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Logistical reasons and slow recruitment
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Myocardial infarction (MI) frequently recurs after non-ST elevation MI (NSTEMI) that may be related to insufficient vulnerable plaque identification using invasive coronary angiography. Furthermore, the natural behaviour of vulnerable plaques in NSTEMI over time and their relation with biomarkers need further exploration. More accurate identification and assessing long-term behaviour of vulnerable plaques may improve therapeutic strategies and clinical outcome. The investigators hypothesize that fully integrated 18Fluoride Sodium-Fluoride (18F-NaF) Positron Emission Tomography/Cardiac Magnetic Resonance imaging (PET/CMR) increases the ability to detect vulnerable plaques as compared to coronary angiography.
This prospective study in 33 consecutive patients with NSTEMI aims to:
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| Measure | Description | Time Frame |
|---|---|---|
| The frequency of coronary vulnerable plaques in non-ST-elevation myocardial infarction (NSTEMI) using 18Fluoride Sodium-Fluoride (18F-NaF) Positron Emission Tomography/Cardiac Magnetic Resonance (PET/CMR). | 0 to 6 months | |
| The frequency of coronary vulnerable plaques in NSTEMI using routine invasive coronary angiography. | 0 to 6 months |
| Measure | Description | Time Frame |
|---|---|---|
| The location of vulnerable plaques within the coronary arteries using 18F-NaF PET at baseline and follow-up. | 0 to 6 months | |
| Based on the AHA 17-segment model, the segmental location of MI using CMR at baseline and follow-up. | 0 to 6 months |
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Inclusion Criteria:
Exclusion Criteria:
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Thirty-three patients, 18-85 years old and admitted with non-ST elevation myocardial infarction (NSTEMI). After informed consent, patients wil receive standard, guideline-based clinical care that includes invasive coronary angiography. Plasma biomaker will be sampled serially, and a comprehensive Sodium 18F-Fluoride Positron Emission Tomography/Cardiac Magnetic Resonance imaging (18F-NaF PET/CMR) will be performed at baseline (<72 hours) and at 6 months, or earlier when patients suffer recurrent myocardial infarction < 6months. Patients will be followed for one year during regular outpatient clinic visits.
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| Name | Affiliation | Role |
|---|---|---|
| Joachim Wildberger, MD, PhD | Maastricht University Medical Center | Principal Investigator |
| Harry J. Crijns, MD, PhD | Maastricht University Medical Center | Principal Investigator |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| Maastricht University Medical Center | Maastricht | Limburg | 6202 AZ | Netherlands |
| PubMed Identifier | Type | Citation | Retractions |
|---|---|---|---|
| 15983262 | Background | Libby P, Theroux P. Pathophysiology of coronary artery disease. Circulation. 2005 Jun 28;111(25):3481-8. doi: 10.1161/CIRCULATIONAHA.105.537878. | |
| 10807742 | Background | Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000 May;20(5):1262-75. doi: 10.1161/01.atv.20.5.1262. No abstract available. |
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| ID | Term |
|---|---|
| D009203 | Myocardial Infarction |
| D017202 | Myocardial Ischemia |
| ID | Term |
|---|---|
| D006331 | Heart Diseases |
| D002318 | Cardiovascular Diseases |
| D014652 | Vascular Diseases |
| D007238 | Infarction |
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Biomarkers
| The frequency of systemic vulnerable plaques as assessed with 18F-NaF PET/CMR at baseline and follow-up. | 0 to 6 months |
