Risk of Peri-implant Fracture With Long Versus Short Cephalomedullary Nailing for Geriatric Patients With Intertrochanteric Femur Fracture.

Intramedullary fixation using a short or long cephalomedullary nail (CMN) for treating hip fractures has gained popularity in recent years. We evaluated reoperation rates requiring device removal of short or long CMNs for patients 65 years and older. A retrospective study was performed at a level I trauma center over a 10-year period (2005-2015). Patients 65 years and older who were treated for intertrochanteric hip fractures with CMNs were included. This study included 893 patients (600 patients treated with a short CMN vs 293 treated with a long CMN). Patients in both cohorts were comparable in age, sex, and Injury Severity Score. There was no significant difference in comorbidities between the short and long CMN groups. Hospital length of stay (7.13 vs 6.88 days, P=.407) and intensive care unit length of stay (4.97 vs 4.63 days, P=.732) were not significantly different between the short and long CMN cohorts, respectively. The in-hospital mortality rate also did not vary between the 2 groups (1.3% for short CMN vs 2.7% for long CMN, P=.139). A significantly higher proportion of patients treated with a long CMN were discharged to a skilled nursing facility (63.4% vs 56.1%, P=.042). The overall reoperation rate was also comparable, 4.7% and 3.4% in the short CMN and long CMN groups, respectively (P=.367). No difference was found between the 2 treatment modalities (short or long CMN) for the elderly population. Both implants had similar rates of reoperation and implant failure. There is a cost consideration, with increasing length of the nail corresponding to increased cost. [Orthopedics. 2022;45(5):304-309.].

Angiotensin II induces afterdepolarizations via reactive oxygen species and calmodulin kinase II signaling.

Renin-angiotensin system inhibitors significantly reduce the incidence of arrhythmias. However, the underlying mechanism(s) is not well understood. We aim to test the hypothesis that angiotensin II (Ang II) induces early afterdepolarizations (EADs) and triggered activities (TAs) via the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-ROS-calmodulin kinase II (CaMKII) pathway. ROS production was analyzed in the isolated rabbit myocytes loaded with ROS dye. Ang II (1-2 µM) increased ROS fluorescence in myocytes, which was abolished by Ang II type 1 receptor blocker losartan, NADPH oxidase inhibitor apocynin, and antioxidant MnTMPyP, respectively. Action potentials were recorded using the perforated patch-clamp technique. EADs emerged in 27 out of 41 (66%) cells at 15.8 ± 1.6 min after Ang II (1-2 µM) perfusion. Ang II-induced EADs were eliminated by losartan, apocynin, or trolox. The CaMKII inhibitor KN-93 (n=6) and inhibitory peptide (AIP) (n=4) also suppressed Ang II-induced EADs, whereas the inactive analogue KN-92 did not. Nifedipine, a blocker of L-type Ca current (I(Ca)(2+)(,L)), or ranolazine, an inhibitor of late Na current (I(Na)(+)), abolished Ang II-induced EADs. The effects of Ang II on major membrane currents were evaluated using voltage clamp. While Ang II at same concentrations had no significant effect on total outward K(+) current, it enhanced I(Ca.L) and late I(Na), which were attenuated by losartan, apocynin, trolox, or KN-93. We conclude that Ang II induces EADs via intracellular ROS production through NADPH oxidase, activation of CaMKII, and enhancement of I(Ca,L) and late I(Na). These results provide evidence supporting a link between renin-angiotensin system and cardiac arrhythmias.