Monocyte count to high-density lipoprotein ratio predicts occlusion of the infarct-related artery in STEMI

Yıl 2017, Cilt: 8 Sayı: 3, 91 - 96, 01.06.2017

Regayip Zehir Taner Sarak Suleyman Barutcu Vedat Şimşek Muhammed Karadeniz Hüseyin Kandemir

https://doi.org/10.18663/tjcl.287859

Öz

 Aim: Patency of infarct-related
artery (IRA) in patients with ST-segment elevation myocardial infarction
(STEMI) before primary percutaneous coronary intervention (pPCI) is associated
with better clinical outcomes. However, there were limited data regarding the
predictors of IRA patency before pPCI in the setting of STEMI. We intended to
evaluate the association of monocyte count to high-density lipoprotein ratio
(MHR) with IRA patency in STEMI.

Material and Methods: A total of
726 patients were recruited. IRA patency was determined by the thrombolysis in
myocardial infarction (TIMI) flow grade. According TIMI flow grade in the IRA
before PCI, the study population was divided into two groups as TIMI 0,1 or 2
group (occluded IRA, n=624) and TIMI 3 group (patent IRA, n=102). Blood samples
were collected on admission to calculate MHR. Of all patients, 92 (20.4%)
patients revealed pre-pPCI TIMI 3 flow in IRA.

Results: The MHR was significantly
higher in occluded IRA group (22.4 ± 5.4 vs 17.8 ± 6.9, P < 0.001). Glucose,
troponin I, and platelet to lymphocyte ratio (PLR) levels were also higher in
occluded IRA group (P < 0.05). Multivariate regression analysis demonstrated
the MHR on admission (odds ratio [OR]: 1.191; 95% confidence interval [CI]:
1.116-1.272, P < 0.001) and pre-hospital use of prasugrel or ticagrelor (OR:
7.045; CI: 1.687-29.414, P = 0.007) as independent predictors of IRA patency.

Conclusion: IRA
patency is more frequently found in patients having received fast acting

antiplatelet
therapy before pPCI and a higher MHR value independently predicts it.

Anahtar Kelimeler

monocyte count to high-density lipoprotein ratio, ST-segment elevation myocardial infarction, infarct-related artery patency

Monosit sayısı /yüksek yoğunluklu lipoprotein oranı, STEMI'de enfarktla ilişkili arterin oklüzyonunu öngörür

Öz

Amaç:
ST segment yükselmeli miyokard enfarktüsü (STEMI) olan hastalarda, primer
perkütan koroner girişim (pPKI) öncesi enfarktüs ilişkili arter acıklığı daha
iyi klinik sonuçlar ile ilişkilidir. Bununla birlikte, STEMI ortamında pPKI
öncesinde IRA açıklığının öngördürücüleri ile ilgili sınırlı veri vardır. STEMI'de
monosit sayısı /yüksek yoğunluklu lipoprotein oranı (MHR) ile enfarktla
ilişkili arterin acıklığı arasındaki ilişkiyi değerlendirmek istedik.

Gereç
ve Yöntemler: Toplam 726 hasta çalışmaya alındı. IRA açıklığı, miyokard
enfarktüsünde tromboliz (TIMI)  akım
sınıflaması ile belirlendi. PKI öncesi IRA'da TIMI akım derecesine göre çalışma
popülasyonu, TIMI 0,1 veya 2 grup (tıkalı IRA, n=624) ve TIMI 3 grubu (patent
IRA, n=102) olmak üzere iki gruba ayrıldı. MHR hesaplamak için basvuruda kan
örnekleri toplandı. Tüm hastaların 92'sinde (%20,4) IRA'da pre-pPKI TIMI 3
akımı vardı.

Bulgular:
MHR, tıkanan IRA grubunda anlamlı derecede yüksekti (22,4 ± 5,4'e karşılık 17,8
± 6,9, P < ,001). Tıkalı IRA grubunda, glikoz, troponin İ ve
trombosit/lenfosit oranı (PLR) düzeyleri de yüksekti (P < 0.05). Çok
değişkenli regresyon analizinde, başvuru sırasındaki MHR değeri (odds oranı
[1,391]; %95 güven aralığı [CI]: 1,116-1,272, P < 0,001) ve prasugrel veya
tikagrelorun hastane öncesi kullanımı (OR: 7,045; CI:1,687-29,414, P = 0,007)
IRA açıklığının bağımsız öngördürücüleri olarak bulundu.

