Population
Healthy and diseased cardiomyocytes, specifically focusing on heart failure and hypertrophic cardiomyopathy
Design
Review
Key result
Inhibition of the late sodium current (INaL) with agents like ranolazine offers a potential therapeutic approach to address arrhythmogenesis and diastolic dysfunction in heart failure and hypertrophic cardiomyopathy.
Authors
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May support INaL inhibition trials in HF and HCM; hypothesis-generating until randomized outcome data emerge.
Intracellular sodium overload, driven by enhanced late sodium current, contributes to arrhythmogenesis and contractile dysfunction in heart failure and hypertrophic cardiomyopathy, making it a promising therapeutic target.
Coppini et al. (2013) conducted a review in Heart failure and hypertrophic cardiomyopathy. Late sodium current (INaL) inhibitors (e.g., ranolazine) was evaluated. Inhibition of the late sodium current (INaL) with agents like ranolazine offers a potential therapeutic approach to address arrhythmogenesis and diastolic dysfunction in heart failure and hypertrophic cardiomyopathy.
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