Association of Neutrophil-Lymphocyte Ratio with the Presence and Severity of Degenerative Aortic Valve Stenosis

  • Murathan Küçük
  • Mustafa Uçar
  • Fulya Avcı Demir
  • Atakan Yanıkoğlu
  • Aytül Belgi Yildirim
Keywords: Aortic stenosis, inflammation, neutrophils


Objective: In different studies, it has been shown that degenerative aortic stenosis and atherosclerosis had a common pathogenic mechanism. The goal of this study was to examine the association between NLR and the presence and severity of degenerative aortic valve stenosis.Methods: Echocardiographic data (from May 2011 to September 2013) of our cardiology department was reviewed retrospectively. After evaluation according to exclusion criteria’s, a total of 103 patients with degenerative AS and a control group of 35 age- and gender- matched patients who had normal echocardiographic findings were included in the study.Results: The level of NLR was highest in severe AS. The neutrophil-lymphocyte ratio was significantly higher in severe AS group than for the mild and moderate AS group (1.95±0.42, 2.31±0.69, 2.67±0.73; p<0.001 respectively). In comparison of the degenerative aortic stenosis groups with the control group, NLR in all aortic stenosis groups was found to be significantly higher than the control group (p<0.001). In addition, there was a statistically significant correlation between NLR and transaortic peak pressure gradient in patients with degenerative aortic stenosis (r: 0.626, p<0.001).Conclusion: The NLR, which is an inexpensive and readily available marker of chronic inflammation, may be useful in predicting the presence and severity of degenerative aortic stenosis.


Dweck MR, Boon NA, Newby DE. Calcific aortic stenosis: A disease of the valve and the myocardium. J Am Coll Cardiol. 2012;60:1854–63.

Mazzone A, Epistolato MC, De Caterina R, Starti S, Vittorini S , Sbrana S, et al. Neoangiogenesis, T-lymphocyte infiltration, and heat shock protein- 60 are biological hallmarks of an immunomediated inflammatory process in end-stage calcified aortic valve stenosis. J Am Coll Cardiol. 2004, 43:1670-6.

Rajamannan NM, Gersh B, Bonow RO. Calcific aortic stenosis: from bench to the bedside – emerging clinical and cellular concepts. Heart. 2003, 89:801-5.

Freeman RV, Otto CM.Spectrum of calcific aortic valve disease: pathogenesis, disease progression, and treatment strategies. Circulation . 2005, 111:3316-6.

Bhat T, Teli S, Rijal J, Bhat H, Raza M , Khoueiry G, et al. Neutrophil to lymphocyte ratio and cardiovascular diseases: a review. Expert Rev Cardiovasc Ther. 2013;11 :55-9.

Kaya MG. Inflammation and coronary artery disease: as a new biomarker neutrophil/lymphocyte ratio [in Turkish]. Turk Kardiyol Dern Ars. 2013;41 :191-92.

Losi MA, Brevetti G, Schiano V, Barbati G, Parisi V, Contaldi C, et al. Aortic valve sclerosis in patients with peripheral and/or coronary arterial disease. Echocardiography. 2010;27:608–12.

O'Brien KD, Reichenbach DD, Marcovina SM, Kuusisto J , Alpers CE, Otto CM , et al. Apolipoprotein B, (a), and E accumulate in the morphologically early lesion of degenerative valvular aortic stenosis. Arterioscler Thromb. 1996, 16:523-32.

Helske S, Lindstedt KA, Laine M, Mayranpaa M, Werkkala K, Lommi J, et al. Induction of local angiotensin II-producing systems in stenotic aortic valves. J Am Coll Cardiol. 2004;44:1859–66.

Pohle K, Maffert R, Ropers D , Moshage W, Stilianakis N, Daniel WG ,et al. Progression of aortic valve calcification: association with coronary atherosclerosis and cardiovascular risk factors. Circulation. 2001;104:1927–32.

O’Brien KD. Pathogenesis of calcific aortic valve disease: a disease process comes of age (and a good deal more). Arterioscler Thromb Vasc Biol .2006;26:1721–8.

Otto CM, Kuusisto J, Reichenbach DD, Gown AM, O’Brien KD. Characterization nof the early lesion of ‘degenerative’ valvular aortic stenosis. Histological and immunohistochemical studies. Circulation.1994;90:844–53.

Gunduz H, Akdemir R, Binak E, Tamer A, Keser N , Uyan C, et al. Can serum lipid and CRP levels predict the "severity" of aortic valve stenosis? Acta Cardiol .2003, 58:321-6.

Galante A, Pietroiusti A, Vellini M, Piccola P, Possati G , De Bonis M ,et al. C-reactive protein is increased in patients with degenerative aortic valvular stenosis. J Am Coll Cardiol. 2001, 38:1078-82.

Sanchez PL, Mazzone A. C-reactive protein in degenerative aortic valve stenosis. Cardiovasc Ultrasound. 2006, 4:24.

Kaya H, Ertas F, Islamoglu Y, Atılgan ZA, Çil H, Çalışkan A, et al. Association between neutrophil to lymphocyte ratio and severity of coronary artery disease . Clin Appl Thromb Hemost. 2014; 20 : 50-4

Dogan M, Akyel A, Cimen T, Bilgin M, Sunman H, Kasapkara HA , et al. Relationship between neutrophil to lymphocyte ratio and slow coronary flow. Clin Appl Thromb Hemost. 2015 ; 21 : 251-4.

Heymans S, Hirsch E, Anker SD, Aukrust P, Balligand JL, Cohen-Tervaert JW, et al. Inflammation as a therapeutic target in heart failure? A scientific statement from the Translational Research Committee of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2009;11:119–29

Uthamalingam S, Patvardhan EA, Subramanian S, Ahmed W, Martin W, Daley M ,et al. Utility of the neutrophil to lymphocyte ratio in predicting long-term outcomes in acute decompensated heart failure. Am J Cardiol. 2011;107;433-8

Avci A, Elnur A, Göksel A, Serdar F, Servet I ,Atilla K, et al. The Relationship between Neutrophil/Lymphocyte Ratio and Calcific Aortic Stenosis. Echocardiography. 2014; 31 : 1031-5

Polat N, Yildiz A, Yuksel M, Bilik MZ, Aydın M, Acet H, et al. Association of Neutrophil-Lymphocyte Ratio With the Presence and Severity of Rheumatic Mitral Valve Stenosis. Clin Appl Thromb Hemost. 2014; 20: 793-8

Sonmez O, Ertem FU, Vatankulu MA, Erdogan E, Tasal A, Kucukbuzcu S, et al. Novel fibro-inflammation markers in assessing left atrial remodeling in non-valvular atrial fibrillation. Med Sci Monit. 2014; 20: 463-70.

Original Research