As indicated by the findings of our study, SII obtained from complete blood cell subtypes provides relevant information according to LVH in patients with hypertension. The level of SII of the patients with LVH is higher than that of the normal ventricular geometry, and its predictive efficacy is more than those of PLR and NLR; which indicates the presence of the LVH. Furthermore, we detected that SII can be an independent and prominent sign of LVH. Thus, we can sugest that this research is the first attempt to reveal the relationship of SII with LVH in patients with hypertension.
Hypertension is admitted as the widely seen risk factor for cardiovascular disease. Despite extensive studies, the exact mechanism underlying hypertension remains to be elucidated. Although low-grade inflammation is considered to have connection with the emergence of hypertension, it has not been clarified whether inflammation is a cause or a consequence of hypertension [14–16].
Many studies indicate that immune cell infiltration of the endothelial, renal and central nervous systems, as well as their counterparts of oxidative stress, activated renin-angiotensin mechanism and increased sympathetic tone can considerably cause the emergence of hypertension [17, 18]. Studies have demonstrated that immune-modulatory cells infiltrating the heart, perivascular adipose tissue or kidneys contribute to the dysfunction of these organs and may cause hypertension [19, 20]. Therefore, inflammation participates in many conditions that contribute to the development of high blood pressure. Several studies have shown a positive relationship between hypertension and high WBC count, CRP, and IL-6 levels [21, 22]. In another experimental study, it was performed that mice or rats without functional T and B lymphocytes were protected from experimental hypertension [23, 24]. Many studies targeting blood cells such as lymphocytes, monocytes, and neutrophils as well as targeting inflammation indicate their contribution to vascular remodeling and hypertension [25–27].
Being another sign of chronic low-grade systemic inflammation, C-reactive protein has been used in different populations as an indicator of poor cardiovascular outcomes, beyond traditional risk factors. CRP levels are also usually high in patients with hypertension, and high CRP can be detected before the development of arterial hypertension and may be a predictive factor for the disease [28, 29]. Platelet-to-lymphocyte ratio (PLR) and neutrophil-to-lymphocyte ratio (NLR), which also lead to inflammation, have been clearly hypothesized by recent researches that they can act as strong predictive and prognostic markers for the presence of hypertension. Several cross-sectional studies revealed that PLR and NLR were positively linked by hypertension [30, 31]. The results that we obtained through this study are compatible on a large scale with the findings pointed out by those researches. Likewise, we determined that PLR, NLR and SII were remarkably high in the group with LVH in comparison to the group without LVH.
The presence of inflammatory markers is often associated with other HT-mediated organ damage, particularly LVH, and disseminated atherosclerotic vascular disease. Therefore, understanding the relationships between LVH and low-grade markers of systemic inflammation and endothelial disfunction is clinically and prognostically important [32, 33]. LVH is a hypertensive target organ damage that independently and clearly predicts the risk of cardiovascular disease that leads to mortality and morbidity, thus making the diagnose of LVH significant in terms of studies and clinical practise. Although the pathophysiological mechanisms underlying the progression from LVH to the development of cardiovascular events are still unclear, accelerated atherosclerosis due to systemic inflammation and endothelial dysfunction may be cited as the cause. When examined in this context, studies have shown that the cells of inflammation and immune system are heavily effective in the development of coronary atherosclerosis. While the evaluation of the above-mentioned cells alone gives important results about the development of atherosclerosis, these results have become even more important with the use of some ratios such as PLR, NLR and SII. All these rates are presented as the markers for atherosclerosis and are associated with the prevalence of coronary artery disease (CAD) and poor cardiovascular outcomes. Recently, it has been suggested that SII, developed by Hu et al, may provide more valuable information about inflammation because it includes 3 cell types [34]. There are studies in the literature demonstrating that PLR, NLR, and SII can be used as new predictors of prognosis and mortality in patients with CAD [11, 35], but studies on the superiority of these indices over each other are limited. In another research conducted by Erdoğan et al, it has been revealed that SII can be a strong predictor of coronary obstruction, considered hemodynamically significant, in comparison to PLR and NLR, and can serve as an independent predictor of coronary artery occlusion, which may cause a heart attack [36]. In another study, we showed that SII can estimate the grade of high thrombus burden in patients more accurately than PLR and NLR [37]. The findings of our study clearly revealed that the predictability of SII in terms of LVH was stronger than NLR and PLR.
LVH is usually identified as the left ventricular mass index, and it occurs subsequent to the increase of chronic blood pressure and volume overload, which results in cardiac fibrosis and cardiomyocyte hypertrophy. Hypertrophic geometric patterns (eccentric hypertrophy, concentric hypertrophy) have close relationship with poor prognosis for patients with hypertension [38]. In a recent research conveyed by Afşin et al, NLR was found to be higher in eccentric and concentric LV geometric patterns [31]. The outcomes of our study are compatible with the findings revealed by the above-mentioned research. Similarly, we determined that SII was higher in the groups with eccentric and concentric LVH, in comparison to those having normal configuration.
The outcomes of our research should be evaluated with some considerations based on the following limitations. Initially, the study was conducted on relatively a small sample, and we did not record any follow-up data because of the cross-sectional design of the study. Secondly, we included only one measurement of admission complete blood count and calculation of SII in the analysis. As with any new prognostic indicator, the normal reference range for SII was not systematically investigated and established in this study. Finally, despite of numerous researches that revealed association of LVH with cytokines, we couldn’t handle cytokines in our research at all.
In conclusion, our study results suggested that SII can independently predict the presence of LVH, which has not been reported previously. This research revealed that SII could be a strong and cost-effective marker which is easily taken from complete blood cell subtypes for judging LVH. The result of our study showed possible links between SII, NLR, PLR, and LVH in clients having hypertension. Additionally, this predictor of SII is stronger than PLR and NLR, which serve as prominent signs of inflammation. SII can assist researchers predict which clients can have high-risk of LVH and provide a new preventive strategy for LVH by modulating hypertension.