In recent decades, the outcomes of coronary heart disease （CHD） have markedly improved, which can be partly attributed to the use of novel drugs （especially statins and antiplatelet drugs） and partly to the evolut...In recent decades, the outcomes of coronary heart disease （CHD） have markedly improved, which can be partly attributed to the use of novel drugs （especially statins and antiplatelet drugs） and partly to the evolution ofpercutaneous coronary intervention （PCI）. From percutaneous transluminal coronary angioplasty to bare-metal stent and then to drug-eluting stent, every step of PCI is attractive to interventional cardiologist, great progress has been made for patients with CHD. In the past few years, some successor devices for treating CHD have cmerged. Undoubtedly, drug-coated balloon （DCB）, which was recommended by 2014 ESC Guidelines on myocardial revascularization, is a ＂shining star＂ among them. DCB involves a semi-compliant angioplasty balloon coated with an anti-proliferative agent that can exert antirestenotic efficacy by permeating into the vessel wall during balloon contact. This review discusses the conception and merits, preclinical data, emerging clinical indications, and results from clinical trials of this novel interventional technology. Although DCB has shown authentic efficacy in the treatment ofin-stent restenosis, its use in de novo coronary lesions is still in dispute. Hence, concerns and the future direction of DCB are also covered in this paper.展开更多
Background Cilostazol is a type 3 phosphodiesterase inhibitor which has been previously demonstrated to prevent the occurrence of tachyarrhythmia and improve defibrillation efficacy. However, the mechanism for this be...Background Cilostazol is a type 3 phosphodiesterase inhibitor which has been previously demonstrated to prevent the occurrence of tachyarrhythmia and improve defibrillation efficacy. However, the mechanism for this beneficial effect is still unclear. Since cardiac mito-chondria have been shown to play a crucial role in fatal cardiac arrhythmias and that oxidative stress is one of the main contributors to arr-hythmia generation, we tested the effects of cilostazol on cardiac mitochondria under severe oxidative stress. Methods Mitochondria were isolated from rat hearts and treated with H2O2 to induce oxidative stress. Cilostazol, at various concentrations, was used to study its protective effects. Pharmacological interventions, including a mitochondrial permeability transition pore （mPTP） blocker, cyclosporine A （CsA）, and an inner membrane anion channel （IMAC） blocker, 4＇-chlorodiazepam （CDP）, were used to investigate the mechanistic role of cilostazol on cardiac mitochondria. Cardiac mitochondrial reactive oxygen species （ROS） production, mitochondrial membrane potential change and mi-tochondrial swelling were determined as indicators of cardiac mitochondrial function. Results Cilostazol preserved cardiac mitochondrial function when exposed to oxidative stress by preventing mitochondrial depolarization, mitochondrial swelling, and decreasing ROS produc-tion. Conclusions Our findings suggest that cardioprotective effects of cilostazol reported previously could be due to its prevention of car-diac mitochondrial dysfunction caused by severe oxidative stress.展开更多
文摘In recent decades, the outcomes of coronary heart disease （CHD） have markedly improved, which can be partly attributed to the use of novel drugs （especially statins and antiplatelet drugs） and partly to the evolution ofpercutaneous coronary intervention （PCI）. From percutaneous transluminal coronary angioplasty to bare-metal stent and then to drug-eluting stent, every step of PCI is attractive to interventional cardiologist, great progress has been made for patients with CHD. In the past few years, some successor devices for treating CHD have cmerged. Undoubtedly, drug-coated balloon （DCB）, which was recommended by 2014 ESC Guidelines on myocardial revascularization, is a ＂shining star＂ among them. DCB involves a semi-compliant angioplasty balloon coated with an anti-proliferative agent that can exert antirestenotic efficacy by permeating into the vessel wall during balloon contact. This review discusses the conception and merits, preclinical data, emerging clinical indications, and results from clinical trials of this novel interventional technology. Although DCB has shown authentic efficacy in the treatment ofin-stent restenosis, its use in de novo coronary lesions is still in dispute. Hence, concerns and the future direction of DCB are also covered in this paper.
文摘Background Cilostazol is a type 3 phosphodiesterase inhibitor which has been previously demonstrated to prevent the occurrence of tachyarrhythmia and improve defibrillation efficacy. However, the mechanism for this beneficial effect is still unclear. Since cardiac mito-chondria have been shown to play a crucial role in fatal cardiac arrhythmias and that oxidative stress is one of the main contributors to arr-hythmia generation, we tested the effects of cilostazol on cardiac mitochondria under severe oxidative stress. Methods Mitochondria were isolated from rat hearts and treated with H2O2 to induce oxidative stress. Cilostazol, at various concentrations, was used to study its protective effects. Pharmacological interventions, including a mitochondrial permeability transition pore （mPTP） blocker, cyclosporine A （CsA）, and an inner membrane anion channel （IMAC） blocker, 4＇-chlorodiazepam （CDP）, were used to investigate the mechanistic role of cilostazol on cardiac mitochondria. Cardiac mitochondrial reactive oxygen species （ROS） production, mitochondrial membrane potential change and mi-tochondrial swelling were determined as indicators of cardiac mitochondrial function. Results Cilostazol preserved cardiac mitochondrial function when exposed to oxidative stress by preventing mitochondrial depolarization, mitochondrial swelling, and decreasing ROS produc-tion. Conclusions Our findings suggest that cardioprotective effects of cilostazol reported previously could be due to its prevention of car-diac mitochondrial dysfunction caused by severe oxidative stress.
