Herz

, Volume 40, Issue 3, pp 502–506 | Cite as

Link between aortic valve sclerosis and myocardial no-reflow in ST-segment elevation myocardial infarction

  • L. Korkmaz
  • H. Erkan
  • M.T. Ağaç
  • E. Pelit
  • H. Bektas
  • Z. Acar
  • I. Gurbak
  • F. Kara
  • Ş. Çelik
e-Herz: Original article

Abstract

Objective

The“no-reflow” phenomenon is associated with a worse prognosis at follow-up for patients with acute ST-segment elevation myocardial infarction (STEMI). Predicting and preventing no-reflow is therefore a crucial step in improving the prognosis of STEMI patients. The purpose of this study was to investigate the association between aortic valve sclerosis (AVS) and myocardial no-reflow in patients with STEMI.

Patients and methods

Patients with a first-time diagnosis of STEMI were enrolled consecutively. No-reflow was defined as a final TIMI 3 flow with a myocardial blush of grade < 2, temporary epicardial coronary no-reflow, and distal coronary occlusion. AVS was defined by echocardiography as thickening and calcification of the normal trileaflet aortic valve without obstruction to the left ventricular outflow.

Results

No-reflow developed in 41 patients. In univariate analysis, age, male gender, smoking, culprit lesion Syntax score (SX score), and hypertension were significantly associated with no-reflow. Multivariate binary logistic regression analyses demonstrated age [95 % confidence interval (CI), 1.024–1.096; p=0.001), AVS (95 % CI, 1.002–1.100; p=0.039], culprit lesion SX score (95 % CI, 1.08–1.021 p=0.008), and symptom-to-balloon time (95 % CI, 1.020–1.097; p=0.002) as independent determinants of myocardial no-reflow.

Conclusion

AVS was significantly and independently associated with myocardial no-reflow in STEMI patients.

Keywords

Aortic valve sclerosis Myocardial infarction No-reflow phenomenon ST-segment elevation myocardial infarction Prognosis 

Zusammenhang zwischen Aortenklappensklerose und No-Reflow-Phänomen bei ST-Strecken-Hebungs-Infarkt

Zusammenfassung

Ziel

Das No-Reflow-Phänomen, also das Sistieren des Blutflusses in den Koronarien, geht bei Patienten mit akutem ST-Strecken-Hebungs-Infarkt (STEMI) mit einer schlechteren Prognose im Verlauf einher. Die Vorhersage und Prävention des No-Reflow-Phänomens stellt daher einen entscheidenden Schritt zur Verbesserung der Prognose von Patienten mit STEMI dar. Ziel der vorliegenden Studie war es, den Zusammenhang zwischen Aortenklappensklerose (AVS) und myokardialem No-Reflow-Phänomen bei Patienten mit STEMI zu untersuchen.

Methoden

Patienten mit Erstdiagnose eines STEMI wurden nacheinander in die Studie aufgenommen. Das No-Reflow-Phänomen wurde definiert als letztlich erzielter Fluss des Grades 3 gemäß TIMI („thrombolysis in myocardial infarction“) mit myokardialem Anfärbungsgrad („blush grade“) < 2, temporäres epikardiales koronares No-Reflow-Phänomen und distaler Koronarverschluss. Zur echokardiographischen Definition einer AVS gehören die Verdickung und Verkalkung der normalen dreizipfligen Aortenklappe ohne Obstruktion des linksventrikulären Ausstroms.

Ergebnisse

Bei 41 Patienten fand sich ein No-Reflow-Phänomen. In der univariaten Analyse standen Alter, männliches Geschlecht, Rauchen, Syntax-Score der zugrunde liegenden Läsion (SX score) und Hypertonie in einem signifikanten Zusammenhang mit dem No-Reflow-Phänomen. Die multivariate binäre logistische Regressionsanalyse ergab Alter (95%-Konfidenzintervall, 95%-KI: 1,024–1,096; p: 0,001), AVS (95%-KI: 1,002–1,100; p: 0,039) und SX score (95%-KI: 1,08–1,021; p: 0,008) sowie Zeitdauer zwischen Symptom und Ballondilatation (95%-KI: 1,020–1,097; p: 0,002) als unabhängige Determinanten eines myokardialen No-Reflow-Phänomens.

Schlussfolgerung

Eine AVS stand in signifikanter und unabhängiger Weise mit einem myokardialen No-Reflow-Phänomen bei STEMI-Patienten in Zusammenhang.

