Safety and Feasibility of Subcutaneous Purse-String Suture of the Femoral Vein After Electrophysiological Procedures on Uninterrupted Oral Anticoagulation.

The aim of this study was to compare safety and feasibility of a subcutaneous purse-string suture (PSS) with manual compression (MC) to gain hemostasis in patients after multiple femoral venous punctures undergoing electrophysiological procedures on uninterrupted oral anticoagulation (OAK). A total of 784 patients who underwent catheter ablation for atrial fibrillation (n = 564) or (a)typical atrial flutter (n = 220) were assessed. Four hundred sixty-two patients received PSS (58.9%) and 322 patients (41.1%) received MC to gain hemostasis. All patients were on uninterrupted full-dose OAK. During the procedure, weight-adapted heparin was applied. Venous sheath diameter were 8Fr (n = 2)/11.5Fr (n = 1) for left atrial or 8Fr (n = 1)/6Fr (n = 2) for right atrial procedures. No protamine was administered at the end of the procedure. After PSS, patients' had 6 hours of bed rest compared with 10 hours after MC (sheath removal after 4 hours followed by a bandage for 6 hours). PSS was removed the following day. All patients underwent duplex sonography of the access site the following day. Using the PSS, hemostasis was achieved in 453 of 462 patients (98%). MC leads to hemostasis in all 322 patients. No difference was found between the 2 approaches regarding hematomas (<5 cm or >5 cm), arterio-venous fistulas, or pseudoaneurysms. No major complication such as ipsilateral leg ischemia, the need of vascular surgery, or deep vein thrombosis occurred. In conclusion, PSS is a safe and effective way to gain immediate hemostasis after multiple punctures of the femoral vein in patients undergoing catheter ablation on OAK. PSS avoids MC and leads to shorter patient immobilization.

Selective retroinfusion of GSH and cariporide attenuates myocardial ischemia-reperfusion injury in a preclinical pig model.

OBJECTIVE: Reperfusion after ischemia may contribute to loss of myocardial function and increase in infarct size. Scavenging of reactive oxygen species (ROS) by glutathione (GSH) and inhibition of the sodium-proton-exchanger by cariporide are both capable of reducing myocardial reperfusion injury. We tested the efficacy of both agents applied regionally into the myocardium immediately before reperfusion. METHODS: Neonatal rat cardiomyocytes (NRCMs) were exposed to either hypoxia (H, 8 h)/reoxygenation (R, 1 h) or H2O2 (300 microM) in the presence or absence of GSH (10 mg/ml). In pigs (n=5 per group), percutaneous LAD occlusion was performed for 60 min. Application of GSH (250 mg/kg) and/or cariporide (1 mg/kg) was achieved by pressure-regulated retroinfusion of the anterior cardiac vein draining the ischemic area starting 5 min before reopening of the occluded LAD. Seven days later, subendocardial segment shortening (SES) was analyzed by sonomicrometry. Infarct size was determined by methylene-blue staining of the non-ischemic area and tetrazolium red staining of the viable myocardium in the area at risk (AAR). RESULTS: NRCM incubated with GSH (10 mg/ml) survived H/R or H2O2 (0.3 mM) to a larger extent than untreated cells. In pigs, infarct size of untreated hearts (51 +/- 6% of the AAR) was not significantly altered by GSH or cariporide retroinfusion alone (41 +/- 3% and 42 +/- 6%). In contrast, combined retroinfusion of cariporide and GSH significantly reduced infarct size (29 +/- 3%). SES of the infarcted area was improved only after cariporide/GSH retroinfusion as compared to untreated hearts. Additional systemic application of CD18-antibody IB4 (1.5 mg/kg) did not alter infarct size or SES in comparison to GSH/cariporide retroinfusion alone. CONCLUSION: Timely application of GSH scavenging ROS and cariporide targeting ion imbalance provides cardioprotection to the postischemic heart, which is superior to either treatment alone. The lack of an effect of additional IB4 treatment may indicate that GSH/cariporide retroinfusion itself affects leukocyte-dependent reperfusion injury.

Incidence and relevance of nonreentrant monomorphic ventricular tachycardia in patients with frequent implantable cardioverter defibrillator interventions.

BACKGROUND: Nonreentrant ventricular tachycardia (VT) originates in hearts without structural disease but occasionally can occur in patients with different cardiomyopathies equipped with an implantable cardioverter defibrillator (ICD). METHODS: In a series of 142 ICD recipients with structural heart disease undergoing ablation for recurrent or incessant monomorphic VT, nonreentrant VTs were identified. RESULTS: Nonreentrant VTs were the cause of appropriate ICD interventions in 12 patients (8.4%). The underlying heart disease was nonischemic cardiomyopathy in eight patients, prior myocardial infarction in two patients, and valvular cardiomyopathy in two patients with a mean left ventricular ejection fraction of 42 ± 7%. Unresponsiveness to antitachycardia pacing and repetitive spontaneous re-initiation of the VT after defibrillation was the cause of frequent ineffective ICD interventions including repetitive ICD shocks in these patients. Using ICD interrogation, one or more episodes of a severe electrical storm (≥3 serial efficacious ICD shocks within 15 min) were more frequently documented in patients with nonreentrant VTs (10/12) than in patients with scar-related reentrant VTs (36/115). The origin of the nonreentrant VT was the left ventricular outflow tract in seven patients, the right ventricular outflow tract in three patients, and the tricuspid and mitral annulus in each one patient. Catheter ablation including epicardial mapping in 2 patients eliminated the nonreentrant VT in 11 of 12 patients and prevented recurrent VT storm. CONCLUSIONS: Repetitive nonreentrant VTs may be ineffectively treated by ICD interventions and can be the cause of an electrical storm in different cardiomyopathies.