Nishimura, Rick A.

Background— Lead-related or valve-related endocarditis can complicate cardiovascular implantable electronic device (CIED) infection in patients with both CIED and prosthetic valves. The objective of this study was to determine the outcomes of transvenous lead extraction for CIED infection in patients with prosthetic valves. Methods and Results— We retrospectively screened 794 transvenous lead extraction procedures, between September 1, 2001 and August 31, 2012, at Mayo Clinic to identify patients with prosthetic valves who underwent lead extraction for infection. Demographic, clinical, and follow-up characteristics were analyzed. In total, 51 patients (6%) met the study inclusion criteria, of whom 20 had pocket infection and 31 had lead-related or valve-related, or both, endocarditis or bloodstream infection (mean age, 67 [18] years). Staphylococcal species were the most common pathogens, including Staphylococcus aureus in 20 cases (39%) and coagulase-negative staphylococci in 19 cases (37%). Overall, 127 transvenous leads (median lead age, 52 months) were extracted. Of these leads, 123 (97%) were removed completely. The in-hospital mortality rate was 9.8%; no deaths were attributable to the extraction procedure. Ninety-five percent of patients who survived had no evidence of recurrent device-related or valve-related infection. Conclusions— Transvenous lead extraction seems safe and curative in patients with CIED infection and prosthetic valves. Cure of infection can be achieved in the majority of patients with complete CIED removal and antimicrobial therapy and without valve surgery.

The management of women with mechanical heart valves during pregnancy remains difficult and controversial. There is no ideal anticoagulation regimen for this unique population, as there are inherent risks and benefits of each approach for both mother and fetus. There has been limited data available to guide the clinician in the optimal treatment strategy for an individual patient. The AHA/ACC Guidelines for the Management of Patients with Valvular Heart Disease created class recommendations for this population based upon current evidence, which is summarized in this review.

Background The endothelium modulates vascular tone through release of vasodilating substances, such as endothelium-derived relaxing factors, and vasoconstricting substances, such as endothelin. Endothelin concentrations are elevated in humans with atherosclerosis and in hypercholesterolemic pigs. Furthermore, the endothelium-dependent vasodilator acetylcholine increases endothelin in hypercholesterolemia in association with coronary vasoconstriction. The present study was designed to test the hypotheses that coronary endothelial dysfunction in humans is characterized by enhanced coronary and circulating endothelin and that the vasoconstriction associated with acetylcholine results in further release of coronary endothelin. Methods and Results Coronary and circulating endothelin concentrations were measured at baseline and during intracoronary acetylcholine administration in 20 patients undergoing diagnostic coronary angiography. Patients were divided into two groups on the basis of their response to intracoronary acetylcholine. Group 1 (n=7) demonstrated a normal vasodilatory response, but group 2 (n=13) demonstrated coronary vasoconstriction. Baseline coronary and circulating endothelin concentrations (as determined by coronary sinus and femoral artery measurements, respectively) were higher in patients who responded to acetylcholine with coronary vasoconstriction (group 2) than in group 1 patients (coronary sinus, 15.9±1.0 pg/mL versus 7.1±1.0 pg/mL; femoral, 14.1±0.9 pg/mL versus 6.8±1.0 pg/mL, respectively; P <.01). In response to intracoronary acetylcholine, a further increase in coronary endothelin was observed only in group 2; this increase correlated with changes in coronary artery diameter. Conclusions This study demonstrates that endothelin immunoreactivity is enhanced in the coronary and systemic circulation in humans with coronary endothelial dysfunction. Moreover, acetylcholine further increased coronary endothelin concentration in patients with coronary endothelial dysfunction and was associated with coronary vasoconstriction. These observations strongly support a role for endothelin as an early participant in and marker for coronary endothelial dysfunction in humans.