Inflammation and Nocturnal Pattern of Blood Pressure in Normotensives

Abstract

Blood pressure (BP) normally decreases during sleep, and certain metabolic and cardiovascular alterations may affect this circadian pattern. 1 Leading reasons for a non-dipping BP pattern are obesity, sleep disorders, obstructive sleep apnea, chronic kidney disease, excessive salt consumption, diabetes mellitus, orthostatic hypotension, autonomic dysfunction, and advanced age. 2 An arbitrary cut-off point has been proposed to define patients as "dippers" if their nocturnal BP falls by ≥10% of the daytime mean BP value. 2 A non-dipper BP pattern is associated with high cardiovascular mortality and morbidity in people with both normal BP and hypertension. 3,4 In recent years, hematological parameters such as the neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), monocyte to high-density lipoprotein (HDL) cholesterol ratio (MHR), and systemic immune-inflammation index (SII) have been investigated in different systemic diseases as indicators of inflammation. [5][6][7][8][9][10][11][12] Although studies are searching for

Relationships between Easily Available Biomarkers and Non-Dipper Blood Pressure Pattern in Patients with Stable Coronary Artery Disease

“…A non-dipping BP pattern is associated with elevated risk of atherosclerotic events and HTN-mediated target organ damage, accelerated CAD progression and an increased likelihood of obstructive sleep apnea [ 47 , 48 , 49 ]. Previous studies have documented increased inflammatory markers in both hypertensive and normotensive patients with a non-dipping BP profile [ 17 ]. Atherosclerosis is a dynamic low-grade inflammatory process [ 50 , 51 , 52 , 53 ] and routine inflammatory biomarkers are used for both acute and long-term cardiovascular risk stratification in CAD patients [ 10 , 13 , 54 ].…”

“…Persistently elevated cytokine concentrations promote endothelial dysfunction and impaired vasodilation, explaining the association between chronic inflammation, HTN and accelerated atherosclerosis [ 16 ]. Moreover, previous studies have documented a more pronounced inflammatory response in both hypertensive and normotensive individuals that present a non-dipping BP pattern [ 17 , 18 , 19 ].…”