| Serial serum concentrations of biomarkers of plaque vulnerability and myocardial injury at baseline and follow-up. | 0 to 6 months |
| 15337693 | Background | Cutlip DE, Chhabra AG, Baim DS, Chauhan MS, Marulkar S, Massaro J, Bakhai A, Cohen DJ, Kuntz RE, Ho KK. Beyond restenosis: five-year clinical outcomes from second-generation coronary stent trials. Circulation. 2004 Sep 7;110(10):1226-30. doi: 10.1161/01.CIR.0000140721.27004.4B. Epub 2004 Aug 30. |
| 15623544 | Background | Glaser R, Selzer F, Faxon DP, Laskey WK, Cohen HA, Slater J, Detre KM, Wilensky RL. Clinical progression of incidental, asymptomatic lesions discovered during culprit vessel coronary intervention. Circulation. 2005 Jan 18;111(2):143-9. doi: 10.1161/01.CIR.0000150335.01285.12. Epub 2004 Dec 27. |
| 19381280 | Background | Kim HW, Klem I, Shah DJ, Wu E, Meyers SN, Parker MA, Crowley AL, Bonow RO, Judd RM, Kim RJ. Unrecognized non-Q-wave myocardial infarction: prevalence and prognostic significance in patients with suspected coronary disease. PLoS Med. 2009 Apr 21;6(4):e1000057. doi: 10.1371/journal.pmed.1000057. Epub 2009 Apr 21. |
| 22679059 | Background | Kato K, Yonetsu T, Kim SJ, Xing L, Lee H, McNulty I, Yeh RW, Sakhuja R, Zhang S, Uemura S, Yu B, Mizuno K, Jang IK. Nonculprit plaques in patients with acute coronary syndromes have more vulnerable features compared with those with non-acute coronary syndromes: a 3-vessel optical coherence tomography study. Circ Cardiovasc Imaging. 2012 Jul;5(4):433-40. doi: 10.1161/CIRCIMAGING.112.973701. Epub 2012 Jun 7. |
| 21247313 | Background | Stone GW, Maehara A, Lansky AJ, de Bruyne B, Cristea E, Mintz GS, Mehran R, McPherson J, Farhat N, Marso SP, Parise H, Templin B, White R, Zhang Z, Serruys PW; PROSPECT Investigators. A prospective natural-history study of coronary atherosclerosis. N Engl J Med. 2011 Jan 20;364(3):226-35. doi: 10.1056/NEJMoa1002358. |
| 24224999 | Background | Joshi NV, Vesey AT, Williams MC, Shah AS, Calvert PA, Craighead FH, Yeoh SE, Wallace W, Salter D, Fletcher AM, van Beek EJ, Flapan AD, Uren NG, Behan MW, Cruden NL, Mills NL, Fox KA, Rudd JH, Dweck MR, Newby DE. 18F-fluoride positron emission tomography for identification of ruptured and high-risk coronary atherosclerotic plaques: a prospective clinical trial. Lancet. 2014 Feb 22;383(9918):705-13. doi: 10.1016/S0140-6736(13)61754-7. Epub 2013 Nov 11. |
| 22516444 | Background | Dweck MR, Chow MW, Joshi NV, Williams MC, Jones C, Fletcher AM, Richardson H, White A, McKillop G, van Beek EJ, Boon NA, Rudd JH, Newby DE. Coronary arterial 18F-sodium fluoride uptake: a novel marker of plaque biology. J Am Coll Cardiol. 2012 Apr 24;59(17):1539-48. doi: 10.1016/j.jacc.2011.12.037. |
| 8989146 | Background | Kim RJ, Chen EL, Lima JA, Judd RM. Myocardial Gd-DTPA kinetics determine MRI contrast enhancement and reflect the extent and severity of myocardial injury after acute reperfused infarction. Circulation. 1996 Dec 15;94(12):3318-26. doi: 10.1161/01.cir.94.12.3318. |
| 23166040 | Background | Kwee RM, van Oostenbrugge RJ, Mess WH, Prins MH, van der Geest RJ, ter Berg JW, Franke CL, Korten AG, Meems BJ, van Engelshoven JM, Wildberger JE, Kooi ME. MRI of carotid atherosclerosis to identify TIA and stroke patients who are at risk of a recurrence. J Magn Reson Imaging. 2013 May;37(5):1189-94. doi: 10.1002/jmri.23918. Epub 2012 Nov 16. |
| 3973257 | Background | Ambrose JA, Winters SL, Stern A, Eng A, Teichholz LE, Gorlin R, Fuster V. Angiographic morphology and the pathogenesis of unstable angina pectoris. J Am Coll Cardiol. 1985 Mar;5(3):609-16. doi: 10.1016/s0735-1097(85)80384-3. |
| D007511 |
| Ischemia |
| D010335 | Pathologic Processes |
| D013568 | Pathological Conditions, Signs and Symptoms |
| D009336 | Necrosis |