Effect of Mono- And Combination Antihypertensive Therapy on the Systemic Inflammation Activity in Hypertensive Patients

L.A. Mischenko, H.M. Bozhenko, O.O. Matova, V.V. Radchenko, M.P. Mospan


The aim of the study is to assess the impact of mono- and combination antihypertensive therapy on parameters of systemic inflammation (C-reactive protein, CRP, interleukin 6, IL-6 and tumor necrosis factor α, TNF-α) relative to the dynamic of ambulatory blood pressure.
The study involved 99 patients with essential hypertension (EH) stage I–II, grade I–II who were randomized into 3 treatment groups: 29 patients received monotherapy with telmisartan 40–80 mg/day, 27 persons received S-amlodipine 5 mg/day and 43 patients got a fixed combination of valsartan with amlodipine 160/5 mg/day). Levels of CRP, IL-6 and TNF-α were determined before (after the 7-day non-drug period) and after 6 months of treatment.
It was found that treatment with telmisartan reduces serum CRP level by 13.9 % and IL-6 by 36.4 %, but does not affect the blood concentration of TNF-α. Monotherapy with calcium antagonist S-amlodipine results in reduction of blood levels of inflammatory cytokines IL-6 by 39 % and TNF-α by 11.9 %. The use of a fixed combination of valsartan with amlodipine produces a more significant antihypertensive effect, but it is not accompanied by more expressive reduction of CRP and IL-6 levels than under monothe­rapy, which accounted for 12.5 and 31.5 %.
Blood pressure reduction is associated with the decrease of acti­vity of low-grade inflammation. Reduction of serum concentration of TNF-α correlates with a decrease of systolic and diastolic BP at day- and night-time, and reduction of CRP associates with changes in 24-hour and average daily systolic BP, 24-hour SBP index and its night-time variability.
Our data confirm that monotherapy with angiotensin II receptor blockers (telmisartan) and calcium antagonists (S-amlodipine) reduces activity of low grade inflammation and when used its combinations (valsartan with amlodipine). This effect directly correlates with a decrease in ambulatory blood pressure indexes.


hypertension; blood pressure; systemic inflammation; C-reactive protein; interleukin 6; tumor necrosis factor α; antihypertensive therapy


Cachofeiro V., Miana M., Heras N. et al. Inflammation: a link between hypertension and atherosclerosis // Curr. Hypertens. Rev. — 2009. — Vol. 5. — P. 40-8.

Міщенко Л.А. Роль нетрадиційних чинників серцево-судинного ризику в патогенезі гіпертонічної хвороби // Український кардіологічний журнал. — 2012. — № 3. — С. 15-21.

Osman R., L’Allier P.L., Elgharib N. et al. Critical appraisal of C-reactive protein throughout the spectrum of cardiovascular di­sease // Vasc. Health Risk. Manag. — 2006. — Vol. 2(3). — P. 221-37.

Patel P., Dokainish H., Tsai P., Lakkis N. Update on the association of inflammation and atrial fibrillation // J. Cardiovasc. Electrophysiol. — 2010. — Vol. 21. — P. 1064-70.

Niskanen L., Laaksonen D.E., Nyssonen K. et al. Inflammation, abdominal obesity and smoking as predictors of hypertension // Hypertension. — 2004. — Vol. 44. — P. 859-865.

Hage F.G. C reactive protein and hypertension // J. Hum. Hypertens. — 2014. — Vol. 28. — P. 410-5.

Міщенко Л.А., Свіщенко Є.П., Яринкіна О.А. Предиктори прогресування ураження сонних артерій у хворих на гіпертонічну хворобу // Серце і судини. — 2013. — № 1. — С. 47-53.

Міщенко Л.А. Предиктори прогресування гіпертрофії лівого шлуночка у хворих на гіпертонічну хворобу // Український кардіологічний журнал. — 2012. — № 6. — С. 110-116

Sander K., Horn C.S., Briesenick C. et al. High-sensitivity C-reactive protein is independently associated with early carotid artery progression in women but not in men / The INVADE study // Stroke. — 2007. — Vol. 38. — P. 2881-2886.

