Gradual Versus Abrupt Reperfusion During Primary Percutaneous Coronary Interventions in ST‐Segment–Elevation Myocardial Infarction (GUARD)
Background Intramyocardial edema and hemorrhage are key pathological mechanisms in the development of reperfusion‐related microvascular damage in ST‐segment–elevation myocardial infarction. These processes may be facilitated by abrupt restoration of intracoronary pressure and flow triggered by prima...
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Wiley
2022-05-01
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Series: | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
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Online Access: | https://www.ahajournals.org/doi/10.1161/JAHA.121.024172 |
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author | Murat Sezer Javier Escaned Christopher J. Broyd Berrin Umman Zehra Bugra Ilke Ozcan Mehmet Rasih Sonsoz Alp Ozcan Adem Atici Emre Aslanger Z. Irem Sezer Justin E. Davies Niels van Royen Sabahattin Umman |
author_facet | Murat Sezer Javier Escaned Christopher J. Broyd Berrin Umman Zehra Bugra Ilke Ozcan Mehmet Rasih Sonsoz Alp Ozcan Adem Atici Emre Aslanger Z. Irem Sezer Justin E. Davies Niels van Royen Sabahattin Umman |
author_sort | Murat Sezer |
collection | DOAJ |
description | Background Intramyocardial edema and hemorrhage are key pathological mechanisms in the development of reperfusion‐related microvascular damage in ST‐segment–elevation myocardial infarction. These processes may be facilitated by abrupt restoration of intracoronary pressure and flow triggered by primary percutaneous coronary intervention. We investigated whether pressure‐controlled reperfusion via gradual reopening of the infarct‐related artery may limit microvascular injury in patients undergoing primary percutaneous coronary intervention. Methods and Results A total of 83 patients with ST‐segment–elevation myocardial infarction were assessed for eligibility and 53 who did not meet inclusion criteria were excluded. The remaining 30 patients with totally occluded infarct‐related artery were randomized to the pressure‐controlled reperfusion with delayed stenting (PCRDS) group (n=15) or standard primary percutaneous coronary intervention with immediate stenting (IS) group (n=15) (intention‐to‐treat population). Data from 5 patients in each arm were unsuitable to be included in the final analysis. Finally, 20 patients undergoing primary percutaneous coronary intervention who were randomly assigned to either IS (n=10) or PCRDS (n=10) were included. In the PCRDS arm, a 1.5‐mm balloon was used to achieve initial reperfusion with thrombolysis in myocardial infarction grade 3 flow and, subsequently, to control distal intracoronary pressure over a 30‐minute monitoring period (MP) until stenting was performed. In both study groups, continuous assessment of coronary hemodynamics with intracoronary pressure and Doppler flow velocity was performed, with a final measurement of zero flow pressure (primary end point of the study) at the end of a 60‐minute MP. There were no complications associated with IS or PCRDS. PCRDS effectively led to lower distal intracoronary pressures than IS over 30 minutes after reperfusion (71.2±9.37 mm Hg versus 90.13±12.09 mm Hg, P=0.001). Significant differences were noted between study arms in the microcirculatory response over MP. Microvascular perfusion progressively deteriorated in the IS group and at the end of MP, and hyperemic microvascular resistance was significantly higher in the IS arm as compared with the PCDRS arm (2.83±0.56 mm Hg.s.cm−1 versus 1.83±0.53 mm Hg.s.cm−1, P=0.001). The primary end point (zero flow pressure) was significantly lower in the PCRDS group than in the IS group (41.46±17.85 mm Hg versus 76.87±21.34 mm Hg, P=0.001). In the whole study group (n=20), reperfusion pressures measured at predefined stages in the early reperfusion period showed robust associations with zero flow pressure values measured at the end of the 1‐hour MP (immediately after reperfusion: r=0.782, P<0.001; at the 10th minute: r=0.796, P<0.001; and at the 20th minute: r=0.702, P=0.001) and peak creatine kinase MB level (immediately after reperfusion: r=0.653, P=0.002; at the 10th minute: r=0.597, P=0.007; and at the 20th minute: r=0.538, P=0.017). Enzymatic myocardial infarction size was lower in the PCRDS group than in the IS group with peak troponin T (5395±2991 ng/mL versus 8874±1927 ng/mL, P=0.006) and creatine kinase MB (163.6±93.4 IU/L versus 542.2±227.4 IU/L, P<0.001). Conclusions In patients with ST‐segment–elevation myocardial infarction, pressure‐controlled reperfusion of the culprit vessel by means of gradual reopening of the occluded infarct‐related artery (PCRDS) led to better‐preserved coronary microvascular integrity and smaller myocardial infarction size, without an increase in procedural complications, compared with IS. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT02732080. |
first_indexed | 2024-04-10T04:35:19Z |
format | Article |
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institution | Directory Open Access Journal |
issn | 2047-9980 |
language | English |
last_indexed | 2024-04-10T04:35:19Z |
publishDate | 2022-05-01 |
publisher | Wiley |
record_format | Article |
series | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
spelling | doaj.art-8c19a9aaff354d6e8bc08b083a28418e2023-03-10T04:02:36ZengWileyJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease2047-99802022-05-01111010.1161/JAHA.121.024172Gradual Versus Abrupt Reperfusion During Primary Percutaneous Coronary Interventions in ST‐Segment–Elevation Myocardial Infarction (GUARD)Murat Sezer0Javier Escaned1Christopher J. Broyd2Berrin Umman3Zehra Bugra4Ilke Ozcan5Mehmet Rasih Sonsoz6Alp Ozcan7Adem Atici8Emre Aslanger9Z. Irem Sezer10Justin E. Davies11Niels van Royen12Sabahattin Umman13Department of Cardiology Istanbul Faculty of Medicine Istanbul University Istanbul TurkeyHospital Clínico San CarlosInstituto de Investigación Sanitaria San CarlosUniversidad Complutense de Madrid Madrid SpainThe Prince Charles Hospital Chermside Brisbane AustraliaDepartment of Cardiology Istanbul Faculty of Medicine Istanbul University Istanbul TurkeyDepartment of Cardiology Istanbul Faculty of Medicine Istanbul University Istanbul TurkeyDepartment of Cardiovascular Medicine Mayo Clinic Rochester MNDepartment of Cardiology Istanbul Faculty of Medicine Istanbul University Istanbul TurkeyDepartment of Cardiology Istanbul Faculty of Medicine Istanbul University Istanbul TurkeyDepartment of Cardiology Istanbul Faculty of Medicine Istanbul University Istanbul TurkeyMarmara UniversitySchool of Medicine Istanbul TurkeyAcibadem Atakent Hastanesi, Halkali Istanbul TurkeyHammersmith Hospital Imperial College London London United KingdomRadboud University Medical Center Nijmegen NetherlandsDepartment of Cardiology Istanbul Faculty of Medicine Istanbul University Istanbul TurkeyBackground Intramyocardial edema and hemorrhage are key pathological mechanisms in the development of reperfusion‐related microvascular damage in ST‐segment–elevation myocardial infarction. These processes may be facilitated by abrupt restoration of intracoronary pressure and flow triggered by primary percutaneous coronary intervention. We investigated whether pressure‐controlled reperfusion via gradual reopening of the infarct‐related artery may limit microvascular injury in patients undergoing primary percutaneous coronary intervention. Methods and Results A total of 83 patients with ST‐segment–elevation myocardial infarction were assessed for eligibility and 53 who did not meet inclusion criteria were excluded. The remaining 30 patients with totally occluded infarct‐related artery were randomized to the pressure‐controlled reperfusion with delayed stenting (PCRDS) group (n=15) or standard primary percutaneous coronary intervention with immediate stenting (IS) group (n=15) (intention‐to‐treat population). Data from 5 patients in each arm were unsuitable to be included in the final analysis. Finally, 20 patients undergoing primary percutaneous coronary intervention who were randomly assigned to either IS (n=10) or PCRDS (n=10) were included. In the PCRDS arm, a 1.5‐mm balloon was used to achieve initial reperfusion with thrombolysis in myocardial infarction grade 3 flow and, subsequently, to