Schlüsselwörter

Aortenklappensklerose Herzinfarkt Fehlende Perfusion ST-Strecken-Hebungs-Infarkt Prognose 

Notes

Compliance with ethical guidelines

Conflict of interest. L. Korkmaz, H. Erkan, M.T. Ağaç, M. Pelit, H. Bektas, Z. Acar, I. Gurbak, F. Kara, and Ş. Çelik state that there are no conflicts of interest. All studies on humans described in the present manuscript were carried out with the approval of the responsible ethics committee and in accordance with national law and the Helsinki Declaration of 1975 (in its current, revised form). Informed consent was obtained from all patients included in studies.

References

  1. 1.
    Schwartz BG, Kloner RA (2012) Coronary no reflow. J Mol Cell Cardiol 52(4):873–882CrossRefPubMedGoogle Scholar
  2. 2.
    Heusch G, Kleinbongard P, Böse D et al (2009) Coronary microembolization: from bedside to bench and back to bedside. Circulation 120(18):1822–1836CrossRefPubMedGoogle Scholar
  3. 3.
    Otto S, Seeber M, Fujita B et al (2012) Microembolization and myonecrosis during elective percutaneous coronary interventions in diabetic patients: an intracoronary Doppler ultrasound study with 2-year clinical follow-up. Basic Res Cardiol 107(5):289CrossRefPubMedGoogle Scholar
  4. 4.
    Magro M, Nauta ST, Simsek C et al (2012) Usefulness of the SYNTAX score to predict “no reflow” in patients treated with primary percutaneous coronary intervention for ST-segment elevation myocardial infarction. Am J Cardiol 109:601–606CrossRefPubMedGoogle Scholar
  5. 5.
    Valero SJ, Moreno R, Reyes RM et al (2008) Pharmacological approach of no- reflowphenomenon related with percutaneous coronary interventions. Cardiovasc Hematol Agents Med Chem (2):125–129CrossRefGoogle Scholar
  6. 6.
    Vignali L, Talanas G, Saia F et al (2007) Genetic association between the 1976T_C polymorphism in the adenosine A2 receptor and angiographic no-reflow phenomenon (abstr). Il giornale italiano di Cardiologia Invasiva 3(Suppl 1):109Google Scholar
  7. 7.
    Shah SJ, Ristow B, Ali S et al (2007) Acute myocardial infarction in patients with versus without aortic valve sclerosis and effect of statin therapy (from the Heart and Soul Study). Am J Cardiol 99:1128–1133CrossRefPubMedCentralPubMedGoogle Scholar
  8. 8.
    Antonini-Canterin F, Di Bello V, Di Salvo G et al (2009) Relation of carotid intima-media thickness and aortic valve sclerosis (from the ISMIR study [”Ispessimento Medio Intimale e Rischio Cardiovascolare”] of the Italian Society of Cardiovascular Echography). Am J Cardiol 103:1556–1561CrossRefPubMedGoogle Scholar
  9. 9.
    Korkmaz L, Adar A, Ata Korkmaz A et al (2012) Aortic knob calcification and coronary artery lesion complexity in non-ST-segment elevation acute coronary syndrome patients. Turk Kardiyol Dern Ars 40:606–611CrossRefPubMedGoogle Scholar
  10. 10.
    Korkmaz L, Adar A, Korkmaz AA et al (2012) Atherosclerosis burden and coronary artery lesion complexity in acute coronary syndrome patients. Cardiol J 19:295–300CrossRefPubMedGoogle Scholar
  11. 11.
    Jaffe R, Dick A, Strauss BH (2010) Prevention and treatment of microvascular obstruction-related myocardial injury and coronary no-reflow following percutaneous coronary intervention: a systematic approach. JACC Cardiovasc Interv 3:695–704CrossRefPubMedGoogle Scholar
  12. 12.
    Niccoli G, Cosentino N, Spaziani C et al (2011) New strategies for the management of no-reflow after primary percutaneous coronary intervention. Expert Rev Cardiovasc Ther 9:615–630CrossRefPubMedGoogle Scholar
  13. 13.
    Harrison RW, Aggarwal A, Ou FS et al (2013) Incidence and outcomes of no-reflow phenomenon during percutaneous coronary intervention among patients with acute myocardial infarction. Am J Cardiol 111:178–184CrossRefPubMedGoogle Scholar
  14. 14.
    Wong DT, Puri R, Richardson JD et al (2013) Myocardial ‘no-reflow’- Diagnosis, pathophysiology and treatment. Int J Cardiol doi:10.1016/j.ijcard.2012.12.049CrossRefGoogle Scholar
  15. 15.
    Magro M, Springeling T, Geuns RJ van, Zijlstra F (2013) Myocardial ‘no-reflow’ prevention. Curr Vasc Pharmacol 11:263–277PubMedGoogle Scholar
  16. 16.