Sanz-Rosa D., Oubina M.P., Cideil E. et al. Effect of AT1 receptor antagonism on vascular and circulating inflammatory mediators in SHR: role of NF κB/ I κB system // Am. J. Physiol. Heart Circ. Phisiol. — 2005. — Vol. 288. — Р. 111-115.

Ceconi C., Fox K.M., Remme W.J. ACE inhibition with perindopril and biomarkers of atherosclerosis and thrombosis: results from the PERTINENT study // Atherosclerosis. — 2009. — Vol. 204(1). — P. 273-275.

Mitrovic V., Klein H.H., Krekel N. et al. Influence of the ­angiotensin converting enzyme inhibitor ramipril on high sensitivity C-reactive protein (hs-CRP) in patients with documented atherosclerosis // Z. Kardiol. — 2005. — Vol. 94. — P. 336-342.

Derosa G., Maffioli P., Salvadeo S.A. et al. Candesartan effect on inflammation in hypertension // Hypertens. Res. — 2010. — Vol. 33. — P. 209-213.

Fliser D., Buchholz K., Haller H. et al. European Trial on Olmesartan and Pravastatin in Inflammation and Atherosclerosis (EUTOPIA) investigators. Antiinflammatory effects of angiotensin II subtype I receptor blockade in hypertensive patients with microinflammation // Circulation. — 2004. — Vol. 110. — P. 1103-1107.

Manabe S. Effects of angiotensin II receptor blockade with valsartan on pro-inflammatory cytokines in patients with essential hypertension // J. Cardivsc. Pharmacol. — 2005. — Vol. 46. — P. 735-739.

Shurtz-Swirski R., Farah R., Sela S. The effect of calcium channel blocker lercanidipine on lowgrade inflammation para­meters in essential hypertension patients // Harefuah. — 2006. — Vol. 45(12). — P. 895-899.

Farah R., Shurtz-Swirski R. The combined effect of calcium channel blocker Lercanidipine and antioxidants on low-grade systemic inflammation parameters in essential hypertensive patients // Minerva Cardioangiol. — 2008. — Vol. 56. — P. 467-476.

Yasunari K., Maeda K., Watanabe T. et al. Comparative effects of valsartan versus amlodipine on left ventricular mass and reactive oxygen species formation by monocytes in hypertensive patients with left ventricular hypertrophy // J. Am. Col. Cardiol. — 2004. — Vol. 43. — P. 2116-2123.

Ridker P.M., Danielson E., Rifai N. et al. Valsartan, blood pressure reduction, and C-reactive protein: primary report of the ­Val-MARC trial // Hypertens. — 2006. — Vol. 48. — P. 73-79.

Ruilope L.M., Malacco E., Khder Y. et al. Efficacy and tole­rability of combination therapy with valsartan plus hydrochlorothiazide compared with amlodipine monotherapy in hypertensive patients with other cardiovascular risk factors: the VAST study // Clin. Ther. — 2005. — Vol. 27(5). — P. 578-587.

Giardina J.B., Green G.M., Cockrell K.L. et al. TNF enhances contraction and inhibits endothelial NO-cGMP relaxation in systemic vessels of pregnant rats // Am. J. Physio. Regul. Integr. Comp.Physiol. — 2002. — Vol. 283. — P. 130-143.

LaMarca B.B., Cockrell K., Sullivan E. et al. Role of endothelin in mediating tumor necrosis factor-induced hypertension in pregnant rats // Hypertension. — 2005. — Vol. 46. — P. 82-86.

Sriramula S., Haque M., Majid D.S. et al. Involvement of tumor necrosis factor-alpha in angiotensin II-mediated effects on salt appetite, hypertension, and cardiac hypertrophy // Hypertension. — 2008. — Vol. 51. — P. 1345-1351.

Brands M.W., Banes-Berceli A.K., Inscho E.W. et al. Interleukin 6 knockout prevents angiotensin II hypertension: role of renal vasoconstriction and Janus kinase 2/signal transducer and activator of transcription 3 activation // Hypertension. — 2010. — Vol. 56. — P. 879-884.

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