# The Non-Dipping Blood Pressure Phenotype Is Independently Linked to Systemic Inflammation and Atherogenic Burden

## TL;DR

This study finds that non-dipping blood pressure is linked to inflammation and atherogenic factors, even in people without metabolic disease.

## Contribution

The study identifies independent associations between non-dipping blood pressure and systemic inflammation and atherogenic burden in individuals without overt metabolic disease.

## Key findings

- Non-dippers had higher LDL cholesterol, AIP, and SIRI compared to dippers.
- SIRI and AIP were independently associated with non-dipping in hierarchical regression models.
- Combined inflammatory-metabolic assessment improved model explanatory power.

## Abstract

Background: A non-dipping blood pressure pattern, defined as an insufficient nocturnal decline in systolic blood pressure, is associated with increased cardiovascular risk and target organ damage. While metabolic abnormalities contribute to circadian blood pressure dysregulation, the independent roles of systemic inflammation and atherogenic burden in individuals without overt metabolic disease remain insufficiently characterized. We aimed to evaluate the associations of systemic inflammatory response index (SIRI) and atherogenic index of plasma (AIP) with nocturnal blood pressure pattern. Methods: This retrospective cross-sectional study included 469 adults who underwent 24 h ambulatory blood pressure monitoring (ABPM) at a single tertiary cardiology outpatient clinic. Participants were classified as dippers (≥10% nocturnal systolic BP decline) or non-dippers (<10%). Hierarchical logistic regression models were constructed sequentially: Model 1 (age, sex), Model 2 (Model 1 + AIP, fasting glucose), and Model 3 (Model 2 + SIRI). Discriminative performance was assessed using receiver operating characteristic (ROC) analysis. Results: Non-dipping was present in 62.5% of participants. LDL cholesterol, AIP, and SIRI were higher in non-dippers, whereas CRP was higher in dippers. In hierarchical regression, AIP was independently associated with non-dipping in Model 2 (OR = 3.672, p = 0.003). After addition of SIRI, SIRI remained independently associated (OR = 1.913, p < 0.001), and model explanatory power increased (Nagelkerke R2 = 0.104). AIP, fasting glucose (inverse association), and age also remained significant. Individual discrimination was modest for SIRI (AUC = 0.572) and AIP (AUC = 0.576), while the multivariable model achieved an area under the curve (AUC) of 0.660. Non-dipping prevalence increased across SIRI quartiles (p for trend = 0.009). Conclusions: Both inflammatory and atherogenic burden were associated with a non-dipping blood pressure pattern in individuals without overt metabolic disease. Although the discriminative capacity was modest, combined inflammatory–metabolic assessment may provide additional biological insight into circadian blood pressure dysregulation.