Özge ÇAKMAK KARAASLAN, Firdevs Ayşenur EKİZLER, Murat Oğuz ÖZİLHAN, Cem ÇOTELİ, Sefa ÜNAL, Orhan MADEN

Akut Miyokardit Hastalarında Monosit/HDL Kolestrol Oranı ile Klinik Sonlanımlar Arasındaki İlişki

Amaç: Miyokardit, kalp kasının enflamatuvar bir hastalığıdır. Enflamasyon ve oksidatif stresin miyokardit patogenezinde önemli bir rol oynadığı bilinmektedir. Bu çalışmanın amacı akut miyokardit hastalarında klinik sonlanım noktaları ile monosit/yüksek yoğunluklu lipoprotein (HDL) oranı arasında ilişkininin değerlendirilmesidir. Gereç ve Yöntem: Mart 2009-Mart 2017 yılları arasında, akut miyokardit tanısı ile kardiyak manyetik rezonans çekilen ardışık 156 hasta çalışmaya alındı. Hastalar klinik sonlanım noktalarına göre ikiye ayrıldı. Klinik sonlanım noktası malign aritmi, takip süresince kardiyovasküler ölüm gerçekleşmesi ve yeni başlangıçlı kalp yetmezliği olarak tanımlandı. Bulgular: Klinik sonlanım izlenen hastalarda yüksek C-reaktif protein seviyesi, düşük yüksek yoğunluklu lipoprotein kolesterol ve glukoz değerleri, azalmış ejeksiyon fraksiyonu izlendi (hepsi için p

The Relationship Between Monocyte/HDL Cholesterol Ratio and Clinical Outcomes in Acute Myocarditis Patients

Objectives: Myocarditis is an inflammatory disease of the heart muscle. Inflammation and oxidative stress are known to play an important role in myocarditis pathogenesis. The aim of this study is to evaluate the relationship between clinical endpoints and monocyte/high-density lipoprotein (HDL) ratio in acute myocarditis patients. Materials and Methods: Between March 2009 and March 2017, 156 consecutive patients who underwent cardiac magnetic resonance with the diagnosis of acute myocarditis were included in the study. The patients were divided into two groups according to clinical endpoints. The clinical endpoint was defined as malignant arrhythmia, cardiovascular death during follow-up, and new-onset heart failure. Results: High C-reactive protein level, low high density lipoprotein cholesterol and glucose levels, and low ejection fraction were found in patients with clinical endpoints. (p

