全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...
PLOS ONE  2013 

Positive Association of Coronary Calcium Detected by Computed Tomography Coronary Angiography with Periprocedural Myocardial Infarction

DOI: 10.1371/journal.pone.0082835

Full-Text   Cite this paper   Add to My Lib

Abstract:

Background Periprocedural myocardial infarction (PMI) may occur in approximately 5% to 30% of patients undergoing percutaneous coronary intervention. Whether the morphology of coronary plaque calcium affects the occurrence of PMI is unknown. Materials and Methods A total of 616 subjects with stable angina and normal baseline cardiac troponin I levels who had undergone computed tomography angiography (CTA) were referred to elective percutaneous coronary intervention. The morphology of coronary calcium was determined by CTA analysis. PMI was defined as an elevation in 24-h post-procedural cardiac troponin I levels of > 5 times the upper limit of normal with either symptoms of myocardial ischemia, new ischemic electrocardiographic changes, or documented complications during the procedure. Logistic regression was performed to identify the effect of the morphology of coronary calcium on the occurrence of PMI. Results According to the presence or morphology of coronary calcium as shown by CTA, 210 subjects were grouped in the heavy calcification group, 258 in the mild calcification group, 40 in the spotty calcification group and 108 in the control group. The dissection rate was significantly higher in the heavy calcification group than in the control group (7.1 % vs. 1.9%, p = 0.03). The occurrence of PMI in the heavy calcification group was significantly higher than that in the control group (OR 4.38, 95% CI 1.80–10.65, p = 0.001). After multivariate adjustment, the risk of PMI still remained significantly higher in the heavy calcification group than in the control group (OR 4.04, 95% CI 1.50–10.89, p = 0.003). Conclusions The morphology of coronary calcium determined by CTA may help to predict the subsequent occurrence of PMI. A large amount of coronary calcium may be predictive of PMI.

