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Published on: July 7, 2016

Spironolactone has antiarrhythmic activity in ischaemic cardiac patients without cardiac failure

Nimit C Shah, Stuart D Pringle, Peter T Donnan

    Journal of Hypertension
    |October 9, 2007
    PubMed

    Insights

    Endogenous aldosterone can promote arrhythmias in patients with coronary artery disease (CAD) without heart failure. Aldosterone blockade reduced ventricular extrasystoles and lengthened the QT interval, suggesting a role in cardiac events.

    Area of Science:

    • Cardiology
    • Endocrinology
    • Pharmacology

    Background:

    • Aldosterone blockade reduces sudden death in heart failure patients, potentially via anti-arrhythmic or anti-coronary event effects.
    • The impact of aldosterone on arrhythmias and endothelial function in patients with coronary artery disease (CAD) but without heart failure remains unclear.

    Purpose of the Study:

    • To investigate if endogenous aldosterone contributes to arrhythmias or endothelial dysfunction in CAD patients without heart failure.
    • To explore the underlying mechanisms of aldosterone's potential pro-arrhythmic effects.

    Main Methods:

    • A randomized, placebo-controlled, double-blind crossover study involving 98 CAD patients without heart failure.
    • Assessed endothelial function using forearm venous occlusion plethysmography.
    • Measured ventricular extrasystoles, procollagen III N-terminal peptide (PIIINP), and QT interval length to evaluate arrhythmias and their determinants.

    Main Results:

    • Spironolactone significantly reduced ventricular extrasystoles by 75% (P < 0.003).
    • Spironolactone decreased the QT interval (P < 0.001) and a collagen marker (PIIINP) (P < 0.001).
    • No significant changes were observed in endothelial dysfunction or heart rate variability.

    Conclusions:

    • Endogenous aldosterone appears to be an arrhythmogenic factor in CAD patients without heart failure, even with standard therapy.
    • Aldosterone may promote myocardial fibrosis and prolong the QTc interval, contributing to arrhythmias.
    • Further research is needed to fully elucidate aldosterone's role and therapeutic implications in this patient population.
    Abstract

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