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Protective Effects of Low-Intensity Pulsed Ultrasound on Cardiac Electrophysiological Function in a Rat Model of
Zhong-Hao Lin1,2,3, Qiu-Lu Yu1,2,3, Bing-Hua Yi1,2,3
1Department of Cardiology The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University Wenzhou Zhejiang China.
Insights
Low-intensity pulsed ultrasound (LIPUS) offers a promising noninvasive treatment for ischemic cardiomyopathy (ICM). LIPUS reduces inflammation, fibrosis, and arrhythmias by activating the cholinergic anti-inflammatory pathway and involving caveolin-1.
Area of Science:
- Cardiology
- Biomedical Engineering
- Regenerative Medicine
Background:
- Ischemic cardiomyopathy (ICM) is a severe heart condition characterized by ventricular remodeling, impaired function, and increased risk of fatal arrhythmias, often linked to chronic inflammation.
- Low-intensity pulsed ultrasound (LIPUS) is known for its anti-inflammatory effects in various conditions and is explored here for potential cardiac benefits.
Purpose of the Study:
- To investigate the cardioprotective effects of LIPUS in a rat model of ICM.
- To elucidate the underlying mechanisms, including the role of the cholinergic anti-inflammatory pathway and caveolin-1 (Cav-1).
Main Methods:
- Ischemic cardiomyopathy (ICM) was induced in rats by ligating the left anterior descending artery.
- Rats were treated with LIPUS, and the cholinergic anti-inflammatory pathway was modulated via vagotomy.
- Cardiac-specific Cav-1 overexpression was achieved using adeno-associated virus serotype 9 for mechanistic studies.
Main Results:
- LIPUS treatment significantly reduced ventricular remodeling, improved cardiac electrophysiological function, and decreased collagen and inflammatory cytokine expression.
- Vagotomy diminished the beneficial effects of LIPUS, indicating the involvement of the cholinergic pathway.
- Overexpression of Cav-1 restored the positive effects of LIPUS, suggesting its crucial downstream role.
Conclusions:
- LIPUS demonstrates direct anti-inflammatory and antifibrotic effects, improves cardiac autonomic function, and protects connexin-43 (Cx43), reducing malignant arrhythmia risk in ICM.
- The cholinergic anti-inflammatory pathway and Cav-1 are identified as key mechanisms mediating LIPUS's cardioprotective effects.
- LIPUS presents a novel, noninvasive therapeutic strategy for managing ischemic cardiomyopathy.
Background:
Ischemic cardiomyopathy (ICM) is the end stage of ischemic heart disease, in which ventricular remodeling contributes to a fatal ventricular arrhythmia, worsens heart function and unfavorable outcomes, and is related to persistent chronic inflammation. Low-intensity pulsed ultrasound (LIPUS) is an effective treatment modality for osteoarthropathy and has been illustrated to regulate the overactive inflammatory response in various diseases. Here, we aim to investigate whether LIPUS can perform cardiac protective effects in ICM and explore its possible mechanism.
Methods:
The left anterior descending artery of adult male Sprague-Dawley rats was ligated for 4 weeks to develop ICM and then treated with LIPUS. Vagotomy was applied to suppress the cholinergic anti-inflammatory pathway. Cardiac-specific Cav-1 (caveolin-1) overexpression in ICM on arrhythmias, excitation-contraction coupling, and cardiac remodeling was investigated using the intramyocardial injection of an adeno-associated virus serotype 9 system.
Results:
The results showed that LIPUS alleviated ventricular remodeling, improved cardiac electrophysiological function, and reduced the cardiac expression of collagens and inflammatory cytokines. Vagotomy suppressed the improvement of LIPUS. The overexpression of Cav-1 reset the influence of vagotomy.
Conclusions:
We found that LIPUS had a direct effect on regional anti-inflammation and antifibrosis, improved cardiac autonomic function and heart failure, protected the Cx43 (connexin-43) protein, and reduced the risk of malignant arrhythmia during ICM. The cholinergic anti-inflammatory pathway was one of the potential critical mechanisms involved, and Cav-1 might play an important role downstream. Our study provided a new, promising, and noninvasive strategy for treating ICM.