Sonuçlar:
IRA açıklığı, pPKI öncesi hızlı etkili antitrombosit tedavi  alan hastalarda daha sık görülmektedir ve
daha düşük bir MHR değeri IRA açıklığını bağımsız bir şekilde tahmin eder.

Anahtar Kelimeler

monosit sayısı / yüksek yoğunluklu lipoprotein oranı, ST segment yükselmesi miyokard enfarktüsü, infarkla ilişkili arter açıklığı

Kaynakça

• 1. Stone GW, Cox D, Garcia E, et al. Normal flow (TIMI-3) before mechanical reperfusion therapy is an independent determinant of survival in acute myocardial infarction: analysis from the primary angioplasty in myocardial infarction trials. Circulation. 2001; 104: 636-641.
• 2. Westerhout CM, Bonnefoy E, Welsh RC, Steg PG, Boutitie F, Armstrong PW. The influence of time from symptom onset and reperfusion strategy on 1-year survival in ST-elevation myocardial infarction: a pooled analysis of an early fibrinolytic strategy versus primary percutaneous coronary intervention from CAPTIM and WEST. Am Heart J 2011; 161:283e290.
• 3. Birdsall HH, Green DM, Trial J, et al. Complement C5a, TGF-beta 1, and MCP-1, in sequence, induce migration of monocytes into ischemic canine myocardium within the first one to five hours after reperfusion. Circulation 1997; 95:684–92.
• 4. Reddy VS, Bui QT, Jacobs JR, et al. Relationship between serum low-density lipoprotein cholesterol and in hospital mortality following acute myocardial infarction (the lipid paradox). Am J Cardiol. 2015; 115:557-62.
• 5. Çiçek G, Kundi H, Bozbay M, Yayla C, Uyarel H. The relationship between admission monocyte HDL-C ratio with short-term and long-term mortality among STEMI patients treated with successful primary PCI. Coron Artery Dis. 2016; 27:176-84.
• 6. Kundi H, Kiziltunc E, Cetin M, et al. Association of monocyte/HDL-C ratio with SYNTAX scores in patients with stable coronary artery disease. Herz. 2016 Jan 11. [Epub ahead of print].
• 7. Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Circulation. 2012; 126: 2020–35.
• 8. The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group. N Engl J Med. 1985; 312 :932–6.
• 9. Hilgendorf I, Swirski FK, Robbins CS. Monocyte fate in atherosclerosis. Arterioscler Thromb Vasc Biol. 2015;3 5: 272–9.
• 10. Bath PM, Gladwin A-M, Martin JF. Human monocyte characteristics are altered in hypercholesterolaemia. Atherosclerosis 1991; 90:175–181.
• 11. Moreno PR, Purushothaman KR, Fuster V, O’Connor WN. Intimomedial interface damage and adventitial inflammation is increased beneath disrupted atherosclerosisin the aorta: implications for plaque vulnerability. Circulation 2002; 105: 2504–11.
• 12. Navab M, Reddy ST, Van Lenten BJ, et al. High-density lipoproteinand 4F peptide reduce systemic inflammation by modulating intestinal oxidized lipid metabolismnovel hypotheses and review of literature. Arterioscler Thromb Vasc Biol 2012; 32: 2553– 2560.
• 13. Karabacak M, Kahraman F, Sert M, et al. Increased plasma monocyte chemoattractant protein-1 levels in patients with isolated low high-density lipoprotein cholesterol. Scand J Clin Lab Invest. 2015; 75: 327-32.
• 14. 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: 240-4.
• 15. Cetin EHO, 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: 967–77.
• 16. Balta S, Celik T, Ozturk C, et al. The relation between monocyte to HDL ratio and no-reflow phenomenon in the patients with acute ST-segment elevation myocardial infarction. Am J Emerg Med. 2016; 34: 1542-7.
• 17. Rakowski T, Dudek D, Dziewierz A, et al. Impact of infarct-related artery patency before primary PCI on outcome in patients with STsegment elevation myocardial infarction: the HORIZONS-AMI trial. Eurointervention. 2013; 8:1307-1314.
• 18. Yayla Ç, Akboğa MK, Canpolat U, et al. Platelet to Lymphocyte Ratio Can be a Predictor of Infarct-Related Artery Patency in Patients With ST-Segment Elevation Myocardial Infarction. Angiology. 2015; 66: 831-6.
• 19. Authors/Task Force members. Windecker S, Kolh P, Alfonso F, et al. 2014 ESC/EACTS guidelines on myocardial revascularization: the Task Force on myocardial revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS) developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J 2014; 35: 2541.