pp 1–5 | Cite as

Decreased platelet-to-lymphocyte ratio as predictor of thrombogenesis in nonvalvular atrial fibrillation

  • Zuo K. 
  • Yang X. Email author
Original articles



Inflammation plays a key role in the progression of atrial fibrillation and its related prothrombotic state. The platelet-to-lymphocyte ratio (PLR) is an easily obtainable biomarker of inflammatory burden. Decreased left atrial appendage flow velocity (LAA-FV) reflects blood stasis, and left atrial strain is a manifestation of atrial remodeling. This study examined the role of PLR in reflecting decreased LAA-FV and its correlation with impaired left atrial strain.


In 54 patients with nonvalvular atrial fibrillation, LAA-FV and left atrial strain were measured by echocardiography. The PLR was calculated from a complete blood count.


The PLR was lower in the group of patients with decreased LAA-FV (84.22 [IQR, 69.87–98.17 cm/s] vs. 103.27 [IQR, 90.37–127.16 cm/s]; p = 0.018). PLR was predictive of decreased LAA-FV with a sensitivity of 66.7% and a specificity of 83.3%. In a receiver operator characteristic curve analysis, using a cut-off value of 88.16, the area under the curve for PLR as a predictor of decreased LAA-FV was 0.726 (p = 0.018). Furthermore, the patients with a PLR of < 88.16 had a lower left atrial strain than those with a PLR of > 88.16 (0.38 vs. 0.77, p = 0.02).


The PLR was lower in patients with nonvalvular atrial fibrillation and with a decreased LAA-FV. Its correlation with left atrial strain might indicate the role of inflammation in the progression of atrial remodeling and in the prothrombotic state.


Atrial remodeling Stroke Inflammation Platelet-to-lymphocyte ratio Strain 

Verminderter Thrombozyten-Lymphozyten-Quotient als Prädiktor der Thrombogenese bei nichtvalvulärem Vorhofflimmern



Entzündungsprozesse spielen eine wesentliche Rolle bei der Progression des Vorhofflimmerns und dem damit verbundenen erhöhten Thromboserisiko. Der Thrombozyten-Lymphozyten-Quotient („platelet-to-lymphocyte ratio“, PLR) ist ein einfach bestimmbarer Biomarker der Entzündungslast. Eine verminderte Flussgeschwindigkeit im linken Herzohr („left atrial appendage flow velocity“, LAA-FV) ist ein Hinweis auf eine Stase des Bluts, linksatriale Deformation ein Zeichen für atriales Remodeling. In der vorliegenden Studie wurde die Rolle des PLR als Hinweis auf eine verminderte LAA-FV und sein Zusammenhang mit einer beeinträchtigten linksatrialen Deformation untersucht.


Bei 54 Patienten mit nichtvalvulärem Vorhofflimmern wurden LAA-FV und linksatriale Deformation mittels Echokardiographie bestimmt. Der PLR wurde aus dem großen Blutbild errechnet.


Der PLR war in der Gruppe der Patienten mit verminderter LAA-FV niedriger (84,22 [Interquartilsabstand, „interquartile range“, IQR: 69,87–98,17 cm/s] vs. 103,27 [IQR: 90,37–127,16 cm/s]; p = 0,018). Mit einer Sensitivität von 66,7% und einer Spezifität von 83,3% war der PLR ein Prädiktor für eine verminderte LAA-FV. In einer ROC-Analyse („receiver operator characteristic curve“) betrug bei Verwendung eines Grenzwerts von 88,16 die Fläche unter der Kurve für den PLR als Prädiktor einer verminderten LAA-FV 0,726 (p = 0,018). Darüber hinaus bestand bei den Patienten mit einem PLR von < 88,16 eine geringere linksatriale Deformation als bei jenen mit einem PLR von > 88,16 (0,38 vs. 0,77; p = 0,02).


Ein niedrigerer PLR lag bei Patienten mit nichtvalvulärem Vorhofflimmern und einer verminderten LAA-FV vor. Sein Zusammenhang mit der linksatrialen Deformation könnte einen Hinweis auf die Bedeutung von Entzündungsprozessen bei der Progression des atrialen Remodelings und bei erhöhtem Thromboserisiko darstellen.


