Bursts of reperfusion arrhythmias occur independently of area at risk size and are the first marker of reperfusion injury. (15th November 2018)

• Record Type: Journal Article
• Authors: van der Weg, Kirian; Kuijt, Wichert J.; Bekkers, Sebastiaan C.A.M.; Tijssen, Jan G.P.; Green, Cynthia L.; Smulders, Martijn W.; Lemmert, Miguel E.; Krucoff, Mitchell W.; Gorgels, Anton P.M.
• Is Part Of: International journal of cardiology. Volume 271(2018)
• Page Start: 240
• Page End: 246
• Publication Date: 2018-11-15
• Subjects: AAR area at risk -- DE-CMR delayed enhancement cardiovascular magnetic resonance imaging -- ECG electrocardiogram -- ESA infarct endocardial surface area -- IS infarct size -- LV left ventricle -- MVO microvascular obstruction -- PCI percutaneous coronary intervention -- SPECT single-photon emission computed tomography -- STEMI ST elevation myocardial infarction -- TIMI thrombolysis in myocardial infarction -- VA ventricular arrhythmias -- VPC ventricular premature complex; Myocardial infarction -- Electrocardiography -- Arrhythmias -- Magnetic resonance imaging -- Myocardial reperfusion injury; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2018.05.083
• Languages: English
• ISSNs: 0167-5273

Abstract

Abstract: Background: The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger infarct size (IS). However it is unclear whether the initial area at risk (AAR), also a determining factor for IS, is responsible for this correlation. We hypothesized that IS would be significantly larger in the presence of VA, while AAR would not differ. Methods: 68 STEMI patients from the MAST study with 24-hour, continuous, 12‑lead Holter monitoring initiated prior to primary percutaneous coronary intervention (PCI) resulting in TIMI 3 flow post PCI were included. VA bursts were identified against subject-specific background VA rates using a previously validated statistical outlier method. IS, and infarct endocardial surface area (ESA) were obtained using CMR at mean 4.9 days after admission. Holter and CMR results were determined in core laboratories blinded to all other data. Results: VA bursts were present in 69% (45/65) of patients. No significant differences were found for demographic characteristics, comorbidities, infarct location, number of diseased coronary vessels, or duration of ischemia between groups with and without VA burst. IS was significantly smaller in the group without VA bursts (median 9.3% vs 17.0%; p = 0.025). Infarct ESA did not significantly differ between the population with and without VA burst; median 24.3% vs 20.0%; p = 0.15. Conclusion: VA bursts are a marker for larger IS independent of AAR, assessed by surrogate markers. These findings support the hypothesis that VA bursts are a marker of reperfusion damage occurring downstream at myocellular level. Highlights: Infarct size is larger in the presence of VA Burst. AAR does not differ between the groups with or without VA Burst. These findings suggest VA Burst to be the first marker of reperfusion injury.