PDF

___

1. Fung G, Luo H, Qiu Y, et al. Myocarditis. Circ Res. 2016;118:496-514.
2. Watanabe M, Panetta GL, Piccirillo F, et al. Acute Epstein-Barr related myocarditis: An unusual but life-threatening disease in an immunocompetent patient. J Cardiol Cases. 2019;21:137-140.
3. Rose NR. Viral myocarditis. Curr Opin Rheumatol. 2016;28:383-389.
4. Ancuta P, Wang J, Gabuzda D. CD16+ monocytes produce IL-6, CCL2, and matrix metalloproteinase-9 upon interaction with CX3CL1-expressing endothelial cells. J Leukoc Biol. 2006;80:1156-1164.
5. Biswas SK. Does the Interdependence between Oxidative Stress and Inflammation Explain the Antioxidant Paradox? Oxid Med Cell Longev. 2016;2016:5698931.
6. Parthasarathy S, Barnett J, Fong LG. High-density lipoprotein inhibits the oxidative modification of low-density lipoprotein. Biochim Biophys Acta. 1990;1044:275-283.
7. Murphy AJ, Woollard KJ, Hoang A, et al. High-density lipoprotein reduces the human monocyte inflammatory response. Arterioscler Thromb Vasc Biol. 2008;28:2071-2077.
8. Kanbay M, Solak Y, Unal HU, et al. Monocyte count/HDL cholesterol ratio and cardiovascular events in patients with chronic kidney disease. Int Urol Nephrol. 2014;46:1619-1625.
9. Canpolat U, Çetin EH, Cetin S, et al. Association of Monocyte-to- HDL Cholesterol Ratio with Slow Coronary Flow is Linked to Systemic Inflammation. Clin Appl Thromb Hemost. 2016;22:476-482.
10. Cetin EH, Cetin MS, Canpolat U, et al. Monocyte/HDL-cholesterol ratio predicts the definite stent thrombosis after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction. Biomark Med. 2015;9:967-977.
11. Canpolat U, Aytemir K, Yorgun H, et al. The role of preprocedural monocyteto- high-density lipoprotein ratio in prediction of atrial fibrillation recurrence after cryoballoon-based catheter ablation. Europace. 2015;17:1807-1815.
12. Karataş MB, Çanga Y, Özcan KS, et al. Monocyte to high-density lipoprotein ratio as a new prognostic marker in patients with STEMI undergoing primary percutaneous coronary intervention. Am J Emerg Med. 2016;34:240-244.
13. Caforio AL, Pankuweit S, Arbustini E, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J. 2013;34:2636-2648.
14. Abdel-Aty H, Zagrosek A, Schulz-Menger J, et al. Delayed enhancement and T2-weighted cardiovascular magnetic resonance imaging differentiate acute from chronic myocardial infarction. Circulation. 2004;109:2411-2416.
15. Aletras AH, Tilak GS, Natanzon A, et al. Retrospective determination of the area at risk for reperfused acute myocardial infarction with T2-weighted cardiac magnetic resonance imaging: histopathological and displacement encoding with stimulated echoes (DENSE) functional validations. Circulation. 2006;113:1865-1870.
16. Abdel-Aty H, Boyé P, Zagrosek A, et al. Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: comparison of different approaches. J Am Coll Cardiol. 2005;45:1815-1822.
17. Laissy JP, Messin B, Varenne O, et al. MRI of acute myocarditis: a comprehensive approach based on various imaging sequences. Chest. 2002;122:1638-1648.
18. Miller DD, Holmvang G, Gill JB, et al. MRI detection of myocardial perfusion changes by gadolinium-DTPA infusion during dipyridamole hyperemia. Magn Reson Med. 1989;10:246-255.
19. Friedrich MG, Sechtem U, Schulz-Menger J, et al. Cardiovascular magnetic resonance in myocarditis: A JACC White Paper. J Am Coll Cardiol. 2009;53:1475-1487.
20. Fabre A, Sheppard MN. Sudden adult death syndrome and other nonischaemic causes of sudden cardiac death. Heart. 2006;92:316-320.
21. Shao L, Ma A, Figtree G, et al. Combination Therapy With Coenzyme Q10 and Trimetazidine in Patients With Acute Viral Myocarditis. J Cardiovasc Pharmacol. 2016;68:150-154.
22. Kanda T, Takahashi T. Interleukin-6 and cardiovascular diseases. Jpn Heart J. 2004;45:183-193.
23. Medeiros NI, Fares RC, Franco EP, et al. Differential Expression of Matrix Metalloproteinases 2, 9 and Cytokines by Neutrophils and Monocytes in the Clinical Forms of Chagas Disease. PLoS Negl Trop Dis. 2017;11:0005284.
24. Fares RC, Gomes Jde A, Garzoni LR, et al. Matrix metalloproteinases 2 and 9 are differentially expressed in patients with indeterminate and cardiac clinical forms of Chagas disease. Infect Immun. 2013;81:3600-3608.
25. Bautista-López NL, Morillo CA, López-Jaramillo P, et al. Matrix metalloproteinases 2 and 9 as diagnostic markers in the progression to Chagas cardiomyopathy. Am Heart J. 2013;165:558-566.
26. Bracamonte-Baran W, Čiháková D. Cardiac Autoimmunity: Myocarditis. Adv Exp Med Biol. 2017;1003:187-221.
27. Soran H, Schofield JD, Durrington PN. Antioxidant properties of HDL. Front Pharmacol. 2015;6:222.
28. Ganjali S, Gotto AM Jr, Ruscica M, et al. Monocyte-to-HDL-cholesterol ratio as a prognostic marker in cardiovascular diseases. J Cell Physiol. 2018;233:9237-9246.
29. Ekizler FA, Cay S. A novel marker of persistent left ventricular systolic dysfunction in patients with peripartum cardiomyopathy: monocyte countto- HDL cholesterol ratio. BMC Cardiovasc Disord. 2019;19:114.
30. Kundi H, Gok M, Kiziltunc E, et al. Relation Between Monocyte to High- Density Lipoprotein Cholesterol Ratio With Presence and Severity of Isolated Coronary Artery Ectasia. Am J Cardiol. 2015;116:1685-1689.
31. Ammirati E, Veronese G, Brambatti M, et al. Fulminant Versus Acute Nonfulminant Myocarditis in Patients With Left Ventricular Systolic Dysfunction. J Am Coll Cardiol. 2019;74:299-311.
32. Berg J, Kottwitz J, Baltensperger N, et al. Cardiac Magnetic Resonance Imaging in Myocarditis Reveals Persistent Disease Activity Despite Normalization of Cardiac Enzymes and Inflammatory Parameters at 3-Month Follow-Up. Circ Heart Fail. 2017;10:004262.
33. Ammirati E, Cipriani M, Moro C, et al. Clinical Presentation and Outcome in a Contemporary Cohort of Patients With Acute Myocarditis: Multicenter Lombardy Registry. Circulation. 2018;138:1088-1099.