Atriales Remodeling Schlaganfall Entzündung Thrombozyten-Lymphozyten-Quotient Deformation 


Compliance with ethical guidelines

Conflict of interest

K. Zuo and X. Yang declare that they have no competing interests.

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1975 Helsinki declaration and its later amendments or comparable ethical standards. Informed consent was obtained from all individual participants included in the study.


  1. 1.
    Van den Berg MP, van Gelder IC, van Veldhuisen DJ (2002) Impact of atrial fibrillation on mortality in patients with chronic heart failure. Eur J Heart Fail 4:571–575CrossRefPubMedGoogle Scholar
  2. 2.
    Delgado V, Di Biase L, Leung M et al (2017) Structure and function of the left atrium and left atrial appendage. J Am Coll Cardiol 70:3157–3172CrossRefPubMedGoogle Scholar
  3. 3.
    Klesen A, Jakob D, Emig R, Kohl P, Ravens U, Peyronnet R (2018) Cardiac fibroblasts active players in (atrial) electrophysiology? Herzschrittmacherther Elektrophysiol 29(1):62–69CrossRefPubMedGoogle Scholar
  4. 4.
    Lee JM, Shim J, Uhm J‑S (2014) Impact of increased orifice size and decreased flow velocity of left atrial appendage on stroke in nonvalvular atrial fibrillation. Am J Cardiol 113:963–969CrossRefPubMedGoogle Scholar
  5. 5.
    Pagola J, González-Alujas T, Flores A et al (2014) Left atria strain is a surrogate marker for detection of atrial fibrillation in cryptogenic strokes. Stroke 45(8):164–166CrossRefGoogle Scholar
  6. 6.
    Altintas O, Tasal A, Niftaliyev E, Kucukdagli OT, Asil T (2016) Association of platelet-to-lymphocyte ratio with silent brain infarcts in patients with paroxysmal atrial fibrillation. Neurol Res. CrossRefPubMedGoogle Scholar
  7. 7.
    Lang RM, Badano LP, Mor-Avi V et al (2015) Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American society of echocardiography and the European association of cardiovascular imaging. Eur Heart J Cardiovasc Imaging 16(3):233–270CrossRefPubMedGoogle Scholar
  8. 8.
    Zuo K, Sun L, Yang X, Lyu X, Li K (2017) Correlation between cardiac rhythm, left atrial appendage flow velocity, and CHA2DS2-VASc score: study based on transesophageal echocardiography and 2‑dimensional speckle tracking. Clin Cardiol 40(2):120–125CrossRefPubMedGoogle Scholar
  9. 9.
    Vianna-Pinton R, Moreno CA, Baxter CM, Lee KS, Tsang TS, Appleton CP (2009) Two-dimensional speckle-tracking echocardiography of the left atrium. Feasibility and regional contraction and relaxation differences in normal subjects. J Am Soc Echocardiogr 22:299–305CrossRefPubMedGoogle Scholar
  10. 10.
    Pollick C, Taylor D (1991) Assessment of left trial appendage function by transesophageal echocardiography. Implications for the development of thrombus. Circulation 84:223–231CrossRefPubMedGoogle Scholar
  11. 11.
    Zabalgoitia M, Halperin J, Pearce LA, Blackshear JL, Asinger RW, Hart RG (1998) Transesophageal echocardiographic correlates of clinical risk of thromboembolism in nonvalvular atrial fibrillation. Stroke prevention in atrial fibrillation III investigators. J Am Coll Cardiol 31:1622–1626CrossRefPubMedGoogle Scholar
  12. 12.
    Shiroshita-Takeshita A, Brundel BJJM, Nattel S (2005) Atrial fibrillation: basic mechanisms, remodeling and triggers. J Interv Card Electrophysiol 13:181–193CrossRefPubMedGoogle Scholar
  13. 13.
    King JB, Azadani PN, Suksaranjit P et al (2017) Left atrial fibrosis and risk of cerebrovascular and cardiovascular events in patients with atrial fibrillation. J Am Coll Cardiol 70:1311–1321CrossRefPubMedGoogle Scholar
  14. 14.
