TY - JOUR
T1 - Microvascular resistance of the culprit coronary artery in acute ST-elevation myocardial infarction
AU - Carrick, David
AU - Haig, Caroline
AU - Carberry, Jaclyn
AU - May, Vannesa Teng Yue
AU - McCartney, Peter
AU - Welsh, Paul
AU - Ahmed, Nadeem
AU - McEntegart, Margaret
AU - Petrie, Mark C.
AU - Eteiba, Hany
AU - Lindsay, Mitchell
AU - Hood, Stuart
AU - Watkins, Stuart
AU - Mahrous, Ahmed
AU - Rauhalammi, Samuli M.O.
AU - Mordi, Ify
AU - Ford, Ian
AU - Radjenovic, Aleksandra
AU - Sattar, Naveed
AU - Oldroyd, Keith G.
AU - Berry, Colin
N1 - Funding Information:
We thank the patients who participated in this study and the staff in the Cardiology and Radiology Departments, Golden Jubilee National Hospital. We thank Peter Weale and Patrick Revell (Siemens Healthcare). This project was supported by research collaboration with Siemens Healthcare. This research was supported by a British Heart Foundation Project Grant (PG/11/2/28474), the National Health Service, and the Chief Scientist Office. Professor Berry was supported by a Senior Fellowship from the Scottish Funding Council. P. Welsh is supported by a British Heart Foundation Intermediate Fellowship (FS/12/62/29889).
Funding Information:
FUNDING. A British Heart Foundation Project Grant (PG/11/2/28474), the National Health Service, the Chief Scientist Office, a Scottish Funding Council Senior Fellowship, a British Heart Foundation Intermediate Fellowship (FS/12/62/29889), and a nonfinancial research agreement with Siemens Healthcare.
Funding Information:
DC coordinated the study, obtained informed consent from all of the participants, and coordinated and analyzed the MRI scans. He collected the clinical data, participated in the statistical analyses, interpreted the results, and drafted the manuscript. MM, MCP, HE, ML, SW, and SH obtained informed assent, collected data, interpreted the results, and contributed to the manuscript. CH and IF contributed to study design, analyzed and interpreted the data, and contributed to the manuscript. AM assessed the source data for serious adverse events during follow-up that were potentially relevant to the prespecified health outcomes. IM, NA, SMOR, and AR contributed to the analysis of the MRI scans in STEMI patients and in healthy volunteers and contributed to the manuscript. PM analyzed the ECGs. JC and VTYM undertook quantitative coronary analysis of the angiograms. PW and NS undertook the analysis of blood samples for NT-proBNP and IL-6 and contributed to the manuscript. KGO helped to conceive the idea for the study, collected data, interpreted the results, and contributed to the manuscript. CB is PI for the British Heart Foundation project grant and chief investigator for the clinical study. CB conceived the idea for the study and obtained the funding and IRB approvals. He participated in patient recruitment, collected clinical data, interpreted the results, and jointly wrote the manuscript. CB takes responsibility for the manuscript.
Publisher Copyright:
© 2016 American Society for Clinical Investigation. All rights reserved.
PY - 2016/5/5
Y1 - 2016/5/5
N2 - BACKGROUND. Failed myocardial reperfusion is common and prognostically important after acute ST-elevation myocardial infarction (STEMI). The purpose of this study was to investigate coronary flow reserve (CFR), a measure of vasodilator capacity, and the index of microvascular resistance (IMR; mmHg × s) in the culprit artery of STEMI survivors. METHODS. IMR (n = 288) and CFR (n = 283; mean age [SD], 60 [12] years) were measured acutely using guide wire-based thermodilution. Cardiac MRI disclosed left ventricular pathology, function, and volumes at 2 days (n = 281) and 6 months after STEMI (n = 264). All-cause death or first heart failure hospitalization was independently adjudicated (median follow-up 845 days).RESULTS. Myocardial hemorrhage and microvascular obstruction occurred in 89 (42%) and 114 (54%) patients with evaluable T2*-MRI maps. IMR and CFR were associated with microvascular pathology (none vs. microvascular obstruction only vs. microvascular obstruction and myocardial hemorrhage) (median [interquartile range], IMR: 17 [12.0-33.0] vs. 17 [13.0-39.0] vs. 37 [21.0-63.0], P < 0.001; CFR: 1.7 [1.4-2.5] vs. 1.5 [1.1-1.8] vs. 1.4 [1.0-1.8], P < 0.001), whereas thrombolysis in myocardial infarction blush grade was not. IMR was a multivariable associate of changes in left ventricular end-diastolic volume (regression coefficient [95% CI] 0.13 [0.01, 0.24]; P = 0.036), whereas CFR was not (P = 0.160). IMR (5 units) was a multivariable associate of all-cause death or heart failure hospitalization (n = 30 events; hazard ratio [95% CI], 1.09 [1.04, 1.14]; P < 0.001), whereas CFR (P = 0.124) and thrombolysis in myocardial infarction blush grade (P = 0.613) were not. IMR had similar prognostic value for these outcomes as <50% ST-segment resolution on the ECG. CONCLUSIONS. IMR is more closely associated with microvascular pathology, left ventricular remodeling, and health outcomes than the angiogram or CFR.
AB - BACKGROUND. Failed myocardial reperfusion is common and prognostically important after acute ST-elevation myocardial infarction (STEMI). The purpose of this study was to investigate coronary flow reserve (CFR), a measure of vasodilator capacity, and the index of microvascular resistance (IMR; mmHg × s) in the culprit artery of STEMI survivors. METHODS. IMR (n = 288) and CFR (n = 283; mean age [SD], 60 [12] years) were measured acutely using guide wire-based thermodilution. Cardiac MRI disclosed left ventricular pathology, function, and volumes at 2 days (n = 281) and 6 months after STEMI (n = 264). All-cause death or first heart failure hospitalization was independently adjudicated (median follow-up 845 days).RESULTS. Myocardial hemorrhage and microvascular obstruction occurred in 89 (42%) and 114 (54%) patients with evaluable T2*-MRI maps. IMR and CFR were associated with microvascular pathology (none vs. microvascular obstruction only vs. microvascular obstruction and myocardial hemorrhage) (median [interquartile range], IMR: 17 [12.0-33.0] vs. 17 [13.0-39.0] vs. 37 [21.0-63.0], P < 0.001; CFR: 1.7 [1.4-2.5] vs. 1.5 [1.1-1.8] vs. 1.4 [1.0-1.8], P < 0.001), whereas thrombolysis in myocardial infarction blush grade was not. IMR was a multivariable associate of changes in left ventricular end-diastolic volume (regression coefficient [95% CI] 0.13 [0.01, 0.24]; P = 0.036), whereas CFR was not (P = 0.160). IMR (5 units) was a multivariable associate of all-cause death or heart failure hospitalization (n = 30 events; hazard ratio [95% CI], 1.09 [1.04, 1.14]; P < 0.001), whereas CFR (P = 0.124) and thrombolysis in myocardial infarction blush grade (P = 0.613) were not. IMR had similar prognostic value for these outcomes as <50% ST-segment resolution on the ECG. CONCLUSIONS. IMR is more closely associated with microvascular pathology, left ventricular remodeling, and health outcomes than the angiogram or CFR.
UR - http://www.scopus.com/inward/record.url?scp=85055599358&partnerID=8YFLogxK
U2 - 10.1172/jci.insight.85768
DO - 10.1172/jci.insight.85768
M3 - Article
C2 - 27699259
AN - SCOPUS:85055599358
SN - 2379-3708
VL - 1
JO - JCI Insight
JF - JCI Insight
IS - 6
M1 - e85768
ER -