388 research outputs found
Old Dog, New Tricks - Usefulness of the ECG in Monitoring Acute Rejection Post Cardiac Transplantation
Electrocardiographic abnormalities have been described in the setting of acute rejection following orthotopic cardiac transplantation. The following is a brief commentary related to an interesting case report by Goldraich et al. which was recently published in the VAD Journal
Pouvoirs locaux et organisation du territoire des cités pinéniciennes sous l'Empire perse achéménide
Este articula trata de las ciudades fenicias y de la organizaciôn de sus territorios durante el Edad del Hierro lll/Perfodo Persa (del s. vi al s. iv a.C). Una descripciôn geogrâfica de las ciudades-estados fenicias es propuesta segûn la documentaciàn conocida actualmente. Las estructuras social-politicas de estas ciudades son estudiadas y caracterizadas en comparaciôn con los otros estados del Prôximo Oriente y con las ciudades griegas contemporâneas (poleis). Se trata también de la situaciôn de las ciudades fenicias en el cuadro politico del imperio perso, en particular de las relaciones entre el gobierno central y los gobiernos locales autónomos.This paper deals witfi the Ptioenician local powers and the organization of tfieir territories during the Iran Age lll/Persian Period (vith-ivth B.C.). A geograpfiical description of the Phoenician city-states is proposed from the présent state of documentation. The socio-political structures of thèse cities are studied and characterized in comparison with the neighbouring Near Eastern states and the contemporaneous Greek cities (poleis). The place of the Phoenician cities in the political framework of the Persian empire is aiso analysed, in particular the relations between the central power and the local autonomous powers
CMR of LV non-compaction cardiomyopathy: association of clinical presentation and prognosis with cardiac phenotype
Left ventricular non-compaction (LVNC) is a rare congenital disorder characterized by two layered myocardium; trabeculated (non-compacted) and a non-trabeculated (compacted). LVNC is increasingly being recognized due to better imaging technology as a cause for heart failure and sudden cardiac death; however, data on clinical and imaging characteristics remains limited
Snaring of the Right Ventricular Lead During Cavotricuspid Isthmus Ablation
The presence of a right ventricular (RV) lead may interfere with cavotricuspid isthmus (CTI) ablation. We present a new option of lifting the RV lead from the CTI allowing a successful ablation of a CTI-dependent flutter without compromising lead integrity and functionality
Flecainide Toxicity Resulting in Pacemaker Latency and Intermittent Failure to Capture
BACKGROUND Flecainide is a class Ic antiarrhythmic agent used in the treatment of supraventricular and ventricular arrhythmias. It is associated with a potent adverse effect profile; however, the effects of flecainide toxicity in the setting of a pacemaker have not been well described. We describe a unique case of flecainide toxicity secondary to acute kidney injury in the setting of a dual-chamber pacemaker, resulting in ventricular capture latency and intermittent failure to capture.
CASE REPORT The patient was a 91-year-old female with a history of atrial fibrillation maintained in sinus rhythm on flecainide, who presented complaining of purple visual disturbances and syncope. She was found to be hypotensive and bradycardic, with a heart rate between 30 to 40 beats per minute. Lab work was notable for creatinine at 2.12 mg/dL. A 12-lead ECG demonstrated atrial and ventricular pacing with severely widened QRS complex and a significant latency between the pacemaker ventricular spike and the ventricular capture. The pacemaker was interrogated, revealing a significant increase in ventricular threshold from 0.75 V at 0.5 ms at baseline to 5.0 V at 1 ms to obtain consistent capture. After multiple boluses of IV sodium bicarbonate, the QRS acutely narrowed, latency interval improved, and consistent pacing capture was achieved. The flecainide level drawn on arrival was 3.09 mcg/mL.
