Coronary vasomotor function in infarcted and remote myocardium after primary percutaneous coronary intervention
ObjectiveIn patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery and in remote myocardium supplied by angiographically normal vessels. The aim was to investigate the temporal evolution of coronary vasodila...
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| Published in | Heart (British Cardiac Society) Vol. 101; no. 19; pp. 1577 - 1583 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
BMJ Publishing Group LTD
01.10.2015
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1355-6037 1468-201X 1468-201X |
| DOI | 10.1136/heartjnl-2015-307825 |
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| Abstract | ObjectiveIn patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery and in remote myocardium supplied by angiographically normal vessels. The aim was to investigate the temporal evolution of coronary vasodilatory reserve in patients with AMI by use of [15O]H2O positron emission tomography, after successful percutaneous coronary intervention.Methods44 patients with AMI and successful revascularisation by percutaneous coronary intervention were included. Subjects were examined 1 week and 3 months after AMI with [15O]H2O positron emission tomography to assess the coronary flow reserve (CFR). CFR was defined as the ratio of myocardial blood flow (MBF) during hyperaemia and rest. Additionally, 45 age-matched and sex-matched subjects underwent similar scanning procedures and served as controls.ResultsAt baseline, CFR averaged 1.81±0.66 in infarcted myocardium versus 2.51±0.81 in remote myocardium (p<0.01). In comparison, CFR in the control group averaged 4.16±1.45 (p=0.001 vs both). During follow-up, the CFR increased to 2.74±0.85 in infarcted myocardium (p<0.01), and to 2.85±0.70 in remote myocardium (p<0.01). This was predominantly due to an increase in hyperaemic MBF, from 1.62±0.54 mL/min/g to 2.19±0.68 mL/min/g in infarcted myocardium (p<0.001), and 2.17±0.54 mL/min/g to 2.60±0.65 mL/min/g in remote myocardium (p<0.001).ConclusionsCFR in infarcted and remote myocardium is impaired 1 week after AMI. After 3 months vasomotor function partially recovers. However, as compared with control patients, MBF remains impaired in culprit and reference territories in patients with AMI.Clinical trial registrationNTR3164. |
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| AbstractList | ObjectiveIn patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery and in remote myocardium supplied by angiographically normal vessels. The aim was to investigate the temporal evolution of coronary vasodilatory reserve in patients with AMI by use of [15O]H2O positron emission tomography, after successful percutaneous coronary intervention.Methods44 patients with AMI and successful revascularisation by percutaneous coronary intervention were included. Subjects were examined 1week and 3months after AMI with [15O]H2O positron emission tomography to assess the coronary flow reserve (CFR). CFR was defined as the ratio of myocardial blood flow (MBF) during hyperaemia and rest. Additionally, 45 age-matched and sex-matched subjects underwent similar scanning procedures and served as controls.ResultsAt baseline, CFR averaged 1.81 plus or minus 0.66 in infarcted myocardium versus 2.51 plus or minus 0.81 in remote myocardium (p<0.01). In comparison, CFR in the control group averaged 4.16 plus or minus 1.45 (p=0.001 vs both). During follow-up, the CFR increased to 2.74 plus or minus 0.85 in infarcted myocardium (p<0.01), and to 2.85 plus or minus 0.70 in remote myocardium (p<0.01). This was predominantly due to an increase in hyperaemic MBF, from 1.62 plus or minus 0.54 mL/min/g to 2.19 plus or minus 0.68mL/min/g in infarcted myocardium (p<0.001), and 2.17 plus or minus 0.54 mL/min/g to 2.60 plus or minus 0.65mL/min/g in remote myocardium (p<0.001).ConclusionsCFR in infarcted and remote myocardium is impaired 1week after AMI. After 3months vasomotor function partially recovers. However, as compared