    Zghaib T, Keramati A, Chrispin J et al (2018) Multimodal examination of atrial fibrillation substrate correlation of left atrial bipolar voltage using multi-electrode fast automated mapping, point-by-point mapping, and magnetic resonance image intensity ratio. JACC Clin Electrophysiol 4(1):59–68CrossRefPubMedGoogle Scholar
  15. 15.
    Marrouche NF, Wilber D, Hindricks G et al (2014) Association of atrial tissue fibrosis identified by delayed enhancement MRI and atrial fibrillation catheter ablation: the DECAAF study. JAMA 311(5):498–506CrossRefPubMedGoogle Scholar
  16. 16.
    Leung M, van Rosendael PJ, Abou R et al (2017) Left atrial function to identify patients with atrial fibrillation at high risk of stroke: new insights from a large registry. Eur Heart J. CrossRefPubMedGoogle Scholar
  17. 17.
    Kadappu KK, Abhayaratna K, Boyd A et al (2016) Independent echocardiographic markers of cardiovascular involvement in chronic kidney disease: the value of left atrial function and volume. J Am Soc Echocardiogr 29:359–367CrossRefPubMedGoogle Scholar
  18. 18.
    Fukushima K, Fukushima N, Kato K et al (2016) Correlation between left atrial appendage morphology and flow velocity in patients with paroxysmal atrial fibrillation. Eur Heart J Cardiovasc Imaging 17:59–66PubMedGoogle Scholar
  19. 19.
    Conway DS, Buggins P, Hughes E, Lip GY (2004) Relationship of interleukin-6 and C‑reactive protein to the prothrombotic state in chronic atrial fibrillation. J Am Coll Cardiol 43:2075–2082CrossRefPubMedGoogle Scholar
  20. 20.
    Lip GY, Patel JV, Hughes E, Hart RG (2007) High-sensitivity C‑ reactive protein and soluble CD40 ligand as indices of inflammation and platelet activation in 880 patients with nonvalvular atrial fibrillation: relationship to stroke risk factors, stroke risk stratification schema, and prognosis. Stroke 38:1229–1237CrossRefPubMedGoogle Scholar
  21. 21.
    Falk E (2006) Pathogenesis of atherosclerosis. J Am Coll Cardiol 47(8 Suppl):C7–C12CrossRefPubMedGoogle Scholar
  22. 22.
    Temiz A, Gazi E, Güngör Ö et al (2014) Platelet/lymphocyte ratio and risk of in-hospital mortality in patients with ST-elevated myocardial infarction. Med Sci Monit 20:660–665CrossRefPubMedPubMedCentralGoogle Scholar
  23. 23.
    Smyth SS, McEver RP, Weyrich AS et al (2009) Platelet functions beyond hemostasis. J Thromb Haemost 7:1759–1766CrossRefPubMedGoogle Scholar
  24. 24.
    Henn V, Slupsky JR, Gräfe M et al (1998) CD40 ligand on activated platelets triggers an inflammatory reaction of endothelial cells. Nature 391:591–594CrossRefPubMedGoogle Scholar
  25. 25.
    Langer HF, Gawaz M (2008) Platelet-vessel wall interactions in atherosclerotic disease. Thromb Haemost 99:480–486CrossRefPubMedGoogle Scholar
  26. 26.
    Kurtul A, Yarlioglues M, Murat S et al (2014) Usefulness of the platelet-to-lymphocyte ratio in predicting angiographic reflow after primary percutaneous coronary intervention in patients with acute ST-segment elevation myocardial infarction. Am J Cardiol 114:342–347CrossRefPubMedGoogle Scholar
  27. 27.
    Azab B, Shah N, Akerman M, McGinn JT Jr (2012) Value of platelet/lymphocyte ratio as a predictor of all-cause mortality after non-ST-elevation myocardial infarction. J Thromb Thrombolysis 34:326–334CrossRefPubMedGoogle Scholar

Copyright information

© Springer Medizin Verlag GmbH, ein Teil von Springer Nature 2018

Authors and Affiliations

  1. 1.Heart Center & Beijing Key Laboratory of HypertensionBeijing Chaoyang Hospital, Capital Medical UniversityBeijingChina

Personalised recommendations