Percutaneous, Antegrade Access of the Superficial Femoral Artery can be Safely Used in Procedures for the Treatment of Lower Extremity Limb Ischemia.

BACKGROUND: Recent studies have shown that antegrade access for treatment of infrainguinal peripheral vascular disease is associated with decreased radiation exposure and contrast use without a significant increase in access complication, although data are limited on antegrade superficial femoral artery (SFA) access for larger sheath sizes. We aim to describe a single institution's contemporary experience with percutaneous antegrade SFA access. METHODS: A retrospective review of percutaneous, infrainguinal endovascular interventions for arterial occlusive disease at a major academic institution was conducted between 2018 and 2020. Antegrade, percutaneous, SFA access cases were included. Information on demographics, indication, sheath size, arteries treated, type of intervention, concurrent pedal access, closure devices, and complications was collected and analyzed. RESULTS: A total of 45 patients with an average body mass index of 25.25 were identified. Indications for intervention included tissue loss (64.4%), rest pain (6.7%), claudication (13.3%), and acute limb ischemia (11.1%). Of which, 80.0% of patients had multilevel interventions. Angioplasty was performed in 68.8% of patients, stenting in 8.3%, atherectomy in 15.6%, and thrombectomy in 7.3%. Nearly a quarter of cases involved concurrent pedal access. Maximum sheath size was 4F for 4.4% of patients, 5F for 28.9%, 6F for 46.7%, 7F for 11.1%, and 8F for 8.9%. The closure device was utilized in 75.6% of cases, with no closure device failures. In the entire cohort, there were no demonstrated access site complications. CONCLUSIONS: This study demonstrates percutaneous, antegrade SFA access for complex endovascular interventions for infrainguinal occlusive disease can be effectively utilized, even with larger sheath size. Moreover, routine use of closure devices is safe, improving patient comfort and expediting time to ambulation.

Intracoronary delivery of recombinant TIMP-3 after myocardial infarction: effects on myocardial remodeling and function.

Ischemia-reperfusion (IR) and myocardial infarction (MI) cause adverse left ventricular (LV) remodeling and heart failure and are facilitated by an imbalance in matrix metalloproteinase (MMP) activation and the endogenous tissue inhibitors of metalloproteinase (TIMPs). We have identified that myocardial injections of recombinant TIMP-3 (rTIMP-3; human full length) can interrupt post-MI remodeling. However, whether and to what degree intracoronary delivery of rTIMP-3 post-IR is feasible and effective remained to be established. Pigs (25 kg) underwent coronary catheterization and balloon occlusion of the left anterior descending coronary artery (LAD) for 90 min whereby at the final 4 min, rTIMP-3 (30 mg, n = 9) or saline was infused in the distal LAD. LV echocardiography was performed at 3-28 days post-IR, and LV ejection fraction (EF) and LV end-diastolic volume were measured. LV EF fell and LV end-diastolic volume increased from baseline (pre-IR) values (66 ± 1% and 40 ± 1 ml, respectively, means ± standard deviation) in both groups; however, the extent of LV dilation was reduced in the rTIMP-3 group by 40% at 28 days post-IR (P < 0.05) and the fall in LV EF was attenuated. Despite equivalent plasma troponin levels (14 ± 3 ng/ml), computed MI size at 28 days was reduced by over 45% in the rTIMP-3 group (P < 0.05), indicating that rTIMP-3 treatment abrogated MI expansion post-IR. Plasma NH2-terminal pro-brain natriuretic peptide levels, an index of heart failure progression, were reduced by 25% in the rTIMP-3 group compared with MI saline values (P < 0.05). Although the imbalance between MMPs and TIMPs has been recognized as a contributory factor for post-MI remodeling, therapeutic strategies targeting this imbalance have not been forthcoming. This study is the first to demonstrate that a relevant delivery approach (intracoronary) using rTIMP can alter the course of post-MI remodeling.NEW & NOTEWORTHY Myocardial ischemia and reperfusion injury remain significant causes of morbidity and mortality whereby alterations in the balance between matrix metalloproteinase and tissue inhibitor of metalloproteinase have been identified as contributory biological mechanisms. This novel translational study advances the concept of targeted delivery of recombinant proteins to modify adverse myocardial remodeling in ischemia-reperfusion injury.