CONCLUSIONS Flecainide increases the ventricular capture threshold for pacemakers. Toxicity in these patients may present with pacemaker ventricular capture latency or failure to capture
Visualizing Mutation-Specific Differences in the Trafficking-Deficient Phenotype of Kv11.1 Proteins Linked to Long QT Syndrome Type 2
KCNH2 encodes the Kv11.1 α-subunit that underlies the rapidly activating delayed-rectifier K+ current in the heart. Loss-of-function KCNH2 mutations cause long QT syndrome type 2 (LQT2), and most LQT2-linked missense mutations inhibit the trafficking of Kv11.1 channel protein to the cell surface membrane. Several trafficking-deficient LQT2 mutations (e.g., G601S) generate Kv11.1 proteins that are sequestered in a microtubule-dependent quality control (QC) compartment in the transitional endoplasmic reticulum (ER). We tested the hypothesis that the QC mechanisms that regulate LQT2-linked Kv11.1 protein trafficking are mutation-specific. Confocal imaging analyses of HEK293 cells stably expressing the trafficking-deficient LQT2 mutation F805C showed that, unlike G601S-Kv11.1 protein, F805C-Kv11.1 protein was concentrated in several transitional ER subcompartments. The microtubule depolymerizing drug nocodazole differentially affected G601S- and F805C-Kv11.1 protein immunostaining. Nocodazole caused G601S-Kv11.1 protein to distribute into peripheral reticular structures, and it increased the diffuse immunostaining of F805C-Kv11.1 protein around the transitional ER subcompartments. Proteasome inhibition also affected the immunostaining of G601S- and F805C-Kv11.1 protein differently. Incubating cells in MG132 minimally impacted G601S-Kv11.1 immunostaining, but it dramatically increased the diffuse immunostaining of F805C-Kv11.1 protein in the transitional ER. Similar results were seen after incubating cells in the proteasome inhibitor lactacystin. Differences in the cellular distribution of G601S-Kv11.1 and F805C-Kv11.1 protein persisted in transfected human inducible pluripotent stem cell derived cardiomyocytes. These are the first data to visually demonstrate mutation-specific differences in the trafficking-deficient LQT2 phenotype, and this study has identified a novel way to categorize trafficking-deficient LQT2 mutations based on differences in intracellular retention
Search for proton radioactivity in <SUP>65</SUP>As, <SUP>69</SUP>Br and <SUP>77</SUP>Y
A search for proton radioactivity in 65As, 69Br and 77Y, produced as residues of fusion reactions, was carried out at the Orsay Tandem accelerator. The residues were collected at the image point of the spectrometer Soleno and implanted into the gaseous medium of an ionization chamber which was also used to detect the radioactivity protons. No such protons have been observed in the energy range of 250–600 keV and in the half-life interval of 10 μs-100 ms, within a production cross section sensitivity of 1 μb.Facultad de Ciencias Exacta
Acute Effects of Implantable Cardioverter-Defibrillator Shocks on Biomarkers of Myocardial Injury, Apoptosis, Heart Failure, and Systemic Inflammation
Background: Implantable cardioverter‐defibrillator (ICD) shocks are potentially associated with myocardial injury, altered hemodynamics, apoptosis, and inflammatory signaling. Their precise cellular impact can be explored after defibrillation testing (DFT) via biomarkers. We evaluated changes in biomarkers after ICD shocks during DFT.
Methods: We prospectively enrolled outpatients presenting for first implantation of a cardiac device. Biomarkers indicative of myocardial injury, inflammation, and apoptosis were measured before and after implantation, and compared between patients receiving DFT (DFT+) to those not (DFT−).
Results: Sixty‐three patients were enrolled, 40 in the DFT+ group and 23 in the DFT− group. Average levels of troponin I, hsCRP, Calprotectin, N‐terminal pro B‐type natriuretic peptide (NTproBNP), and sFas increased by \u3e50% after cardiac device implantation compared to baseline. Increase in troponin never exceeded the 50‐fold upper limit of normal (2 ng/mL). Troponin trended higher in the DFT+ group at 8 hours (median 0.18 ng/mL, interquartile range [IQR] 0.11–0.48) versus the DFT− group (0.10 ng/mL, IQR 0.06–0.28, P = 0.0501); NTproBNP had a similar trend (P = 0.0581). sFas significantly increased in the DFT+ group from baseline (median 4663 pg/mL, IQR 2908–5679) to 24 hours (5039 pg/mL, IQR 3274–6261; P = 0.0338) but not in the DFT− group (P = 0.4705).
Conclusion: DFT testing is associated with acutely increased plasma levels of troponin and sFas, a biomarker of apoptosis, along with a trend toward higher NTproBNP
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