Changes in non-culprit lesion severity on follow-up coronary angiography after primary percutaneous coronary ıntervention

Yıl 2021, Cilt: 11 Sayı: 4, 537 - 542, 31.07.2021

Fuat Caner , Selahattin Turen , Aydın Yıldırım

https://doi.org/10.16899/jcm.851281

Öz

Aim: Non-culprit lesion severity has often been exaggerated at the time of acute ST segment elevation myocardial infarction (STEMI). We aimed to determine changes in non-culprit lesions severity on follow-up coronary angiography (CAG) and independent predictors of these changes.
Material and Methods: We retrospectively evaluated the changes in non-culprit lesion stenosis on follow-up CAG which was done within 2 months after primary percutaneous coronary intervention (P-PCI) in patients presenting with STEMI.
Results: 154 patients were included in this study and 207 non-culprit lesions (percentage diameter stenosis (PDS) ≥50%) were compared using quantitative coronary analyses (QCA). Minimal lumen diameter (1.30 ± 0.38 mm vs. 1.54 ± 0.46 mm, p<0.001) and reference vessel diameter (2.88 ± 0.66 mm vs. 2.92 ± 0.64 mm, p=0.001) were increased significantly and PDS (54.49 ± 9.38 vs. 47.5 ± 11.17, p<0.001) and percentage area stenosis (78.38 ± 8.65 vs. 71.29 ± 11.84, p= <0.001) were decreased significantly. There was no significant change in lesion length (13.52 ± 5.59 mm vs. 13.25 ± 5.31 mm, p= 0.078). 65 (31.4%) of these significant lesions (PDS ≥50% by QCA) were regressed (less than 50%) on follow-up CAG. In multivariable analyses; current smoking, clopidogrel use after the P-PCI and history of coronary artery disease were the independent predictors of decrease in PDS.
Conclusion: Significant exaggeration of non-culprit lesion stenosis severity occurs at the time of acute STEMI.

Anahtar Kelimeler

Primary percutaneous coronary intervention, multi-vessel disease, non-culprit lesion, quantitative coronary analysis

Primer perkütan koroner girişimlerde sorumlu olmayan lezyonların kontrol koroner anjiyografide değişimleri

Öz

Amaç: Akut ST segment yükselmeli miyokard enfarktüsü (STEMI) sırasında sorumlu olmayan lezyonlar sıklıkla olduklarından daha ciddi görünürler. Kontrol koroner anjiyografi (KAG)'de sorumlu olmayan lezyonların şiddetindeki değişiklikleri ve bu değişikliklerin bağımsız prediktörlerini belirlemeyi amaçladık.
Gereç ve Yöntem: STEMI ile başvuran ve primer perkütan koroner girişimden (P-PKG) sonraki 2 ay içinde kontrol KAG yapılan hastalarda sorumlu olmayan lezyonlardaki değişiklikleri retrospektif olarak değerlendirdik.
Bulgular: Bu çalışmaya 154 hasta dahil edildi ve 207 (yüzde çap darlığı (YÇD) ≥50%) sorumlu olmayan lezyon kantitatif koroner analizler (QCA) kullanılarak karşılaştırıldı. Minimal lümen çapı (1,30 ± 0,38 mm'ye karşı 1,54 ± 0,46 mm, p <0,001) ve referans damar çapı (2,88 ± 0,66 mm'ye karşı 2,92 ± 0,64 mm, p = 0,001) önemli ölçüde arttı ve YÇD (54,49 ± 9,38'e karşı 47.5 ± 11.17, p <0.001) ve yüzde alan darlığı (78.38 ± 8.65 vs. 71.29 ± 11.84, p= <0.001) anlamlı olarak azaldı. Lezyon uzunluğunda anlamlı değişiklik izlenmedi (13,52 ± 5,59 mm'ye karşı 13,25 ± 5,31 mm, p= 0,078). Bu önemli lezyonların 65'i (% 31.4) (QCA'ya göre YÇD ≥% 50) kontrol KAG'de geriledi (% 50'den az). Çok değişkenli analizlerde; mevcut sigara kullanımı, P-PKG'den sonra klopidogrel kullanımı ve koroner arter hastalığı öyküsü, YÇD'deki azalmanın bağımsız prediktörleri idi.
Sonuç: Akut STEMI sırasında sorumlu olmayan lezyonlardaki darlıkların derecesi önemli ölçüde daha artmış olarak izlenmektedir.

