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Evaluation of the neutrophil-lymphocyte ratio in newly diagnosed nondiabetic hypertensive patients with ascending aortic dilatation

Evaluation of the neutrophil-lymphocyte ratio in newly diagnosed nondiabetic hypertensive patients with ascending aortic dilatation

Blood Pressure Monitoring 21(4): 238-243

Ascending aortic dilatation (AAD), more often encountered in hypertensive individuals compared with normotensive individuals, is an important cause of mortality in adults. Neutrophil-to-lymphocyte ratio (NLR), as an oxidative stress and proinflammatory marker, has recently emerged as a useful indicator to predict cardiovascular risk and adverse outcomes. The aim of our study was to investigate the relationship between NLR and AAD in patients with hypertension. A total of 135 newly diagnosed and untreated hypertensive patients were enrolled in this study. Ninety-three consecutive hypertensive patients with AAD and 42 consecutive hypertensive patients with normal ascending aortic diameter were recruited into the study by comprehensive transthoracic echocardiography. NLR was calculated using the complete blood count. In the comparison of laboratory parameters between the hypertensive patients with AAD and hypertensive patients with normal ascending aortic diameter, NLR was found to be statistically significantly higher in the aortic dilatation group than in the control group (2.72±1.1 vs. 1.87±0.5, P<0.001). There was a statistically significant positive correlation between the ascending aortic diameter and NLR (r=0.524, P<0.001). According to multiple logistic regression analysis (ascending aortic diameter set as the dependent variable), smoking [odds ratio (OR): 1.57, 95% confidence interval (CI): 1.14-1.98, P=0.008], NLR (OR: 2.01, 95% CI: 1.57-3.25, P<0.001), and γ-glutamyl transferase (OR: 1.98, 95% CI: 1.59-2.74, P=0.001) were found to be independent predictors of AAD. NLR as a marker of chronic low-grade inflammation may play a role in the pathogenesis of aneurysm of the ascending aorta in hypertensive patients.

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Accession: 057818509

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PMID: 27003944

DOI: 10.1097/MBP.0000000000000187

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