This study demonstrates that low decibel infrasound (4-20 Hz, 79.75-86.11 dB) significantly inhibits angiotensin II (Ang II)-induced proliferation and collagen synthesis in cultured rat cardiac fibroblasts by modulating the miR-29a/TGF-β/Smad3 signaling pathway, offering a potential novel therapeutic strategy for combating cardiac fibrosis. By showing that infrasound counteracts Ang II-induced reductions in miR-29a expression and subsequent increases in TGF-β secretion and Smad3 phosphorylation, the findings suggest that low-intensity infrasound could serve as a non-invasive intervention to mitigate fibrosis-related heart conditions, such as those associated with hypertension and coronary heart disease. The necessity of miR-29a for these effects, confirmed through RNAi knockdown, underscores its critical role in the mechanism, while the contrast with high-intensity infrasound’s harmful effects highlights the importance of optimizing frequency and intensity for clinical applications, warranting further investigation into safe and effective therapeutic doses.

Owners of the Infrasound 8 device and the CHI Palm might use them to help with heart-related issues caused by stress or strain on the heart, such as those linked to high blood pressure or heart disease. The study suggests that using the device at low settings (The Acute setting of the CHI Palm) for 2 hours daily could reduce excessive cell growth and fibrous tissue buildup in the heart, which might help keep the heart healthier and less stiff. They could expect some improvement in how the heart handles stress, but further testing is needed.