OBJECTIVE: Inflammation plays an important role in the pathogenesis of atherosclerosis. The lymphocyte-to-monocyte ratio (LMR) may reflect a systemic inflammatory status. We investigated the association between the LMR and coronary artery disease (CAD) in patients with stable angina pectoris.
PATIENTS AND METHODS: A total of 221 consecutive patients who had been routinely referred for coronary angiography, for stable angina pectoris and 72 patients with normal coronary arteries were included in the present study. We analyzed the relation between the LMR and the angiographic severity of CAD. The SYNTAX score (SxS) was used for assessing the severity of coronary atherosclerosis.
RESULTS: The neutrophil-to-lymphocyte ratio (N/L ratio), platelet size distribution width (PDW), neutrophil and uric acid levels were significantly higher in the stable angina pectoris group than in the control group. The LMR was significantly lower in the stable angina pectoris group than in the control group (4.5±3.2 vs. 6±2.9, p < 0.001). The MPV/L ratios were similar in both groups. Patients with elevated SYNTAX scores (>32) had lower LMR values (3.2±1.5 vs. 4.6±3, p = 0.002). The monocyte count/HDL-C ratio (MHR) was significantly higher in patients with stable CAD than in the control group (0.015±0.008 vs 0.009±0.004, p < 0.001); however, it was similar in the higher SYNTAX score (>32) and lower SYNTAX score groups (0.018±0.007 vs. 0.014±0.008, p = 0.056). Using multivariate logistic regression analysis, we found that only the LMR was an independent predictor of the high SYNTAX scores in patients with stable angina pectoris.
CONCLUSIONS: The LMR, an inexpensive and easily measurable laboratory variable, is significantly associated with the presence of CAD and high SYNTAX scores in patients with stable angina pectoris.Free PDF Download
To cite this article
N. Kose, F. Akin, T. Yildirim, G. Ergun, I. Altun
The association between the lymphocyte-to-monocyte ratio and coronary artery disease severity in patients with stable coronary artery disease
Eur Rev Med Pharmacol Sci
Vol. 23 - N. 6