Anahtar Kelimeler

Primer perkütan koroner girişim, çoklu damar hastalığı, sorumlu olmayan lezyon, kantitatif koroner analiz

Kaynakça

• Mandelzweig L, Battler A, Boyko V, et al. The second Euro Heart Survey on acute coronary syndromes: characteristics, treatment, and outcome of patients with ACS in Europe and the Mediterranean Basin in 2004. Eur Heart J. 2006;27:2285-93.
• Yeh RW, Sidney S, Chandra M, et al. Population trends in the incidence and outcomes of acute myocardial infarction. N Engl J Med. 2010;362:2155-65.
• Steg PG, James SK, Atar D, Badano LP, Blömstrom-Lundqvist C, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012;33(20):2569-619.
• O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;127:e362-425.
• Widimsky P, Holmes DR Jr. How to treat patients with ST-elevation acute myocardial infarction and multi-vessel disease? Eur Heart J 2011;32:396-403.
• Cavender MA, Milford-Beland S, Roe MT, Peterson ED, Weintraub WS, Rao SV. Prevalence, predictors, and in-hospital outcomes of non-infarct artery intervention during primary percutaneous coronary intervention for ST-segment elevation myocardial infarction (from the National Cardiovascular Data Registry). Am J Cardiol 2009;104:507–513.
• Kahn JK. Evidence for dynAMEc coronary vasoconstriction of non-infarct vessels during acute myocardial infarction. Cathet Cardiovasc Diagn. 1995;36(4):371-3.
• Hanratty CG, Koyama Y, Rasmussen HH, Nelson GI, Hansen PS, Ward MR. Exaggeration of nonculprit stenosis during acute myo¬cardial infarction: implication for immediate multivessel revascu-larization. J Am Coll Cardiol. 2002;40:911-6.
• Gibson CM, Ryan KA, Murphy SA, et al. Impaired coronary blood flow in nonculprit arteries in the setting of acute myocardial infarction. The TIMI Study Group.Thrombolysis In Myocardial Infarction.J Am Coll Cardiol 1999;34: 974–82.
• Glass CK, Witztum JL. Atherosclerosis: the road ahead. Cell 2001;104:503–516.
• Libby P. Current concepts of the pathogenesis of the acute coronary syndromes. Circulation 2001;104:365–372
• Falk E, Shah PK, Fuster V. Atherothrombosis and thrombosis-prone plaques. In: Fuster V, Alexander RW, O’Rourke RA, et al., eds. Hurst’s the Heart, 2004. New York: McGraw-Hill, pp. 1123–39.
• Bogaty P, Hackett D, Davies G, Maseri A. Vasoreactivity of the culprit lesion in unstable angina. Circulation 1994;90:5-11.
• Remme WJ, Kruijssen DA, Look MP, Bootsma, de Leeuw PW: Systemic and cardiac neuroendocrine activation and severity of myocardial ischemia in humans. J Am Coll Cardiol 1994;23:82-91
• Slavíková J, Kuncová J, Topolcan O. Plasma catecholamines and ischemic heart disease. Clin Cardiol 2007;30:326–330.
• Wald DS, Morris JK, Wald NJ, et al. Randomized trial of preventive angioplasty in myocardial infarction. N Engl J Med. 2013 Sep 19;369 (12):1115-23.
• Chesebro JH, Knatterud G, Roberts R, et al. Thrombolysis in Myocardial Infarction (TIMI) Trial. Phase I: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge. Circulation 1987;76:142-5.
• Salvatore Davide Tomasello, Luca Costanzo, Alfredo Ruggero Galassi. Quantitative Coronary Angiography in the Interventional Cardiology, Advances in the Diagnosis of Coronary Atherosclerosis, Prof.Suna Kirac (Ed.), 2011. ISBN: 978-953-307-286-9, InTech, Available from: http://www.intechopen.com/books/advances-in-the-diagnosis-of-coronary-atherosclerosis/quantitativecoronary-angiography-in-the-interventional-cardiology
• Sahin M, Demir S, Kocabay G, et al. Coronary vessel diameters during and after primary percutaneous coronary artery intervention. Herz 2014;39(4):515-21.
• Cristea E, Stone GW, Mehran R et al (2011) Chang¬es in reference vessel diameter in ST-segment el¬evation myocardial infarction after primary per¬cutaneous coronary intervention: implications for appropriate stent sizing. Am Heart J 2011;162(1):173–7.
• Libby P. Inflammation in atherosclerosis. Nature 2002;420: 868–74.
• Davies MJ. The pathophysiology of acute coronary syndromes. Heart 2000;83:361–66.
• Nicod P, Rehr R, Winniford MD, Campbell WB, Firth BG, Hillis LD. Acute systemic and coronary hemodynamic and serologic responses to cigarette smoking in long term smokers with atherosclerotic coronary artery disease. J Am Coll Cardiol 1984;4(5):964–71.
• Puranik R, Celermajer DS. Smoking and endothelial function. Progress in Cardiovascular Diseases 2003;45(6):443–58.