INTRODUCTION: Inflammatory markers have been reported to be elevated in hypertension. AIM: We compared levels of inflammatory markers between hypertensives (HT) with target organ damage (TOD) but without associated clinical conditions (ACC), n=55, HT with ACC, n=42, HT without TOD/ACC, n=22 and normotensive controls, n=41. METHODS: Serum levels of CRP, fibrinogen, TNF-alpha and anti-HSP60 antibodies were measured. Hypertensive complications were assessed on the basis of clinical history and the following investigations: M-mode echocardiography (left ventricular hypertrophy), Doppler: mitral and pulmonary vein flow and isovolumetric relaxation time (diastolic dysfunction), vascular ultrasound (common carotid artery intima-media thickness--IMT), pulse wave velocity (carotid-femoral arterial stiffness) and creatinine concentration (renal function). RESULTS: HT with TOD had higher concentrations of CRP than controls (1.71 vs 0.76 mg/l, p <0.0001); higher fibrinogen and TNF-a vs controls and also vs HT without TOD/ACC (2.80 vs 2.53 vs 2.49 g/l, p <0.0001) and (2.49 vs 2.00 vs 1.83 pg/ml, p=0.04), respectively. HT without TOD/ACC did not differ from the control group in inflammatory marker concentrations. HT with ACC did not differ from HT with TOD in inflammatory marker concentrations. There were no differences in anti-HSP60 antibody concentrations between all groups. In multiple regression analysis only IMT was influenced by inflammatory markers: fibrinogen (beta=0.2, p=0.02) and TNF-alpha, (beta=0.17, p=0.05). CONCLUSIONS: We conclude that inflammatory markers are elevated in HT with TOD and are not elevated in uncomplicated HT without TOD.
INTRODUCTION: Inflammatory markers have been reported to be elevated in hypertension. AIM: We compared levels of inflammatory markers between hypertensives (HT) with target organ damage (TOD) but without associated clinical conditions (ACC), n=55, HT with ACC, n=42, HT without TOD/ACC, n=22 and normotensive controls, n=41. METHODS: Serum levels of CRP, fibrinogen, TNF-alpha and anti-HSP60 antibodies were measured. Hypertensive complications were assessed on the basis of clinical history and the following investigations: M-mode echocardiography (left ventricular hypertrophy), Doppler: mitral and pulmonary vein flow and isovolumetric relaxation time (diastolic dysfunction), vascular ultrasound (common carotid artery intima-media thickness--IMT), pulse wave velocity (carotid-femoral arterial stiffness) and creatinine concentration (renal function). RESULTS: HT with TOD had higher concentrations of CRP than controls (1.71 vs 0.76 mg/l, p <0.0001); higher fibrinogen and TNF-a vs controls and also vs HT without TOD/ACC (2.80 vs 2.53 vs 2.49 g/l, p <0.0001) and (2.49 vs 2.00 vs 1.83 pg/ml, p=0.04), respectively. HT without TOD/ACC did not differ from the control group in inflammatory marker concentrations. HT with ACC did not differ from HT with TOD in inflammatory marker concentrations. There were no differences in anti-HSP60 antibody concentrations between all groups. In multiple regression analysis only IMT was influenced by inflammatory markers: fibrinogen (beta=0.2, p=0.02) and TNF-alpha, (beta=0.17, p=0.05). CONCLUSIONS: We conclude that inflammatory markers are elevated in HT with TOD and are not elevated in uncomplicated HT without TOD.
Authors: Maria E Marketou; Joanna E Kontaraki; Evangelos A Zacharis; George E Kochiadakis; Aikaterini Giaouzaki; Gregory Chlouverakis; Panos E Vardas Journal: J Clin Hypertens (Greenwich) Date: 2012-04-17 Impact factor: 3.738