control distal intracoronary pressure over a 30‐minute monitoring period (MP) until stenting was performed. In both study groups, continuous assessment of coronary hemodynamics with intracoronary pressure and Doppler flow velocity was performed, with a final measurement of zero flow pressure (primary end point of the study) at the end of a 60‐minute MP. There were no complications associated with IS or PCRDS. PCRDS effectively led to lower distal intracoronary pressures than IS over 30 minutes after reperfusion (71.2±9.37 mm Hg versus 90.13±12.09 mm Hg, P=0.001). Significant differences were noted between study arms in the microcirculatory response over MP. Microvascular perfusion progressively deteriorated in the IS group and at the end of MP, and hyperemic microvascular resistance was significantly higher in the IS arm as compared with the PCDRS arm (2.83±0.56 mm Hg.s.cm−1 versus 1.83±0.53 mm Hg.s.cm−1, P=0.001). The primary end point (zero flow pressure) was significantly lower in the PCRDS group than in the IS group (41.46±17.85 mm Hg versus 76.87±21.34 mm Hg, P=0.001). In the whole study group (n=20), reperfusion pressures measured at predefined stages in the early reperfusion period showed robust associations with zero flow pressure values measured at the end of the 1‐hour MP (immediately after reperfusion: r=0.782, P<0.001; at the 10th minute: r=0.796, P<0.001; and at the 20th minute: r=0.702, P=0.001) and peak creatine kinase MB level (immediately after reperfusion: r=0.653, P=0.002; at the 10th minute: r=0.597, P=0.007; and at the 20th minute: r=0.538, P=0.017). Enzymatic myocardial infarction size was lower in the PCRDS group than in the IS group with peak troponin T (5395±2991 ng/mL versus 8874±1927 ng/mL, P=0.006) and creatine kinase MB (163.6±93.4 IU/L versus 542.2±227.4 IU/L, P<0.001). Conclusions In patients with ST‐segment–elevation myocardial infarction, pressure‐controlled reperfusion of the culprit vessel by means of gradual reopening of the occluded infarct‐related artery (PCRDS) led to better‐preserved coronary microvascular integrity and smaller myocardial infarction size, without an increase in procedural complications, compared with IS. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT02732080.https://www.ahajournals.org/doi/10.1161/JAHA.121.024172coronary microvascular resistanceintramyocardial hemorrhagemicrovascular injurymyocardial edemaprimary PCIreperfusion injury |
spellingShingle | Murat Sezer Javier Escaned Christopher J. Broyd Berrin Umman Zehra Bugra Ilke Ozcan Mehmet Rasih Sonsoz Alp Ozcan Adem Atici Emre Aslanger Z. Irem Sezer Justin E. Davies Niels van Royen Sabahattin Umman Gradual Versus Abrupt Reperfusion During Primary Percutaneous Coronary Interventions in ST‐Segment–Elevation Myocardial Infarction (GUARD) Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease coronary microvascular resistance intramyocardial hemorrhage microvascular injury myocardial edema primary PCI reperfusion injury |
title | Gradual Versus Abrupt Reperfusion During Primary Percutaneous Coronary Interventions in ST‐Segment–Elevation Myocardial Infarction (GUARD) |
title_full | Gradual Versus Abrupt Reperfusion During Primary Percutaneous Coronary Interventions in ST‐Segment–Elevation Myocardial Infarction (GUARD) |
title_fullStr | Gradual Versus Abrupt Reperfusion During Primary Percutaneous Coronary Interventions in ST‐Segment–Elevation Myocardial Infarction (GUARD) |
title_full_unstemmed | Gradual Versus Abrupt Reperfusion During Primary Percutaneous Coronary Interventions in ST‐Segment–Elevation Myocardial Infarction (GUARD) |
title_short | Gradual Versus Abrupt Reperfusion During Primary Percutaneous Coronary Interventions in ST‐Segment–Elevation Myocardial Infarction (GUARD) |
title_sort | gradual versus abrupt reperfusion during primary percutaneous coronary interventions in st segment elevation myocardial infarction guard |
topic | coronary microvascular resistance intramyocardial hemorrhage microvascular injury myocardial edema primary PCI reperfusion injury |
url | https://www.ahajournals.org/doi/10.1161/JAHA.121.024172 |
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