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Coronary microcirculation in nonculprit vessel territory in reperfused acute myocardial infarction

  • Murat Sezer
  • , Ahmet Tas
  • , Zeynep G Demirtakan
  • , Christopher J Broyd
  • , Alp Ozcan
  • , Hakan Hasdemir
  • , Mehmet Kocaaga
  • , Irem Sezer
  • , Mehmet R Sonsoz
  • , Adem Atici
  • , Ilke Ozcan
  • , Berrin Umman
  • , Zehra Bugra
  • , Justin E Davies
  • , Javier Escaned
  • , Niels van Royen
  • , Sabahattin Umman
  • Istanbul University
  • The Prince Charles Hospital
  • Acibadem University
  • Imperial College London
  • Department of Neurology, Hospital Clinico San Carlos, Instituto de Investigacion Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain.
  • International Hospital Istanbul
  • Prince Charles Hospital
  • Acibadem Mehmet Ali Aydinlar Universitesi
  • Complutense University
  • Department of Cardiology, Radboud University Medical Centre, Nijmegen, the Netherlands

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

BACKGROUND: There is an ongoing debate on the extension of reperfusion-related microvascular damage (MVD) throughout the remote noninfarcted myocardial regions in patients with ST-elevation myocardial infarction (STEMI) that undergo primary percutaneous intervention (pPCI). The aim of this study was to elucidate the impact of reperfusion on remote microcirculatory territory by analyzing hemodynamic alterations in the nonculprit-vessel in relation to reperfusion.

METHODS: A total of 20 patients with STEMI undergoing pPCI were included. Peri-reperfusion temporal changes in hemodynamic parameters were obtained in angiographically normal nonculprit vessels before and 1-h after reopening of the culprit vessel. Intracoronary pressure and flow velocity data were compared using pairwise analyses (before and 1-h after reperfusion).

RESULTS: In the non-culprit vessel, compared to the pre-reperfusion state, mean resting average peak velocity (33.4 ± 9.4 to 25.0 ± 4.9 cm/s, P < 0.001) and mean hyperemic average peak velocity (53.5 ± 14.4 to 42.1 ± 10.66 cm/s, P = 0.001) significantly decreased; whereas baseline (3.2 ± 1.0 to 4.0 ± 1.0 mmHg.cm-1.s, P < 0.001) and hyperemic microvascular resistance (HMR) (1.9 ± 0.6 to 2.4 ± 0.7 mmHg.cm-1.s, P < 0.001) and mean zero flow pressure (Pzf) values (32.5 ± 6.9 to 37.6 ± 8.3 mmHg, P = 0.003) significantly increased 1-h after reperfusion. In particular, the magnitude of changes in HMR and Pzf values following reperfusion were more prominent in patients with larger infarct size and with higher extent of MVD in the culprit vessel territory.

CONCLUSION: Reperfusion-related microvascular injury extends to involve remote myocardial territory in relation to the magnitude of the adjacent infarction and infarct-zone MVD. (GUARD Clinical TrialsNCT02732080).

Original languageEnglish
Article number104495
Pages (from-to)104495
JournalMicrovascular research
Volume147
DOIs
Publication statusPublished - 1 May 2023
Externally publishedYes

Keywords

  • Humans
  • Coronary Circulation
  • Coronary Vessels
  • Microcirculation
  • Myocardial Infarction
  • Percutaneous Coronary Intervention
  • ST Elevation Myocardial Infarction
  • Treatment Outcome
  • Coronary hemodynamics
  • Microvascular damage
  • Microvascular resistance
  • Nonculprit-vessel
  • Primary PCI
  • Reperfusion injury
  • STEMI

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