References

[1]  Prasad A, Herrmann J (2011) Myocardial infarction due to percutaneous coronary intervention. N Engl J Med 364: 453–464.
[2]  Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, et al. (2012) Third universal definition of myocardial infarction. Circulation 126: 2020–2035.
[3]  Nienhuis MB, Ottervanger JP, Bilo HJ, Dikkeschei BD, Zijlstra F (2008) Prognostic value of troponin after elective percutaneous coronary intervention: A meta-analysis. Catheter Cardiovasc Interv 71: 318–324.
[4]  Feldman DN, Kim L, Rene AG, Minutello RM, Bergman G, et al. (2011) Prognostic value of cardiac troponin-I or troponin-T elevation following nonemergent percutaneous coronary intervention: a meta-analysis. Catheter Cardiovasc Interv 77: 1020–1030.
[5]  Babu GG, Walker JM, Yellon DM, Hausenloy DJ (2010) Peri-procedural myocardial injury during percutaneous coronary intervention: an important target for cardioprotection. Eur Heart J 32: 23–31.
[6]  Testa L, Van Gaal WJ, Biondi Zoccai GG, Agostoni P, Latini RA, et al. (2009) Myocardial infarction after percutaneous coronary intervention: a meta-analysis of troponin elevation applying the new universal definition. QJM 102: 369–378.
[7]  Selvanayagam JB, Porto I, Channon K, Petersen SE, Francis JM, et al. (2005) Troponin elevation after percutaneous coronary intervention directly represents the extent of irreversible myocardial injury: insights from cardiovascular magnetic resonance imaging. Circulation 111: 1027–1032.
[8]  Uetani T, Amano T, Ando H, Yokoi K, Arai K, et al. (2008) The correlation between lipid volume in the target lesion, measured by integrated backscatter intravascular ultrasound, and post-procedural myocardial infarction in patients with elective stent implantation. Eur Heart J 29: 1714–1720.
[9]  Hong YJ, Mintz GS, Kim SW, Lee SY, Okabe T, et al. (2009) Impact of plaque composition on cardiac troponin elevation after percutaneous coronary intervention: an ultrasound analysis. JACC Cardiovasc Imaging 2: 458–468.
[10]  Mehran R, Dangas G, Mintz GS, Lansky AJ, Pichard AD, et al. (2000) Atherosclerotic plaque burden and CK-MB enzyme elevation after coronary interventions : intravascular ultrasound study of 2256 patients. Circulation 101: 604–610.
[11]  Watabe H, Sato A, Akiyama D, Kakefuda Y, Adachi T, et al. (2012) Impact of coronary plaque composition on cardiac troponin elevation after percutaneous coronary intervention in stable angina pectoris: a computed tomography analysis. J Am Coll Cardiol 59: 1881–1888.
[12]  Kodama T, Kondo T, Oida A, Fujimoto S, Narula J (2012) Computed tomographic angiography-verified plaque characteristics and slow-flow phenomenon during percutaneous coronary intervention. JACC Cardiovasc Interv 5: 636–643.
[13]  Uetani T, Amano T, Kunimura A, Kumagai S, Ando H, et al. (2010) The association between plaque characterization by CT angiography and post-procedural myocardial infarction in patients with elective stent implantation. JACC Cardiovasc Imaging 3: 19–28.
[14]  Gibbons RJ, Balady GJ, Bricker JT, Chaitman BR, Fletcher GF, et al. (2002) ACC/AHA 2002 guideline update for exercise testing: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines). Circulation 106: 1883–1892.
[15]  Zhao L, Zhang Z, Fan Z, Yang L, Du J (2011) Prospective versus retrospective ECG gating for dual source CT of the coronary stent: comparison of image quality, accuracy, and radiation dose. Eur J Radiol 77: 436–442.
[16]  Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M Jr, et al. (1990) Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol 15: 827–832.
[17]  Kitagawa T, Yamamoto H, Ohhashi N, Okimoto T, Horiguchi J, et al. (2007) Comprehensive evaluation of noncalcified coronary plaque characteristics detected using 64-slice computed tomography in patients with proven or suspected coronary artery disease. Am Heart J 154: 1191–1198.
[18]  Mantel N (1963) Chi-Square Tests with One Degree of Freedom Extensions of the Mantel- Haenszel Procedure. J Am Stat Assoc 58(303): 690–670.
[19]  van Gaal WJ, Ponnuthurai FA, Selvanayagam J, Testa L, Porto I, et al. (2009) The Syntax score predicts peri-procedural myocardial necrosis during percutaneous coronary intervention. Int J Cardiol 135: 60–65.
[20]  Bose D, von Birgelen C, Zhou XY, Schmermund A, Philipp S, et al. (2008) Impact of atherosclerotic plaque composition on coronary microembolization during percutaneous coronary interventions. Basic Res Cardiol 103: 587–597.
[21]  Ewence AE, Bootman M, Roderick HL, Skepper JN, McCarthy G, et al. (2008) Calcium phosphate crystals induce cell death in human vascular smooth muscle cells: a potential mechanism in atherosclerotic plaque destabilization. Circ Res 103: e28–34.
[22]  Iakovou I, Mintz GS, Dangas G, Abizaid A, Mehran R, et al. (2003) Increased CK-MB release is a "trade-off" for optimal stent implantation: an intravascular ultrasound study. J Am Coll Cardiol 42: 1900–1905.
[23]  Zemanek D, Branny M, Martinkovicova L, Hajek P, Maly M, et al.. (2013) Effect of seven-day atorvastatin pretreatment on the incidence of periprocedural myocardial infarction following percutaneous coronary intervention in patients receiving long-term statin therapy. A randomized study. Int J Cardiol: 2013 Apr 2015.
[24]  Schmermund A, Achenbach S, Budde T, Buziashvili Y, Forster A, et al. (2006) Effect of intensive versus standard lipid-lowering treatment with atorvastatin on the progression of calcified coronary atherosclerosis over 12 months: a multicenter, randomized, double-blind trial. Circulation 113: 427–437.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133