Paclitaxel-Coated Balloon Angioplasty Attenuates Progression and Inflammation of Experimental Atherosclerosis: Implications for COVID-19-Associated Cardiovascular Complications

Paclitaxel drug-coated balloons (DCBs) effectively reduce restenosis after percutaneous transluminal angioplasty (PTA), yet concerns regarding their long-term safety have emerged. This study tested the hypothesis that DCBs could attenuate vascular inflammation and halt plaque progression in experimental atherosclerosis. In a rabbit model of diet-induced hypercholesterolemia combined with balloon injury to create nonobstructive aortic lesions, animals underwent DCB-PTA, plain PTA, or sham-PTA (balloon insertion without inflation). Serial intravascular near-infrared fluorescence-optical coherence tomography (NIRF-OCT) assessed inflammation via protease activity, while intravascular ultrasound (IVUS) quantified plaque burden and progression over time. DCB-PTA significantly reduced lesion inflammation on NIRF-OCT and suppressed plaque progression on IVUS compared with plain PTA or sham-PTA. Mechanisms likely include paclitaxel’s anti-inflammatory effects, as evidenced by correlations between reduced inflammation and halted lesion growth, alongside potential favorable remodeling from balloon angioplasty itself. Histology confirmed decreased macrophage content and cathepsin expression in DCB-treated lesions. These results demonstrate that paclitaxel DCBs not only inhibit restenosis but also exert beneficial anti-atherosclerotic effects by attenuating inflammation and plaque advancement in nonobstructive disease. This provides mechanistic reassurance regarding DCB safety and suggests potential utility as regional endovascular therapy for atherosclerosis. In the context of COVID-19-associated cardiovascular complications—where endothelial injury, heightened inflammation, and accelerated atherothrombosis contribute to poor outcomes—these anti-inflammatory and plaque-stabilizing properties of paclitaxel DCBs may offer therapeutic implications for managing vulnerable plaques or post-infectious vascular risk in high-risk patients. Further clinical translation is warranted to explore DCBs in such inflammatory cardiovascular scenarios.