with control patients, MBF remains impaired in culprit and reference territories in patients with AMI.Clinical trial registrationNTR3164. ObjectiveIn patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery and in remote myocardium supplied by angiographically normal vessels. The aim was to investigate the temporal evolution of coronary vasodilatory reserve in patients with AMI by use of [15O]H2O positron emission tomography, after successful percutaneous coronary intervention.Methods44 patients with AMI and successful revascularisation by percutaneous coronary intervention were included. Subjects were examined 1 week and 3 months after AMI with [15O]H2O positron emission tomography to assess the coronary flow reserve (CFR). CFR was defined as the ratio of myocardial blood flow (MBF) during hyperaemia and rest. Additionally, 45 age-matched and sex-matched subjects underwent similar scanning procedures and served as controls.ResultsAt baseline, CFR averaged 1.81±0.66 in infarcted myocardium versus 2.51±0.81 in remote myocardium (p<0.01). In comparison, CFR in the control group averaged 4.16±1.45 (p=0.001 vs both). During follow-up, the CFR increased to 2.74±0.85 in infarcted myocardium (p<0.01), and to 2.85±0.70 in remote myocardium (p<0.01). This was predominantly due to an increase in hyperaemic MBF, from 1.62±0.54 mL/min/g to 2.19±0.68 mL/min/g in infarcted myocardium (p<0.001), and 2.17±0.54 mL/min/g to 2.60±0.65 mL/min/g in remote myocardium (p<0.001).ConclusionsCFR in infarcted and remote myocardium is impaired 1 week after AMI. After 3 months vasomotor function partially recovers. However, as compared with control patients, MBF remains impaired in culprit and reference territories in patients with AMI.Clinical trial registrationNTR3164. In patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery and in remote myocardium supplied by angiographically normal vessels. The aim was to investigate the temporal evolution of coronary vasodilatory reserve in patients with AMI by use of [(15)O]H2O positron emission tomography, after successful percutaneous coronary intervention.OBJECTIVEIn patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery and in remote myocardium supplied by angiographically normal vessels. The aim was to investigate the temporal evolution of coronary vasodilatory reserve in patients with AMI by use of [(15)O]H2O positron emission tomography, after successful percutaneous coronary intervention.44 patients with AMI and successful revascularisation by percutaneous coronary intervention were included. Subjects were examined 1 week and 3 months after AMI with [(15)O]H2O positron emission tomography to assess the coronary flow reserve (CFR). CFR was defined as the ratio of myocardial blood flow (MBF) during hyperaemia and rest. Additionally, 45 age-matched and sex-matched subjects underwent similar scanning procedures and served as controls.METHODS44 patients with AMI and successful revascularisation by percutaneous coronary intervention were included. Subjects were examined 1 week and 3 months after AMI with [(15)O]H2O positron emission tomography to assess the coronary flow reserve (CFR). CFR was defined as the ratio of myocardial blood flow (MBF) during hyperaemia and rest. Additionally, 45 age-matched and sex-matched subjects underwent similar scanning procedures and served as controls.At baseline, CFR averaged 1.81±0.66 in infarcted myocardium versus 2.51±0.81 in remote myocardium (p<0.01). In comparison, CFR in the control group averaged 4.16±1.45 (p=0.001 vs both). During follow-up, the CFR increased to 2.74±0.85 in infarcted myocardium (p<0.01), and to 2.85±0.70 in remote myocardium (p<0.01). This was predominantly due to an increase in hyperaemic MBF, from 1.62±0.54 mL/min/g to 2.19±0.68 mL/min/g in infarcted myocardium (p<0.001), and 2.17±0.54 mL/min/g to 2.60±0.65 mL/min/g in remote myocardium (p<0.001).RESULTSAt baseline, CFR averaged 1.81±0.66 in infarcted myocardium versus 2.51±0.81 in remote myocardium (p<0.01). In comparison, CFR in the control group