in 2012, many studies have been conducted to evaluate the effectiveness, safety, and applicability of this novel pacing approach.Areas covered: This review will cover the current status of leadless pacemaker technology. Available safety and efficacy outcomes, current area of indication, and end-of-life management will be evaluated. Furthermore, future perspectives for clinical practice and new pacing modalities are discussed. Expert opinion: The first-generation leadless pacemakers are a promising innovation that provide safe and efficient single-chamber pacing therapy without the use of transvenous pacemaker leads. Yet, broad implementation of this technology is hampered by limitations of the current leadless devices, such as end-of-life management and its single-chamber pacing indication. Further innovations such as leadless dual-chamber pacing therapy, leadless cardiac synchronization therapy, energy-harvesting leadless pacemakers, communicating leadless pacemakers with subcutaneous implantable cardiac defibrillators, and minimally invasive completely extracardiac pacemakers are currently being developed that have the potential to become major game changers in pacing therapy.
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