Dergiler / İstanbul Kuzey Klinikleri / 2018 / Cilt: 5 - Sayı: 3

Systemic inflammatory activation in patients with acute coronary syndrome secondary to nonatherosclerotic spontaneous coronary artery dissection

Sayfa
186–194
Yayın Tarihi
2022-10-18
DOI
—
🏛️Bu makalenin bibliyografik verileri ve tam metin bağlantısı DergiPark üzerinden sağlanmıştır.
DergiPark Kaydı ↗
✨

Yapay Zeka Hızlı Bakış & Çıkarımlar

AI Insight
⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

Neutrophil–lymphocyte ratio (NLR) and C-reactive protein (CRP) levels were only significantly higher in the NA-SCADACS group [2.01 (1.54–6.17) for NLR and 0.70 (0.13–2.70) for CRP] than in the controls [1.55 (1.27–2.13), p=0.03 for NLR and0.15 (0.10–0.43), p=0.049 for CRP]; however, there were no differences between the NA-SCAD-ACS and CAD-ACS groups [1.91(1.41–2.78) for NLR and 0.41 (0.09–1.10) for CRP, p>0.05 for both comparisons] regarding all tested parameters.CONCLUSION: The degree of inflammatory activation in NA-SCAD-ACS patients was similar to, or even greater than, that inCAD-ACS patients; thus, suggesting a role of inflammation in the pathophysiology of NA-SCAD-ACS.

📌 3 Maddede Bu Makale

🎯
Amaç & Hipotez:OBJECTIVE: Pathological studies have suggested that local inflammation, particularly eosinophilic infiltration of the adventitia, could be related to nonatherosclerotic spontaneous coronary artery dissection (NA-SCAD).
📊
Temel Bulgular & Veri:Our aim was to investigate systemic inflammatory activationin patients with an acute coronary syndrome (ACS) secondary to NA-SCAD.METHODS: The institutional electronic medical database was reviewed, and 22 patients with NA-SCAD-ACS were identifiedafter the review.
💡
Sonuç & Katkı:Neutrophil–lymphocyte ratio (NLR) and C-reactive protein (CRP) levels were only significantly higher in the NA-SCADACS group [2.01 (1.54–6.17) for NLR and 0.70 (0.13–2.70) for CRP] than in the controls [1.55 (1.27–2.13), p=0.03 for NLR and0.15 (0.10–0.43), p=0.049 for CRP]; however, there were no differences between the NA-SCAD-ACS and CAD-ACS groups [1.91(1.41–2.78) for NLR and 0.41 (0.09–1.10) for CRP, p>0.05 for both comparisons] regarding all tested parameters.CONCLUSION: The degree of inflammatory activation in NA-SCAD-ACS patients was similar to, or even greater than, that inCAD-ACS patients; thus, suggesting a role of inflammation in the pathophysiology of NA-SCAD-ACS.
🔬Tür:Literatür & Derleme Çalışması
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Alan Parametreleri

Abstract

OBJECTIVE: Pathological studies have suggested that local inflammation, particularly eosinophilic infiltration of the adventitia, could be related to nonatherosclerotic spontaneous coronary artery dissection (NA-SCAD). However, the role of systemicinflammation in the pathogenesis of NA-SCAD remains unknown. Our aim was to investigate systemic inflammatory activationin patients with an acute coronary syndrome (ACS) secondary to NA-SCAD.METHODS: The institutional electronic medical database was reviewed, and 22 patients with NA-SCAD-ACS were identifiedafter the review. Furthermore, 30 random patients with CAD-ACS and 30 random subjects without any history of CAD or ACSwith demographic and clinical characteristics similar to those of NA-SCAD-ACS patients were identified from the institutionaldatabase to be included in the study.RESULTS: Patients with NA-SCAD-ACS and those with CAD-ACS both had higher white blood cell and neutrophil counts thancontrols. Neutrophil–lymphocyte ratio (NLR) and C-reactive protein (CRP) levels were only significantly higher in the NA-SCADACS group [2.01 (1.54–6.17) for NLR and 0.70 (0.13–2.70) for CRP] than in the controls [1.55 (1.27–2.13), p=0.03 for NLR and0.15 (0.10–0.43), p=0.049 for CRP]; however, there were no differences between the NA-SCAD-ACS and CAD-ACS groups [1.91(1.41–2.78) for NLR and 0.41 (0.09–1.10) for CRP, p>0.05 for both comparisons] regarding all tested parameters.CONCLUSION: The degree of inflammatory activation in NA-SCAD-ACS patients was similar to, or even greater than, that inCAD-ACS patients; thus, suggesting a role of inflammation in the pathophysiology of NA-SCAD-ACS.