averaged 4.16±1.45 (p=0.001 vs both). During follow-up, the CFR increased to 2.74±0.85 in infarcted myocardium (p<0.01), and to 2.85±0.70 in remote myocardium (p<0.01). This was predominantly due to an increase in hyperaemic MBF, from 1.62±0.54 mL/min/g to 2.19±0.68 mL/min/g in infarcted myocardium (p<0.001), and 2.17±0.54 mL/min/g to 2.60±0.65 mL/min/g in remote myocardium (p<0.001).CFR in infarcted and remote myocardium is impaired 1 week after AMI. After 3 months vasomotor function partially recovers. However, as compared with control patients, MBF remains impaired in culprit and reference territories in patients with AMI.CONCLUSIONSCFR in infarcted and remote myocardium is impaired 1 week after AMI. After 3 months vasomotor function partially recovers. However, as compared with control patients, MBF remains impaired in culprit and reference territories in patients with AMI.NTR3164.CLINICAL TRIAL REGISTRATIONNTR3164. Objective In patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery and in remote myocardium supplied by angiographically normal vessels. The aim was to investigate the temporal evolution of coronary vasodilatory reserve in patients with AMI by use of [15 O]H2 O positron emission tomography, after successful percutaneous coronary intervention. Methods 44 patients with AMI and successful revascularisation by percutaneous coronary intervention were included. Subjects were examined 1 week and 3 months after AMI with [15 O]H2 O positron emission tomography to assess the coronary flow reserve (CFR). CFR was defined as the ratio of myocardial blood flow (MBF) during hyperaemia and rest. Additionally, 45 age-matched and sex-matched subjects underwent similar scanning procedures and served as controls. Results At baseline, CFR averaged 1.81±0.66 in infarcted myocardium versus 2.51±0.81 in remote myocardium (p<0.01). In comparison, CFR in the control group averaged 4.16±1.45 (p=0.001 vs both). During follow-up, the CFR increased to 2.74±0.85 in infarcted myocardium (p<0.01), and to 2.85±0.70 in remote myocardium (p<0.01). This was predominantly due to an increase in hyperaemic MBF, from 1.62±0.54 mL/min/g to 2.19±0.68 mL/min/g in infarcted myocardium (p<0.001), and 2.17±0.54 mL/min/g to 2.60±0.65 mL/min/g in remote myocardium (p<0.001). Conclusions CFR in infarcted and remote myocardium is impaired 1 week after AMI. After 3 months vasomotor function partially recovers. However, as compared with control patients, MBF remains impaired in culprit and reference territories in patients with AMI. Clinical trial registration NTR3164. In patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery and in remote myocardium supplied by angiographically normal vessels. The aim was to investigate the temporal evolution of coronary vasodilatory reserve in patients with AMI by use of [(15)O]H2O positron emission tomography, after successful percutaneous coronary intervention. 44 patients with AMI and successful revascularisation by percutaneous coronary intervention were included. Subjects were examined 1 week and 3 months after AMI with [(15)O]H2O positron emission tomography to assess the coronary flow reserve (CFR). CFR was defined as the ratio of myocardial blood flow (MBF) during hyperaemia and rest. Additionally, 45 age-matched and sex-matched subjects underwent similar scanning procedures and served as controls. At baseline, CFR averaged 1.81±0.66 in infarcted myocardium versus 2.51±0.81 in remote myocardium (p<0.01). In comparison, CFR in the control group averaged 4.16±1.45 (p=0.001 vs both). During follow-up, the CFR increased to 2.74±0.85 in infarcted myocardium (p<0.01), and to 2.85±0.70 in remote myocardium (p<0.01). This was predominantly due to an increase in hyperaemic MBF, from 1.62±0.54 mL/min/g to 2.19±0.68 mL/min/g in infarcted myocardium (p<0.001), and 2.17±0.54 mL/min/g to 2.60±0.65 mL/min/g in remote myocardium (p<0.001). CFR in infarcted and remote myocardium is impaired 1 week after AMI. After 3 months vasomotor function partially recovers. However, as compared with control patients, MBF remains impaired in culprit and reference territories in patients with AMI. NTR3164. |
