Coronary microcirculation in nonculprit vessel territory in reperfused acute myocardial infarction

• Published in: Microvascular research Vol. 147; p. 104495
• Main Authors: Sezer, Murat, Tas, Ahmet, Demirtakan, Zeynep G., Broyd, Christopher J., Ozcan, Alp, Hasdemir, Hakan, Kocaaga, Mehmet, Sezer, Irem, Sonsoz, Mehmet R., Atici, Adem, Ozcan, Ilke, Umman, Berrin, Bugra, Zehra, Davies, Justin E., Escaned, Javier, van Royen, Niels, Umman, Sabahattin
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.2023
• Subjects: Coronary Circulation; Coronary hemodynamics; Coronary Vessels; Humans; Microcirculation; Microvascular damage; Microvascular resistance; Myocardial Infarction; Nonculprit-vessel; Percutaneous Coronary Intervention; Primary PCI; Reperfusion injury; ST Elevation Myocardial Infarction; STEMI; Treatment Outcome; Primary PCI; BMR; APV; HMR; Microvascular damage; Microvascular resistance; CFR; Reperfusion injury; Coronary hemodynamics; pPCI; STEMI; IRA; MVD; Pzf; Nonculprit-vessel; APVh
• ISSN: 0026-2862; 1095-9319
• DOI: 10.1016/j.mvr.2023.104495

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. 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). 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. 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). •Reperfusion induces microvascular injury in nonculprit vessel territory.•More severe nonculprit vessel microvascular injury accompanies larger infarct size.•Severity of microvascular damage in culprit and nonculprit vessels is associated.•Reperfusion induces significant perturbations in nonculprit vessel hemodynamics.