Implications of Inflammatory and Oxidative Stress Markers in the Attenuation of Nocturnal Blood Pressure Dipping

Abstract

To date, no model has jointly encompassed clinical, inflammatory, and redox markers with the risk of a non-dipper blood pressure (BP) profile. We aimed to evaluate the correlation between these features and the main twenty-four-hour ambulatory blood pressure monitoring (24-h ABPM) indices, as well as to establish a multivariate model including inflammatory, redox, and clinical markers for the prediction of a non-dipper BP profile. This was an observational study that included hypertensive patients older than 18 years. We enrolled 247 hypertensive patients (56% women) with a median age of 56 years. The results showed that higher levels of fibrinogen, tissue polypeptide-specific antigen, beta-2-microglobulin, thiobarbituric acid reactive substances, and copper/zinc ratio were associated with a higher risk of a non-dipper BP profile. Nocturnal systolic BP dipping showed a negative correlation with beta-globulin, beta-2-microglobulin, and gamma-globulin levels, whereas nocturnal diastolic BP dipping was positively correlated with alpha-2-globulin levels, and negatively correlated with gamma-globulin and copper levels. We found a correlation between nocturnal pulse pressure and beta-2-microglobulin and vitamin E levels, whereas the day-to-night pulse pressure gradient was correlated with zinc levels. Twenty-four-hour ABPM indices could exhibit singular inflammatory and redox patterns with implications that are still poorly understood. Some inflammatory and redox markers could be associated with the risk of a non-dipper BP profile.

Assessing the relationship between lipoprotein(a) levels and blood pressure among hypertensive patients beyond conventional measures. An observational study

“…Beyond its independent association with arterial stiffness and critical hypoperfusion of diastolic flow-dependent organs, recent studies have linked nPP to a pro-inflammatory internal milieu and an unfavorable redox status. These abnormalities promote a sequence of deleterious metabolic effects on the cardiovascular system, potentially including concurrent lipid profile abnormalities [47][48][49] .…”