Abstract
Danqi soft capsule (DQ) is a traditional Chinese medicine containing Salvia miltiorrhiza and Panax notoginseng; it is safe and efficient in treating ischaemic heart diseases. The purpose of the present study was to assess whether DQ could prevent infarct border zone (IBZ) remodelling and decrease ventricular arrhythmias occurrence in post‐myocardial infarction (MI) stage. MI was induced by a ligation of the left anterior descending coronary artery. DQ was administered to the post‐MI rats started from 1 week after MI surgery for 4 weeks. The results showed that DQ treatment significantly attenuated tachyarrhythmia induction rates and arrhythmia score in post‐MI rats. In echocardiography, DQ improved left ventricular (LV) systolic and diastolic function. Histological assessment revealed that DQ significantly reduced fibrotic areas and myocyte areas, and increased connexin (Cx) 43 positive areas in IBZ. Western blot revealed that DQ treatment significantly reduced the protein expression levels of type I and III collagens, α‐smooth muscle actin (α‐SMA), transforming growth factor‐β1 (TGF‐β1) and Smad3 phosphorylation, while increasing Cx43 amounts. Overall, these findings mainly indicated that DQ intervention regulates interstitial fibrosis, Cx43 expression and myocyte hypertrophy by TGF‐β1/Smad3 pathway in IBZ, inhibits LV remodelling and reduces vulnerability to tachyarrhythmias after MI. This study presents a proof of concept for novel antiarrhythmic strategies in preventing IBZ remodelling, modifying the healed arrhythmogenic substrate and thus reducing susceptibility to ventricular arrhythmias in the late post‐MI period.
Highlights
Ventricular arrhythmias represent a major cause of morbidity and mortality in post‐myocardial infarction (MI) patients, even in the current era of coronary revascularization, accounting for a substantial number of sudden cardiac deaths.[1]
Increasing evidence reveals that cardiac remodelling at the in‐ farct border zone (IBZ) induced by MI plays a critical role in the occurrence of ventricular arrhythmias.[3,4]
Previous studies have indicated that abnormal conduction exists in the IBZ, constitut‐ ing the main reason for ventricular tachyarrhythmia (VT) occurrence in MI rats.[3,4]
Summary
Ventricular arrhythmias represent a major cause of morbidity and mortality in post‐myocardial infarction (MI) patients, even in the current era of coronary revascularization, accounting for a substantial number of sudden cardiac deaths.[1]. It is closely associated with changes in ventricular size, shape and function after MI.[5,6] Previous studies have indicated that abnormal conduction exists in the IBZ, constitut‐ ing the main reason for ventricular tachyarrhythmia (VT) occurrence in MI rats.[3,4] IBZ remodelling can be considered a primary target for the prevention of ventricular arrhythmias.[7,8]
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