Multidisciplinary approach to transvenous lead extraction: a single center's experience.

OBJECTIVE: To evaluate the success and complication rates of a single center's multidisciplinary approach to transvenous lead extraction. SETTING: One university hospital. PARTICIPANTS: One hundred ninety-five patients scheduled for transvenous lead extraction. INTERVENTIONS: A multidisciplinary approach to transvenous lead extraction involving cardiac surgery, electrophysiology, perfusion, and cardiac anesthesiology. MEASUREMENTS AND MAIN RESULTS: A case series of 351 lead extractions performed in 195 patients over a 42-month period. Indications, success rates, and complication rates were tracked and retrospectively evaluated and reported. Indications for lead extraction included 53.3% because of lead malfunction, 36.9% because of infection, with the remaining 9.7% from other categories such as venous stenosis. The lead extraction rate was 99.7%, with complete removal in 97.7%. The overall major complication rate was 3.08%. After an initial 1-year period of performing lead extractions, the overall major complication rate reduced to 1.23%. CONCLUSIONS: Transvenous lead extraction generally is a safe procedure, but not without complications. A multidisciplinary approach involving cardiac surgery, electrophysiology, and cardiac anesthesiology allows for successful management and the ability to rapidly manage major complications.

Plasma vasopressin levels in patients with right-sided heart dysfunction and chronic thromboembolic pulmonary hypertension (CTEPH).

OBJECTIVES: Patients with left-sided heart dysfunction and volume overload often have associated elevations in vasopressin from neuroendocrine activation. The authors investigated perioperative levels of vasopressin in patients with isolated right-sided heart dysfunction from chronic thromboembolic pulmonary hypertension. DESIGN: Prospective, observational study. SETTING: Single center, tertiary hospital. PARTICIPANTS: Patients with chronic thromboembolic pulmonary hypertension undergoing pulmonary thromboendarterectomy. INTERVENTIONS: Vasopressin levels were measured in 22 patients during the perioperative period. MEASUREMENTS AND MAIN RESULTS: Vasopressin was undetectable in 8/22 patients at baseline. As a group, vasopressin levels at baseline and after induction of anesthesia were 0.8 pg/mL (median; 0.5-1.5, interquartile range of 25% and 75%) and 0.7 pg/mL (median; 0.5-1.4, interquartile range of 25% and 75%), respectively. During cardiopulmonary bypass (CPB), vasopressin increased to 13.9 pg/mL (median; 6.7-19.9, interquartile range of 25% and 75%). Vasopressin remained elevated after deep hypothermic circulatory arrest (DHCA) at 10.5 pg/mL (median; 6.5-19.9 interquartile range of 25% and 75%) and after CPB at 19.9 pg/mL (median; 11.1-19.9 interquartile range of 25% and 75%). CONCLUSIONS: Vasopressin levels in PTE patients are in the low-to-normal range at baseline and may be a clinically relevant issue in the hemodynamic management of PTE.

DNA damage and mutations induced by arachidonic acid peroxidation.

Endogenous cellular oxidation of omega6-polyunsaturated fatty acids (PUFAs) has long been recognized as a contributing factor in the development of various cancers. The accrual of DNA damage as a result of reaction with free radical and electrophilic aldehyde products of lipid peroxidation is believed to be involved; however, the genotoxic and mutation-inducing potential of specific membrane PUFAs remains poorly defined. In the present study we have examined the ability of peroxidizing arachidonic acid (AA, 20:4omega6) to induce DNA strand breaks, base modifications, and mutations. The time-dependent induction of single-strand breaks and oxidative base modifications by AA in genomic DNA was quantified using denaturing glyoxal gel electrophoresis. Mutation spectra were determined in XP-G fibroblasts and a repair-proficient line corrected for this defect by c-DNA complementation (XP-G(+)). Mutation frequencies were elevated from approximately 5- to 30-fold over the background following reaction of DNA with AA for various times. The XPG gene product was found to be involved in the suppression of mutations after extended reaction of DNA with AA. Arachidonic acid-induced base substitutions were consistent with the presence of both oxidized and aldehyde base adducts in DNA. The frequency of multiple-base substitutions induced by AA was significantly reduced upon correction for the XPG defect (14% vs 2%, P = 0.0015). Evidence is also presented which suggests that the induced frequency of multiple mutations is lesion dependent. These results are compared to published data for mutations stimulated by alpha,beta-unsaturated aldehydes identified as products of lipid peroxidation.