Systemic immune-inflammation index is associated with increased carotid intima-media thickness in hypertensive patients

ABSTRACT

Background

Arterial hypertension causes cardiovascular adverse events mainly through endothelial dysfunction, atherosclerosis, and inflammation. Carotid intima-media thickness (CIMT) is a marker of subclinical atherosclerosis and endothelial dysfunction. Systemic immune-inflammation index (SII) reflects systemic inflammatory and immunity status. This index has strong prognostic value in malignancy and recently was demonstrated to be associated with adverse events in cardiovascular diseases. We aimed to interrogate the relationship between SII and CIMT in patients with hypertension.

Methods

A total of 215 consecutive hypertensive patients were included in the study. CIMT of all patients was obtained by B-mode arterial doppler ultrasound. SII was obtained by the following formula: (platelet × neutrophil/lymphocyte ratio) from admission complete blood count. Patients were divided into two groups by means of CIMT is above or below the value of 0.9 mm. SII and demographic characteristics of patients were compared between groups.

Results

Increased CIMT was detected in 55 (25.6%) of hypertensive patients. The patients with increased CIMT were older and had higher neutrophil count (p < .001), neutrophil to lymphocyte ratio (NLR) (p < .001), C-reactive protein (CRP) (p = .047), CRP to albumin ratio (CAR) (p = .044) and SII (p < .001) Advanced age (OR: 1.054; 95% CI: 1.015–1.095; p = .006), NLR (OR: 3.213; 95% CI: 1.577–6.546; p = .001), and SII (OR: 3.906; 95% CI: 1.887–8.086; p < .001) were independent predictors of increased CIMT in multivariable logistic regression analysis.

Conclusion

SII was an independent predictor of elevated CIMT in hypertensive patients. Preventive approaches for future atherosclerotic cardiovascular diseases can be developed in those with higher SII level.

KEYWORDS:

• Arterial hypertension (AH)
• carotid intima-media thickness (CIMT)
• systemic immune-inflammation index (SII)
• atherosclerosis
• Inflammation

Disclosure statment

The authors declare that they have no conflict of interest.

Additional information

Funding

This research received no grant from any funding agency in the public, commercial or not-for-profit sectors.