| Author | Timmer, Stefan A J Lammertsma, Adriaan A Knaapen, Paul van de Ven, Peter M Van Rossum, Albert C Teunissen, Paul F A Danad, Ibrahim de Waard, Guus A van Royen, Niels Raijmakers, Pieter G |
| Author_xml | – sequence: 1 givenname: Paul F A surname: Teunissen fullname: Teunissen, Paul F A email: p.knaapen@vumc.nl organization: Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands – sequence: 2 givenname: Stefan A J surname: Timmer fullname: Timmer, Stefan A J email: p.knaapen@vumc.nl organization: Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands – sequence: 3 givenname: Ibrahim surname: Danad fullname: Danad, Ibrahim email: p.knaapen@vumc.nl organization: Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands – sequence: 4 givenname: Guus A surname: de Waard fullname: de Waard, Guus A email: p.knaapen@vumc.nl organization: Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands – sequence: 5 givenname: Peter M surname: van de Ven fullname: van de Ven, Peter M email: p.knaapen@vumc.nl organization: Department of Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, The Netherlands – sequence: 6 givenname: Pieter G surname: Raijmakers fullname: Raijmakers, Pieter G email: p.knaapen@vumc.nl organization: Department of Radiology & Nuclear Medicine, VU University Medical Center, Amsterdam, The Netherlands – sequence: 7 givenname: Adriaan A surname: Lammertsma fullname: Lammertsma, Adriaan A email: p.knaapen@vumc.nl organization: Department of Radiology & Nuclear Medicine, VU University Medical Center, Amsterdam, The Netherlands – sequence: 8 givenname: Albert C surname: Van Rossum fullname: Van Rossum, Albert C email: p.knaapen@vumc.nl organization: Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands – sequence: 9 givenname: Niels surname: van Royen fullname: van Royen, Niels email: p.knaapen@vumc.nl organization: Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands – sequence: 10 givenname: Paul surname: Knaapen fullname: Knaapen, Paul email: p.knaapen@vumc.nl organization: Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26246402$$D View this record in MEDLINE/PubMed |
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Effect of rosuvastatin on coronary flow reserve in patients with systemic hypertension publication-title: Am J Cardiol doi: 10.1016/j.amjcard.2014.07.046 – volume: 39 start-page: 102 year: 2012 ident: key-10.1136/heartjnl-2015-307825-11 article-title: Coronary risk factors and myocardial blood flow in patients evaluated for coronary artery disease: a quantitative [15O]H2O PET/CT study publication-title: Eur J Nucl Med Mol Imaging doi: 10.1007/s00259-011-1956-0 – volume: 102 start-page: 24 year: 1981 ident: key-10.1136/heartjnl-2015-307825-8 article-title: Serial plasma catecholamine response early in the course of clinical acute myocardial infarction: relationship to infarct extent and mortality publication-title: Am Heart J doi: 10.1016/0002-8703(81)90408-7 – volume: 301 start-page: H129 year: 2011 ident: key-10.1136/heartjnl-2015-307825-22 article-title: Effects of alcohol septal ablation on coronary microvascular function and myocardial energetics in hypertrophic obstructive cardiomyopathy publication-title: AJP: Heart and Circulatory Physiology – volume: 89 start-page: 1109 year: 1994 ident: key-10.1136/heartjnl-2015-307825-16 article-title: Predictive value of reactive hyperemic response on reperfusion on recovery of regional myocardial function after coronary angioplasty in acute myocardial infarction publication-title: Circulation doi: 10.1161/01.CIR.89.3.1109 – volume: 105 start-page: 2785 year: 2002 ident: key-10.1136/heartjnl-2015-307825-27 article-title: Angiotensin-converting enzyme inhibitors improve coronary flow reserve in dilated cardiomyopathy by a bradykinin-mediated, nitric oxide-dependent mechanism publication-title: Circulation doi: 10.1161/01.CIR.0000017433.90061.2E – volume: 47 start-page: 163 year: 2006 ident: key-10.1136/heartjnl-2015-307825-9 