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A pacemaker is an electrical device implanted in the chest to regulate the heartbeat in persons whose natural heartbeat is irregular, too fast or too slow. Artificial pacemakers can become infected; this occurs in one to three percent of cases. Original implantation of the device can cause infection, but the pacemaker can also develop infection years after placement. An unrelated infection in the body, such as an ear infection, can introduce bacteria into the bloodstream which can lodge on the pacemaker lead (wire); a common cause of this is Staphylococcus aureus bacteria. Evidence of bacterial growth on the device is very difficult to detect, but is important because infection can cause a blood clot, pulmonary embolism, or abscess. One approach to diagnosis is to remove the pacemaker lead by pulling it out through a vein slowly over several days, or if this fails by a surgical procedure. Echocardiography is an approach that it helpful for locating the pacemaker and the infection; it uses ultrasound to visualize the heart and pacemaker without removing the device. While two-dimensional echocardiography has been used, an improved technique is transesophageal (through the esophagus) echocardiography which is able to show small vegetations (bacterial colonies) on the pacemaker more effectively. The case of a 70-year-old man who suffered from a fever unresponsive to antibiotics for seven months is described; he had developed a pacemaker lead infection following an ear infection. Transesophageal echocardiography detected the vegetations and the pacemaker was removed successfully using a new extraction technique, which is described. (Consumer Summary produced by Reliance Medical Information, Inc.)

β-Blocker Effects on SQTS-Mutant K+ Channels Background N588K-KCNH2 and V307L-KCNQ1 mutations lead to a gain-of-function of IKr and IKs thus causing short-QT syndromes (SQT1, SQT2). Combined pharmacotherapies using K+-channel-blockers and β-blockers are effective in SQTS. Since β-blockers can block IKr and IKs, we aimed at determining carvedilol's and metoprolol's electrophysiological effects on N588K-KCNH2 and V307L-KCNQ1 channels. Methods Wild-type (WT)-KCNH2, WT-KCNQ1 and mutant N588K-KCNH2 and V307L-KCNQ1 channels were expressed in CHO-K1 or HEK-293T cells and IKs and IKr were recorded at baseline and during β-blocker exposure. Results Carvedilol (10 μM) reduced IKs tail in WT- and V307L-KCNQ1 by 36.5 ± 5% and 18.6 ± 9% (P < 0.05). IC50 values were 16.3 μM (WT) and 46.1 μM (V307L), indicating a 2.8-fold decrease in carvedilol's IKs-blocking potency in V307L-KCNQ1. Carvedilol's (1 μM) inhibition of the IKr tail was attenuated in N588K-KCNH2 (4.5 ± 3% vs 50.3 ± 4%, WT, P < 0.001) with IC50 values of 2.8 μM (WT) and 25.4 μM (N588K). Carvedilol's IKr end-pulse inhibition, however, was increased in N588K-KCNH2 (10 μM, 60.7 ± 6% vs 36.5 ± 5%, WT, P < 0.01). Metoprolol (100 μM) reduced IKr end-pulse by 0.23 ± 3% (WT) and 74.1 ± 7% (N588K, P < 0.05), IKr tail by 32.9 ± 10% (WT) and 68.8 ± 7% (N588K, P < 0.05), and reduced IKs end-pulse by 18.3 ± 5% (WT) and 57.1 ± 11% (V307L, P < 0.05) and IKs tail by 3.3 ± 1% (WT) and 45.1 ± 13 % (V307L, P < 0.05), indicating an increased sensitivity to metoprolol in SQT mutated channels. Conclusions N588K-KCNH2 and V307L-KCNQ1 mutations decrease carvedilol's inhibition of the IKs or IKr tail but increase carvedilol's IKr end-pulse inhibition and metoprolol's inhibition of tail and end-pulse currents. These different effects on SQT1 and SQT2 mutated channels should be considered when using β-blocker therapy in SQTS patients. [ABSTRACT FROM AUTHOR]