🔖

Bu Makaleye Atıf Yap

KARATAŞ, M. B., GÜNGÖR, B., UZUN, A. O., ONUK, T., ÇALIK, A. N., BEZGİN, T., TANIK, V. O., BOLCA, O., GÜVENÇ, T. S., CANGA, Y. (2022). Systemic inflammatory activation in patients with acute coronary syndrome secondary to nonatherosclerotic spontaneous coronary artery dissection. İstanbul Kuzey Klinikleri, Cilt: 5 - Sayı: 3, 186–194. https://ajindex.com/articles/551511

📄 Tam Metin PDF Okuyucu

📄

PDF görüntüleyici hazırlanıyor...

Kaynakça (15)

  1. Isner JM, Donaldson RF, Fortin AH, Tischler A, Clarke RH. Attenuation of the media of coronary arteries in advanced atherosclerosis. Am J Cardiol 1986;58:937–9
  2. Aqel RA, Zoghbi GJ, Iskandrian A. Spontaneous coronary artery dissection, aneurysms, and pseudoaneurysms: a review. Echocardiography 2004;21:175–82
  3. Saw J, Aymong E, Sedlak T, Buller CE, Starovoytov A, Ricci D, et al. Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes. Circ Cardiovasc Interv 2014;7:645–55
  4. Robinowitz M, Virmani R, McAllister HA. Spontaneous coronary artery dissection and eosinophilic inflammation: a cause and effect relationship? Am J Med 1982;72:923–8
  5. Bateman AC, Gallagher PJ, Vincenti AC. Sudden death from coronary artery dissection. J Clin Pathol 1995;48:781–4
  6. Kajihara H, Tachiyama Y, Hirose T, Takada A, Saito K, Murai T, et al. Eosinophilic coronary periarteritis (vasospastic angina and sudden death), a new type of coronary arteritis: report of seven autopsy cases and a review of the literature. Virchows Arch 2013;462:239–48
  7. Kobayashi M, Cohle SD. A case of sudden cardiac death due to eosinophilic coronary periarteritis: possible significance of coexisting atherosclerosis and eosinophilic inflammation of the esophagus. Cardiovasc Pathol 2016;25:67–71
  8. Crea F, Liuzzo G. Pathogenesis of Acute Coronary Syndromes. J Am Coll Cardiol 2013;61:1–11
  9. Libby P. Inflammation in atherosclerosis. Nature 2002;420:868–74
  10. Berk BC, Weintraub WS, Alexander RW. Elevation of C-reactive protein in “active” coronary artery disease. Am J Cardiol 1990;65:168–72
  11. Tomoda H, Aoki N. Prognostic value of C-reactive protein levels within six hours after the onset of acute myocardial infarction. Am Heart J 2000;140:324–8
  12. Liuzzo G, Biasucci LM, Gallimore JR, Grillo RL, Rebuzzi AG, Pepys MB, et al. The prognostic value of C-reactive protein and serum amyloid a protein in severe unstable angina. N Engl J Med 1994;331:417– 24
  13. Liuzzo G, Biasucci LM, Gallimore JR, Caligiuri G, Buffon A, Rebuzzi AG, et al. Enhanced inflammatory response in patients with preinfarction unstable angina. J Am Coll Cardiol 1999;34:1696–703
  14. Biasucci LM, Vitelli A, Liuzzo G, Altamura S, Caligiuri G, Monaco C, et al. Elevated levels of interleukin-6 in unstable angina. Circulation 1996;94:874–7
  15. Barron HV, Harr SD, Radford MJ, Wang Y, Krumholz HM. The association between white blood cell count a