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[The activity of nonspecific inflammation in hypertensive patients]

E V Oshchepkova, V A Dmitriev, V N Titiov

    Terapevticheskii Arkhiv
    |January 29, 2008
    PubMed

    Insights

    Essential hypertension (EH) is linked to inflammation, with C-reactive protein (CRP) and interleukin-6 (IL-6) correlating with blood pressure (BP). Treatment with indapamide-retard and perindopril showed positive CRP changes, suggesting reduced inflammation.

    Area of Science:

    • Cardiology
    • Clinical Immunology

    Background:

    • Essential hypertension (EH) is a prevalent cardiovascular condition.
    • Nonspecific inflammation, indicated by C-reactive protein (CRP) and interleukin-6 (IL-6), may play a role in EH pathogenesis.
    • Circadian blood pressure (BP) patterns are crucial in hypertension management.

    Purpose of the Study:

    • To investigate the relationship between inflammatory markers (CRP, IL-6) and circadian BP profiles in patients with EH.
    • To evaluate the effect of indapamide-retard and perindopril on CRP levels in hypertensive patients.

    Main Methods:

    • The study included 81 patients with stage I-II EH.
    • CRP and IL-6 levels were measured using turbidimetry and ELISA, respectively.
    • Circadian BP monitoring was performed using the TM 2421 device. Patients received either indapamide-retard or perindopril.

    Main Results:

    • Elevated CRP (>3 mg/l) was found in 55% of patients, correlating positively with 24-h systolic and diastolic BP and abnormal circadian BP rhythms (nondippers).
    • Elevated IL-6 was detected in 30% of patients, showing strong positive correlations with 24-h systolic and diastolic BP.
    • Patients treated with indapamide-retard or perindopril exhibited positive changes in CRP levels.

    Conclusions:

    • Nonspecific inflammation, evidenced by CRP and IL-6, is associated with EH and abnormal BP patterns.
    • Therapy with indapamide-retard may reduce inflammation by alleviating hemodynamic stress.
    • Perindopril's positive effect on CRP dynamics could be attributed to angiotensin II blockade.
    Abstract

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