Baseline hs‐CRP predicts hypertension remission in metabolic syndrome

Abstract

Background: Inflammation, overweight and other cardiovascular risk factors might negatively impact on hypertension remission in metabolic syndrome (MetS), independently of the pharmacological treatment. Here, the potential influence of systemic inflammation (assessed by serum high-sensitivity C-reactive protein [hs-CRP]) on hypertension remission will be investigated in a cohort of hypertensive patients with MetS. Material and Methods: Hypertensive patients with MetS (n = 100) were enrolled, treated under current behavior/dietary/pharmacological recommendations and followed up for 12 months. All patients received medications and nutritional advice based on Mediterranean-like dietary pattern in addition to psychological and physicalactivity counselling. At baseline (T0), 6 (T1) and 12 (T2) months of follow-up, clinical data, haematological and biochemical profiles and serum hs-CRP were measured. Results: As compared to T0, at T2 patients displayed improvements in anthropometric and metabolic profiles. At T2, the hypertension remission rate was 13.0%. Serum hs-CRP did not change overtime in the overall cohort. Surprisingly, patients who experienced hypertension remission were less treated with antihypertensive drugs, but developed a weak improvement in anthropometric measures during follow-up.The hypertension remission group had lower baseline levels of hs-CRP as compared to non-remission. Low baseline hs-CRP (<2 µg/mL, cut-off value identified by ROC curve) predicted hypertension remission, independently of antihypertensive treatment implementation, baseline systolic blood pressure and waist circumference improvement. Conclusions: Remission of hypertension in MetS is independently associated with baseline low CRP levels, which might suggest a critical role for inflammation in sustaining high blood pressure levels. K E Y W O R D SC-reactive protein, hypertension, inflammation, metabolic syndrome, obesity, overweight

Oxidative Stress: A Unifying Paradigm in Hypertension

“…142 Tissue expression of adhesion molecules (VCAM-1, ICAM-1), production of inflammatory mediators (monocyte chemotactic peptide 1, tumour necrosis factor, interleukin [IL] 1, IL-6, 1L-17), activation of proinflammatory signalling pathways (MAPK, STAT) and transcription factors (NF-kB, AP-1, HIF-1), and circulating levels of inflammatory biomarkers (C-reactive protein, PAI-1, ILs) are increased in hypertension. [143][144][145][146] Although it still remains unclear whether inflammation is a cause or an effect of hypertension, it is clear that the immune system and ROS are important players.…”

Serum osteopontin predicts glycaemic profile improvement in metabolic syndrome: A pilot study

“…This is sub‐analysis of a previously published prospective study, which enrolled patients with MetS, as defined by the NCEP‐ATP III criteria, 14 from November 2012 to May 2015. Including and excluding criteria are reported elsewhere 15 . Here, we have further excluded patients with diagnosed T2DM or treated with glucose‐lowering drugs and those with steatosis and non‐alcoholic fatty liver disease (n = 3).…”

“…As previously reported, patients received a nutritional advice based on Mediterranean‐like dietary pattern 15 . Nutritional advice was mainly directed at weight reduction so that a control of total daily energy consumption was recommended (calculated as 20 kcal/kg of ideal body weight per day).…”

Anti‐ApoA‐1 IgGs predict resistance to waist circumference reduction after Mediterranean diet

“…Even more relevant, validated predictors of neither WC/weight loss nor metabolic improvement in patients undergoing bariatric surgery or dietary interventions are still lacking. In this regard, a multitude of pathways involving genetic background, lifestyle, environmental pollution and especially low‐grade chronic inflammation is under investigation 4‐6 . Here, we attempted to deepen knowledge on the potential metabolic role of autoantibodies against apolipoprotein A‐1 (anti‐apoApoA‐1 IgG), the major proteic fraction of high‐density lipoprotein cholesterol (HDL‐c).…”