Key result
Inhibiting leukocyte adhesion emerges as a target for myocardial reperfusion injury, driving ~40 patent filings.
Why the study?
Reperfusion injury of the heart remains an untreated condition despite successful implementation of reperfusion strategies in clinical practice.
Inhibition of leukocyte adhesion and post-ischaemic inflammation has emerged as a therapeutic goal for myocardial reperfusion injury, with numerous patents filed in this area.
Answers are grounded in this paper and cite their sources.
Leukocyte adhesion inhibition warrants no clinical use in reperfusion injury; hypothesis-generating and requires prospective trials.
Reperfusion injury of the heart remains an untreated condition even though reperfusion strategies have been successfully implemented in the clinical standard. Accordingly, low or no reflow phenomena with subsequent myocardial infarction, myocardial and endothelial stunning as well as arrhythmias remain aspects of reperfusion injury of the heart. Since leukocyte recruitment has been linked to these phenomena, inhibition of leukocyte adhesion and of the subsequent post-ischaemic inflammation of the heart has emerged as a therapeutic goal. Around 40 patents from 1997 to the first quarter of 2000 are implicitly or explicitly aimed at myocardial reperfusion injury.
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Kupatt et al. (2000) conducted a review in Myocardial ischaemia reperfusion injury. Inhibition of post-ischaemic inflammation was evaluated. Inhibition of leukocyte adhesion and post-ischaemic inflammation has emerged as a therapeutic goal for myocardial reperfusion injury, with around 40 patents filed between 1997 and 2000.
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