Attenuation of Myocardial Dysfunction in Hypertensive Cardiomyopathy Using Non-R-Wave-Synchronized Cardiac Shock Wave
Fei Li1, Zhe Zhen1,2, Si-Jia Sun1
1Cardiology Division, Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR, China.
Insights
Cardiac shock wave therapy (CSWT) safely reduces cardiac dysfunction in hypertensive cardiomyopathy. This novel treatment enhances blood vessel growth and reduces inflammation, improving heart function.
Area of Science:
- Cardiology
- Regenerative Medicine
Background:
- Hypertensive cardiomyopathy leads to significant cardiac dysfunction.
- Conventional therapies are often insufficient for refractory cases.
- Cardiac shock wave therapy (CSWT) offers a novel approach.
Purpose of the Study:
- To investigate the mechanism and efficacy of non-R-wave-triggered CSWT.
- To assess CSWT's impact on hypertensive cardiomyopathy in a large animal model.
- To evaluate CSWT's effects on myocardial neovascularization and inflammation.
Main Methods:
- Induced sustained hypertension in pigs using angiotensin-II and DOCA.
- Administered two sessions of non-R-wave-triggered CSWT.
- Assessed cardiac function, blood pressure, and myocardial tissue characteristics.
Main Results:
- CSWT attenuated the decrease in cardiac function (+dP/dt, ESPVR) observed in the hypertension group.
- CSWT improved diastolic function (EDPVR) and increased microvascular density.
- CSWT upregulated vascular endothelial growth factor (VEGF) and reduced inflammation.
Conclusions:
- Non-R-wave-triggered CSWT is safe and effective in a large animal model of hypertensive cardiomyopathy.
- CSWT attenuates left ventricular systolic and diastolic dysfunction.
- The therapeutic effects are mediated by enhanced myocardial neovascularization and anti-inflammatory actions.
Abstract:
Cardiac shock wave therapy (CSWT) is a novel therapeutic procedure for patients with angina that is refractory to conventional therapy. We investigated the potential mechanism and therapeutic efficacy of non-R-wave-triggered CSWT to attenuate myocardial dysfunction in a large animal model of hypertensive cardiomyopathy. Sustained elevated blood pressure (BP) was induced in adult pigs using a combination of angiotensin-II and deoxycorticosterone acetate (DOCA). Two sessions of non-R-wave-triggered CSWT were performed at 11 and 16 weeks. At 10 weeks, systolic and diastolic blood pressure, LV posterior wall thickness and intraventricular septum thickness significantly increased in both the hypertension and CSWT groups. At 20 weeks, +dP/dt and end-systolic pressure-volume relationship (ESPVR) decreased significantly in the hypertension group but not the CSWT group, as compared with week 10. A significant improvement in end-diastolic pressure-volume relationship (EDPVR) was observed in the CSWT group. The CSWT group exhibited significantly increased microvascular density and vascular endothelial growth factor (VEGF) expression in the myocardium. Cytokine array demonstrated that the CSWT group had significantly reduced inflammation compared with the hypertension group. Our results demonstrate that non-R-wave-triggered CSWT is safe and can attenuate LV systolic and diastolic dysfunction via enhancement of myocardial neovascularization and anti-inflammatory effect in a large animal model of hypertensive cardiomyopathy.
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