Although less invasive then SAVR, TAVI is associated with a significant rate of access site and non-access site bleeding. These complications are major determinants of therapy outcome, however, the economic consequences are not well defined. The purpose of this study was to determine the relationship between bleeding, in-hospital resource utilization and costs among patients undergoing transfemoral aortic valve implantation (TF-AVI) at a representative university hospital in Germany. Between February 2010 and December 2011, we prospectively enrolled 60 consecutive patients undergoing TAVI using a 18F transfemoral approach at our institution. The relationship between overt bleeding (OVB), defined according to the definitions provided by the Valve Academic Research Consortium, in-hospital resource utilization and in-hospital costs was investigated. The mean age was 82 (±6) years, 53 % were female and the mean EuroScore was 17.2 % (±8, 7). Thirty-eight percent (23/60) of the patients had an OVB following TF-AVI procedure. In-hospital mortality was 8.7 % in the OVB patients (2/23) and 2.7 % among patients without any OVB (1/37; NOVB), which was not statistically significant ( p = 0.3). The total length of stay (LOS) of patients with and without bleeding complication were 15.0 ± 6.4 and 10.4 ± 5.1 days, respectively ( p < 0.01). Time spent on ICU in the OVB group was twice as long as compared to the NOVB group (120.5 ± 98.5 min vs. 63.6 ± 26.5 min, p < 0.01). Consequently, in-hospital costs were statistically significant higher in OVB patients (40.051 ± 9.293€ vs. 33.625 ± 4.368€, p < 0.01). Bleeding is associated with increased resource use and in-hospital costs among TF-AVI patients. Our data indicates that strategies reducing bleeding risk may have the potential to generate important in-hospital costs reductions in TF-AVI patients. [ABSTRACT FROM AUTHOR]

The development of 'transcatheter aortic valve implantation (TAVI)' is changing the field of cardiovascular medicine rapidly. The basic principle of TAVI is the percutaneous implantation of a bioprosthesis mounted in a metal frame. The prosthesis, which is attached to the tip of the catheter, is positioned in the native aortic valve and expanded. The first successful implantation was made by Alain Cribier in 2002. Several smaller mono- and multicenter studies later confirmed the technical feasibility of this procedure. Its true value as an important, therapeutic alternative to open heart surgery in inoperable and high-risk patients is now confirmed in large multicenter registries and by the prospective, randomized PARTNER trial. Decisive for the future acceptance of the procedure and for a possible expansion of the indication spectrum will be (1) continuous further development of the implantation technique and the prosthesis design, (2) reduction of TAVI-associated complications, (3) confirmation of the initial positive long-term results and (4) confirmation of the promising results in the treatment of surgical prosthesis dysfunctions and of patients with low to intermediate risk. [ABSTRACT FROM AUTHOR]

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We have generated transgenic rabbits lacking cardiac slow delayed-rectifier K~ current [IKs; long QT syndrome type I (LQTI)] or rapidly activating delayedrectifier K+ current [IKr; long QT syndrome type 2 (LQT2)]. Rabbits with either genotype have prolonged action potential duration and QT intervals; however, only LQT2 rabbits develop atrioventricular (AV) blocks and polymorphic ventricular tachycardia. We therefore sought to characterize the genotype-specific differences in AV conduction and ventricular refractoriness in LQTI and LQT2 rabbits. We carried out in vivo electrophysiological studies in LQTI, LQT2, and littermate control (LMC) rabbits at baseline, during isoproterenol infusion, and after a bolus of dofetilide and ex vivo optical mapping studies of the AV node! His-region at baseline and during dofetilide perfusion. Under isoflurane anesthesia, LQT2 rabbits developed infra-His blocks, decremental His conduction, and prolongation of the Wenckebach cycle length. In LQTI rabbits, dofetilide altered the His morphology and slowed His conduction, resulting in intra-His block, and additionally prolonged the ventricular refractoriness, leading to pseudo-AV block. The ventricular effective refractory period (VERP) in right ventricular apex and base was significantly longer in LQT2 than LQTI (P < 0.05) or LMC (P < 0.0 I), with a greater VERP dispersion in LQT2 than LQTI rabbits. Isoproterenol reduced the VERP dispersion in LQT2 rabbits by shortening the VERP in the base more than in the apex but had no effect on VERP in LQT1. EPS and optical mapping experiments demonstrated genotype-specific differences in AV conduction and ventricular refractoriness. The occurrence of infra-His blocks in LQT2 rabbits under isoflurane and intra-His block in LQTI rabbits after dofetilide suggest differential regional sensitivities of the rabbit His-Purkinje system to drugs blocking IKr and IKs. [ABSTRACT FROM AUTHOR]