article-title: Quantification of subendocardial and subepicardial blood flow using 15O-labeled water and PET: experimental validation publication-title: J Nucl Med – volume: 23 start-page: 465 year: 2006 ident: key-10.1136/heartjnl-2015-307825-30 article-title: Effects of smoking on coronary blood flow velocity and coronary flow reserve assessed by transthoracic Doppler echocardiography publication-title: Echocardiography doi: 10.1111/j.1540-8175.2006.00242.x – volume: 3 start-page: 695 year: 2010 ident: key-10.1136/heartjnl-2015-307825-5 article-title: Prevention and treatment of microvascular obstruction-related myocardial injury and coronary no-reflow following percutaneous coronary intervention: a systematic approach publication-title: JACC Cardiovasc Interv doi: 10.1016/j.jcin.2010.05.004 – volume: 30 start-page: 1270 year: 1997 ident: key-10.1136/heartjnl-2015-307825-2 article-title: Recovery of myocardial perfusion in acute myocardial infarction after successful balloon angioplasty and stent placement in the infarct-related coronary artery publication-title: J Am Coll Cardiol doi: 10.1016/S0735-1097(97)00300-8 – volume: 97 start-page: 791 year: 2008 ident: key-10.1136/heartjnl-2015-307825-6 article-title: Cardiac positron emission tomography: myocardial perfusion and metabolism in clinical practice publication-title: Clin Res Cardiol doi: 10.1007/s00392-008-0662-9 – volume: 2 start-page: 456 year: 2005 ident: key-10.1136/heartjnl-2015-307825-18 article-title: The role of shear stress in the destabilization of vulnerable plaques and related therapeutic implications publication-title: Nat Clin Pract Cardiovasc Med doi: 10.1038/ncpcardio0298 – volume: 52 start-page: 417 year: 2001 ident: key-10.1136/heartjnl-2015-307825-20 article-title: Minimal impairment of myocardial blood flow responses to exercise in the remodeled left ventricle early after myocardial infarction, despite significant hemodynamic and neurohumoral alterations publication-title: Cardiovasc Res doi: 10.1016/S0008-6363(01)00426-6 – volume: 331 start-page: 222 year: 1994 ident: key-10.1136/heartjnl-2015-307825-1 article-title: Reduced coronary vasodilator function in infarcted and normal myocardium after myocardial infarction publication-title: N Engl J Med doi: 10.1056/NEJM199407283310402 – volume: 22 start-page: 650 year: 1993 ident: key-10.1136/heartjnl-2015-307825-4 article-title: Altered coronary vasodilator reserve and metabolism in myocardium subtended by normal arteries in patients with coronary artery disease publication-title: J Am Coll Cardiol doi: 10.1016/0735-1097(93)90172-W |
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| Snippet | ObjectiveIn patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery... In patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery and in... Objective In patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit... |
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| SubjectTerms | Acute coronary syndromes Adenosine Adult Aged Cardiovascular disease Case-Control Studies Colonies & territories Coronary vessels Coronary Vessels - innervation Female Fractional Flow Reserve, Myocardial Heart attacks Humans Male Medical imaging Middle Aged Myocardial Infarction - diagnosis Myocardial Infarction - physiopathology Myocardial Infarction - therapy Myocardial Perfusion Imaging - methods Oxygen Radioisotopes Percutaneous Coronary Intervention Positron-Emission Tomography Predictive Value of Tests Radiopharmaceuticals Recovery of Function Respiration Studies Time Factors Treatment Outcome Vascular Resistance Vasodilation Vasomotor System - physiopathology |
| Title | Coronary vasomotor function in infarcted and remote myocardium after primary percutaneous coronary intervention |
| URI | https://heart.bmj.com/content/101/19/1577.full https://www.ncbi.nlm.nih.gov/pubmed/26246402 https://www.proquest.com/docview/1780741472 https://www.proquest.com/docview/1711541455 https://www.proquest.com/docview/1808701611 |
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