Transradial catheterization (TRC) has been associated with a lower incidence of major access site related complications as compared to the transfemoral approach. With the increased adoption of transradial access, it is essential to understand the potential major and minor complications of TRC. The most common complication is asymptomatic radial artery occlusion, which rarely leads to clinical events, owing to the dual collateral perfusion of the hand. Adequate anticoagulation, appropriate compression techniques, and smaller sheath size can minimize the risk of radial artery occlusion. Hand ischemia with necrosis has never been reported during TRC with thorough pre-examination of intact collateral circulation. Radial artery spasm is relatively common, and can result in access and procedural failure. It can be prevented by the use of vasodilator cocktails and hydrophilic sheaths. Radial artery perforation can lead to severe forearm hematoma and compartment syndrome if not managed promptly. Careful observation, prompt detection of the hematoma, and management with a pressure bandage dressing are critical to avoid serious complications. Pseudoaneurym and arteriovenous fistula are rare complications, which can likely be managed conservatively without surgical intervention. Nerve injury occurring during access has been reported. Close observation for improvement is necessary, although symptoms usually improve over time. In summary, to prevent access site complications, avoidance of multiple punctures, gentle catheter manipulation, use of guided compression, coupled with careful observation for adverse warning signs such as hematoma, loss of pulse, pain, are critical for safe and effective TRC.

This study suggests that moderate-to-severe ASA might be associated with LA dysfunction in patients with PFO. The resultant similarities to the pathophysiology of AF might represent an additional contributing mechanism for arterial embolism in such patients.

Recently, a growing body of clinical data has shown that the first generation of drug-eluting stents (1st-gen DES) implantation could elicit coronary conduit artery vasomotor dysfunction at nonstented reference segments as late as 12 months after implantation compared with that seen with bare-metal stents. The mechanism of this phenomenon is still not fully understood. Pathological studies have implicated delayed arterial healing and poor re-endothelialization after the 1st-gen DES implantation. Given the vast use of DES globally, a thorough understanding of the early and long-term safety of these devices is paramount. Therefore, this article systematically reviews the current clinical, pathophysiological, and histopathological available data regarding 1st-gen DES-associated vascular endothelial dysfunction. Meanwhile, we will also review the newer generation of DES and emerging endothelial-friendly technology.

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