Drug-coated balloons for treating de novo lesions in large coronary vessels: A case report.

BACKGROUND: Percutaneous transluminal coronary angioplasty, while an effective intervention, can frequently lead to acute occlusion with severe consequences. Although clinical trials have demonstrated the efficacy of drug-coated balloons (DCB) in treating acute coronary artery occlusion and in preventing restenosis, there has been limited exploration on the use of DCB in treating de novo lesions in large vessels. Currently, DCB are only recommended for patients with small vessel lesions and in-stent restenosis lesions, those at high risk of bleeding, and other special groups of patients. CASE SUMMARY: This report presents a case of successful drug-coated balloon treatment of de novo lesions in large coronary vessels. Postoperatively, the patient demonstrated favorable recovery, with subsequent examination results revealing no significant differences from the previous examination. CONCLUSION: The successful treatment of the patient in our case highlights the potential of DCB in the treatment of de novo lesions in large coronary vessels.

Honokiol Protects against Anti-ß1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy.

Myocardial diseases are prevalent syndromes with high mortality rate. The exploration of effective interference is important. Anti-ß1-adrenergic receptor autoantibody (ß1-AAB) is highly correlated with myocardial dysfunction. The actions and underlying mechanisms of honokiol (HNK) in ß1-AAB-positive patients await to be unraveled. In this study, we established a rat model of ß1-AAB positive with myocardial dysfunction. Cardiac function following ß1-AR-ECII administration was analyzed using the VisualSonics Vevo 770 High-Resolution In Vivo Imaging System. The levels of autophagy-related proteins were detected by Western blotting. Our data revealed that HNK reversed ß1-AAB-induced effects and protected myocardial tissues from dysfunction. After HNK treatment, the cardiac contractile ability increased and the LDH activity decreased. HNK attenuated myocardial degeneration. In addition, HNK promoted the activation of the AMP-dependent protein kinase/Unc-51-like autophagy activating kinase (AMPK/ULK) pathway and activated autophagy. These results suggest that HNK protects against ß1-AAB-induced myocardial dysfunction via activation of autophagy and it may be a potentially therapeutic compound for ß1-AAB-positive myocardial diseases.

Astragaloside IV inhibits ventricular remodeling and improves fatty acid utilization in rats with chronic heart failure.

Chronic heart failure (CHF) is the end-stage of many cardiovascular diseases and severely affects the patients' lifespan. Inhibiting ventricular remodeling is thus a primary treatment target for CHF patients. Astragaloside IV (AS-IV) can improve cardiac function and protect myocardial cells. The study aims to investigate the effects of AS-IV on ventricular remodeling and explore its role in regulating energy metabolism using a rat CHF model. Sprague-Dawley rats were divided into five groups (n=20 per group): CHF + benazepril hydrochloride (Benazepril HCL), CHF + low-dose (30 mg.kg-1day-1) AS-IV, CHF + high-dose (60 mg.kg-1day-1) AS-IV, and a sham control group. After 8 weeks of treatment, the cardiac structure and functional parameters were measured. Morphological changes in the myocardial tissue in five groups were evaluated. Protein and mRNA expression of peroxisome proliferator-activated receptor α (PPARα), medium-chain acyl-CoA dehydrogenase (MCAD), and muscle carnitine palmitoyl transferase-1 (MCPT1) were also analyzed. Our results showed that the left ventricular mass index (LVMI), collagen volume fraction (CVF), and free fatty acid (FFA) concentration of CHF group rats increased when compared with sham control group, while the protein and mRNA expressions of PPARα, MCAD, and MCPT1 decreased in CHF. Importantly, treatment with AS-IV (CHF + AS-IV group) showed improved heart function and structure, increased expression of PPARα, MCAD, and MCPT1 and improved FFA utilization in comparison with CHF group. In conclusion, our study shows that AS-IV inhibits ventricular remodeling, improves cardiac function, and decreases FFA concentration of CHF model rats. Our findings suggest a therapeutic potential of using AS-IV in CHF.