Robotic ventral hernia repair: a safe and durable approach.

BACKGROUND: Short-term success following robotic-assisted ventral hernia repair (RVHR) is well established; however, data describing outcomes after the first year are limited. In this study, we followed a cohort of patients with an average of 1.8 years of follow-up to demonstrate the durability of this technique and examine risk factors for recurrence. METHODS: A retrospective analysis of RVHR performed by a single surgeon from 2012 to 2016 was done. The technical approach for hernia repair consisted of tension-free primary fascial closure with placement of preperitoneal mesh when possible. The primary end point of hernia recurrence was determined based on physical examination or imaging documented in the medical record. A logistic regression model was used to identify patient risk factors for recurrence. RESULTS: One hundred and eight RVHRs were performed over 4 years. Mean age was 52.72 ± 13.61 years, BMI was 33.07 ± 7.82 kg/m2, and hernia defect size was 70.1 ± 86.3 cm2. In terms of patient characteristics, 17.6% of patients were diabetic, 13.9% were smokers preoperatively, 72.2% were ASA class 3 or higher, and 29.6% had prior VHR. Primary fascial closure was achieved in all RVHRs, with 23.1% requiring component separation. Mesh was used in 97.2% of patients: 79.5% had preperitoneal mesh and 17.6% had intraperitoneal onlay mesh. Ninety-eight percent of patients had long-term follow-up at a mean of 625.6 days. Recurrence rate was 12%, with one recurrence attributed to an inguinal hernia fixed concurrently with a midline defect. There were no statistically significant differences in gender, age, BMI, ASA class, incidence of diabetes, smoking status, or number of previous hernia repairs. Hernia defect size and perioperative complications including SSO, ileus, obstruction, or any other medical complication were not predictive of recurrence. Technical approach did not affect outcomes. CONCLUSION: RVHR is safe and durable with a low recurrence rate at a mean of 21 months postoperatively. Patient characteristics or type of repair were not predictive of recurrence.

Natriuretic peptides like NO facilitate cardiac vagal neurotransmission and bradycardia via a cGMP pathway.

We tested the hypothesis that natriuretic peptide receptors (NPRs) that are coupled to cGMP production act in a similar way to nitric oxide (NO) by enhancing acetylcholine release and vagal-induced bradycardia. The effects of enzyme inhibitors and channel blockers on the action of atrial natriuretic peptide (ANP), brain-derived natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) were evaluated in isolated guinea pig atrial-right vagal nerve preparations. RT-PCR confirmed the presence NPR B and A receptor mRNA in guinea pig sinoatrial node tissue. BNP and CNP significantly (P < 0.05) enhanced the heart rate (HR) response to vagal nerve stimulation. CNP had no effect on the HR response to carbamylcholine and facilitated the release of [(3)H]acetylcholine during atrial field stimulation. The particulate guanylyl cyclase-coupled receptor antagonist HS-142-1, the phosphodiesterase 3 inhibitor milrinone, the protein kinase A inhibitor H89, and the N-type calcium channel blocker omega-conotoxin all blocked the effect of CNP on vagal-induced bradycardia. Like NO, BNP and CNP facilitate vagal neurotransmission and bradycardia. This may occur via a cGMP-PDE3-dependent pathway increasing cAMP-PKA-dependent phosphorylation of presynaptic N-type calcium channels.