    Kleinbongard P, Böse D, Baars T et al (2011) Vasoconstrictor potential of coronary aspirate from patients undergoing stenting of saphenous vein aortocoronary bypass grafts and its pharmacological attenuation. Circ Res 108(3):344–352CrossRefPubMedGoogle Scholar
  17. 17.
    Marzilli M, Orsini E, Marraccini P, Testa R (2000) Beneficial effects of intracoronary adenosine as an adjunct to primary angioplasty in acute myocardial infarction. Circulation 101:2154–2159CrossRefPubMedGoogle Scholar
  18. 18.
    Ishii H, Ichimiya S, Kanashiro M et al (2005) Impact of a single intravenous administration of nicorandil before reperfusion in patients with ST-segment-elevation myocardial infarction. Circulation 112:1284–1288CrossRefPubMedGoogle Scholar
  19. 19.
    Malmberg K, Ryde’n L, Efendic S et al (1995) Randomized trial of insulin glucose infusion followed by subcutaneous insulin treatment in diabetic patients with acute myocardial infarction (DIGAMI study): effects on mortality at 1 year. J Am Coll Cardiol 26:56–65CrossRefGoogle Scholar
  20. 20.
    Montalescot G, Antoniucci D, Kastrati A et al (2007) Abciximab in primary coronary stenting of ST-elevation myocardial infarction: a European meta-analysis on individual patients’ data with long-term follow-up. Eur Heart J 28:443–449CrossRefPubMedGoogle Scholar
  21. 21.
    Svilaas T, Vlaar PJ, Horst IC van der et al (2008) Thrombus aspiration during primary percutaneous coronary intervention. N Engl J Med 358:557–567CrossRefPubMedGoogle Scholar
  22. 22.
    Skyschally A, Leineweber K, Gres P et al (2006) Coronary microembolization. Basic Res Cardiol 101:373–382CrossRefPubMedGoogle Scholar
  23. 23.
    Sui SJ, Ren MY, Xu FY, Zhang Y (2007) A high association of aortic valve sclerosis detected by transthoracic echocardiography with coronary arteriosclerosis. Cardiology 108:322–330CrossRefPubMedGoogle Scholar
  24. 24.
    Soydinc S, Davutoglu V, Dundar A, Aksoy M (2006) Relationship between aortic valve sclerosis and the extent of coronary artery disease in patients undergoing diagnostic coronary angiography. Cardiology 106:277–282CrossRefPubMedGoogle Scholar
  25. 25.
    Huczek Z, Kochman J, Filipiak KJ et al (2005) Mean platelet volume on admission predicts impaired reperfusion and long-term mortality in acute myocardial infarction treated with primary percutaneous coronary intervention. J Am Coll Cardiol 46:284–290CrossRefPubMedGoogle Scholar
  26. 26.
    Sucu M, Davutoglu V, Sari I et al (2010) Relationship between platelet indices and aortic valve sclerosis. Clin Appl Thromb Hemost 16:563–567CrossRefPubMedGoogle Scholar
  27. 27.
    Erdoğan T, Cetin M, Kocaman SA et al (2013) Aortic valve sclerosis is a high predictive marker of systemic endothelial dysfunction in hypertensive patients. Herz [Epub ahead of print]Google Scholar
  28. 28.
    Zhao J, Yang Y, you S et al (2007) Carvedilol preserves endothelial junctions and reduces myocardial no-reflow after acute myocardial infarction and reperfusion. Int J Cardiol 115:334–341CrossRefPubMedGoogle Scholar
  29. 29.
    Ngo DT, Sverdlov AL, Willoughby SR et al (2009) Determinants of occurrence of aortic sclerosis in an aging population. JACC Cardiovasc Imaging 2:919–927CrossRefPubMedGoogle Scholar
  30. 30.
    Pasceri V, Pristipino C, Pelliccia F et al (2005) Effects of the nitric oxide donor nitroprusside on no-reflow phenomenon during coronary interventions for acute myocardial infarction. Am J Cardiol 95:1358–1361CrossRefPubMedGoogle Scholar
  31. 31.
    Sverdlov AL, Ngo DT, Chapman MJ et al (2011) Pathogenesis of aortic stenosis: not just a matter of wear and tear. Am J Cardiovasc Dis 1:185–199PubMedCentralPubMedGoogle Scholar

Copyright information

© Urban & Vogel 2014

Authors and Affiliations

  • L. Korkmaz
    • 1
  • H. Erkan
    • 1
  • M.T. Ağaç
    • 1
  • E. Pelit
    • 1
  • H. Bektas
    • 1
  • Z. Acar
    • 1
  • I. Gurbak
    • 1
  • F. Kara
    • 1
  • Ş. Çelik
    • 1
  1. 1.Department of CardiologyAhi Evren Cardiovascular and Thoracic Surgery Training and Research HospitalTrabzonTurkey

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