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Polymorphonuclear neutrophils in myocardial ischemia and reperfusion injury

Influence of coronary intervention?

Polymorphkernige Neutrophile bei Myokardischämie und Reperfusionsschaden – Einfluss der Koronarintervention

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Zusammenfassung

Zirkulierende polymorphkernige Neutrophile (PMNs) spielen eine wichtige Rolle bei myokardialer Ischämie und postinterventioneller Reperfusion. Die aktuelle Studie untersucht, ob die Dauer der Ischämie, die Art der Akut–Koronarintervention (Angioplastie versus Angioplastie und Stentimplantation) und die Dauer der Rekanalisationsprozedur selbst beim akuten Myokardinfarkt die inflammatorische Antwort der PMN beeinflusst.

Methoden und Ergebnisse

Bei Patienten mit akutem Myokardinfarkt (AMI; n = 20) wurden das neutrophile Beta–2–Integrin Mac–1 (CD11b/CD18) und L–Selektin (CD62L) zu bestimmten Zeitpunkten vor und nach PTCA oder PTCA und Stentimplantation untersucht. Nach alleiniger PTCA, jedoch nicht nach PTCA mit Stentimplantation stieg Mac–1 signifikant an (136 ± 43%). Dieser Mac–1– Wert fiel nach 60 Minuten wieder ab, sofern die Rekanalisationsprozedur kürzer als 30 Minuten gedauert hatte; nach längerer Rekanalisationsdauer blieb Mac-1 über diesen Zeitpunkt hinaus erhöht. Nach langer präinterventioneller Ischämiedauer (6–24 Stunden nach Symptombeginn) kam es zu einem signifikanten und ausgeprägteren Anstieg von Mac–1 (142 ± 37%); dieser Anstieg konnte durch eine frühe Intervention innerhalb des 6–Stunden–Intervalls nach Symptombeginn verhindert werden. Nach alleiniger PTCA oder nach verspäteter Intervention kam es zu einem signifikanten Abscheren von L–Selektin (77 ± 20%; 77 ± 23%). Eine frühzeitige Intervention oder eine gleichzeitige Stentimplantation verhinderte dieses Abscheren.

Schlussfolgerung

Es konnte gezeigt werden, dass die PMN–Aktivierung durch eine frühzeitige und kurzdauernde Koronarintervention und durch die Stentimplantation verhindert werden kann. Diese verminderte PMN–Aktivierung könnte zum bekannt besseren klinischen Verlauf nach Stenting und früher Koronarintervention beim akuten Myokardinfarkt beitragen.

Summary

Circulating polymorphonuclear neutrophils (PMNs) are known to contribute to the pathophysiology of myocardial ischemia and reperfusion injury. The present study was designed to examine whether the duration of ischemia in myocardial infarction, the type of coronary intervention (angioplasty vs. angioplasty plus stenting) and duration of the procedure itself modulate the inflammatory responses of PMNs.

Methods and results

In patients with acute myocardial infarction (AMI; n = 20) neutrophil β–2–integrin Mac–1 (CD11b/CD18) and L–selectin (CD62L) were determined at different time points before and after PTCA or PTCA plus stenting. After PTCA alone but not after PTCA plus stenting a significant rise in Mac–1 (136 ± 43%) was demonstrated. This elevation decreased after 60 minutes if the duration of the recanalization procedure was shorter than 30 minutes but remained elevated after longer interventions. After delayed intervention a significant and more pronounced increase of Mac–1 (142 ± 37%) was observed, while early intervention prevented this increase. After PTCA alone or delayed intervention a significant shedding of L–selectin (77 ± 20%; 77 ± 23%) was demonstrated. Early intervention or PTCA plus stenting caused no significant changes in L–selectin.

Conclusions

It is concluded that PMN activation is attenuated by early and short intervention as well as by stenting. Induction of PMN activation might contribute to the superior outcome following stenting and early intervention compared to conventional PTCA in particular when performed delayed.

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Authors and Affiliations

  1. Medizinische Klinik und Poliklinik, Innere Medizin III Universitätskliniken des Saarlandes, 66421, Homburg/Saar, Germany

    Andreas Link,  Holger Schwerdt,  Benno Hennen &  Michael Böhm

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  1. Holger Schwerdt
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  2. Benno Hennen
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  3. Michael Böhm
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Correspondence to Andreas Link.

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Link, A., Schwerdt, H., Hennen, B. et al. Polymorphonuclear neutrophils in myocardial ischemia and reperfusion injury. Z Kardiol 93, 605–611 (2004). https://doi.org/10.1007/s00392-004-0105-1

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  • DOI: https://doi.org/10.1007/s00392-004-0105-1

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