Stress and anxiety are potential consequences from arrhythmias and implantable cardioverter defibrillator (ICD) shocks that can contribute to substantial morbidity. We assessed anxiety associated with an ICD and whether cognitive behavioral therapy (CBT) reduces anxiety.

Purpose. The purpose of this article is to show how custom "Y"-lead adapters and standard dual-chamber pacemakers can be used to produce pacing paradigms that will lead to stable experimental models of heart failure and atrial fibrillation.Description. With two custom lead adapters we used both ports of two dual-chamber clinical pacemakers to independently apply various pacing paradigms to either the ventricles or the atria of dogs.Evaluation. Because both ports of the ventricular pacemaker were used to apply stimuli through one lead, the device did not have to be modified to obtain ventricular pacing rates that are sufficiently elevated to lead to tachycardia-induced heart failure. Similarly, simultaneous use of both ports of the atrial pacemaker can be used to apply stimuli through one atrial lead to induce sustained atrial fibrillation.Conclusions. These techniques facilitate induction of experimental models of heart failure and atrial fibrillation without the need for modification of the clinical pacemaker.

Objective: To address the role that alloreactivity may play and better define the window for histoincompatible stem cell transplantation in utero. Subjects, Material and Methods: We studied 9 fetal blood specimens obtained by cardiocentesis during elective abortions in the second trimester by multicolor flow cytometry and in vitro stimulation. Results: Lymphocytes ranged from adult levels (3/9) to >90% leukocytes. Six specimens had T cells within adult range. T cells in the other specimens were reduced, while B cells were conversely elevated. This variability did not correlate with gestational age, or leukocyte composition. Following 4 h of mitogenesis, fetal CD4+ and CD8+ T cells from 1 of 5 specimens showed a response similar to that of maternal T cells, while the other 4 specimens showed a diminished response (0.3 ± 0.2-fold). This heterogeneity did not correlate with gestational age, or lymphocyte subset distribution. Following 18 h of in vitro mitogenesis, fetal T cells from 2 specimens showed a response similar to that of maternal T cells (0.8 ± 0.2-fold). Despite that, one specimen gave a 3-fold greater response in a one-way mixed lymphocyte reaction vs. maternal cells compared to the other specimen. Conclusion: We determine that fetal immunocompetence differs greatly during the second trimester and assessment of host vs. donor reactivity prior to in utero transplantation is likely to potentiate more favorable outcomes.

Opportunistic infections such as pulmonary tuberculosis (TB) increase local HIV-1 replication and mutation. As AIDS progresses, alteration of the HIV-1 gp120 V3 sequence is associated with a shift in viral coreceptor use from CCR5 (CD195) to CXCR4 (CD184). To better understand the effect of HIV/TB coinfection, we screened transcripts from bronchoalveolar lavage cells with high density cDNA arrays and found that CXCR4 mRNA is increased in patients with TB. Surprisingly, CXCR4 was predominately expressed on alveolar macrophages (AM). Mycobacterium tuberculosis infection of macrophages in vitro increased CXCR4 surface expression, whereas amelioration of disease reduced CXCR4 expression in vivo. Bronchoalveolar lavage fluid from TB patients had elevated levels of CCL4 (macrophage inflammatory protein-1β), CCL5 (RANTES), and CX3CL1 (fractalkine), but not CXCL12 (stromal-derived factor-1α). We found that M. tuberculosis infection of macrophages in vitro increased viral entry and RT of CXCR4, using HIV-1, but not of CCR5, using HIV-1. Lastly, HIV-1 derived from the lung contains CD14, suggesting that they were produced in AM. Our results demonstrate that TB produces a permissive environment for replication of CXCR4-using virus by increasing CXCR4 expression in AM and for suppression of CCR5-using HIV-1 by increasing CC chemokine expression. These changes explain in part why TB accelerates the course of AIDS. CXCR4 inhibitors are a rational therapeutic approach in HIV/TB coinfection.

Opportunistic infections such as pulmonary tuberculosis (TB) increase local HIV-1 replication and mutation. As AIDS progresses, alteration of the HIV-1 gp120 V3 sequence is associated with a shift in viral coreceptor use from CCR5 (CD195) to CXCR4 (CD184). To better understand the effect of HIV/TB coinfection, we screened transcripts from bronchoalveolar lavage cells with high density cDNA arrays and found that CXCR4 mRNA is increased in patients with TB. Surprisingly, CXCR4 was predominately expressed on alveolar macrophages (AM). Mycobacterium tuberculosis infection of macrophages in vitro increased CXCR4 surface expression, whereas amelioration of disease reduced CXCR4 expression in vivo. Bronchoalveolar lavage fluid from TB patients had elevated levels of CCL4 (macrophage inflammatory protein-1beta), CCL5 (RANTES), and CX3CL1 (fractalkine), but not CXCL12 (stromal-derived factor-la). We found that M. tuberculosis infection of macrophages in vitro increased viral entry and RT of CXCR4, using HIV-1, but not of CCR5, using HIV-1. Lastly, HIV-1 derived from the lung contains CD14, suggesting that they were produced in AM. Our results demonstrate that TB produces a permissive environment for replication of CXCR4-using virus by increasing CXCR4 expression in AM and for suppression of CCR5-using HIV-1 by increasing CC chemokine expression. These changes explain in part why TB accelerates the course of AIDS. CXCR4 inhibitors are a rational therapeutic approach in HIV/TB coinfection.

Biventricular ICDs may offer increased benefit for patients with severe congestive heart failure and ventricular arrhythmia. Currently there are no approved dedicated biventricular ICDs available. Twenty-one consecutive patients who had approved nondedicated hardware implanted for biventricular pacing and defibrillation were included in this study. All device therapies were evaluated using stored electrograms. During mean follow-up at 13 +/- 7 months, 8 (36%) patients had inappropriate shocks. Ventricular fibrillation therapy was delivered for slow ventricular tachycardia because of double counting in two patients. In one patient, AV nodal reentrant tachycardia below detection rate cut off triggered device therapy because of ventricular double counting. Sinus tachycardia or premature atrial contraction initiating AV conduction and ventricular double counting resulted in shocks in five patients. The number of shocks per patient ranged from 1 to 64. Two patients required transient disconnection of the LV lead and subsequent ICD generator replacement for premature battery depletion. Two patients required AV junction ablation and three needed slow pathway ablation. Two patients were treated by upgrading to a device that was capable of a higher atrial tracking rate. The patients with impaired AV conduction or constant ventricular pacing did not have inappropriate therapy for sinus tachycardia or supraventricular arrhythmia. Use of conventional nondedicated hardware for biventricular pacer/defibrillator is feasible but should be considered only in patients with poor AV node function or less likely to require antitachycardic therapy, to avoid ICD double counting of ventricular sensed events and consequent high incidence of inappropriate therapies.

The effects of extracorporeal shock wave lithotripsy (ESWL) were tested on four advanced generation implantable cardioverter‐defibrillators (ICDs) in vitro and in vivo in two patients. During in vitro testing, advancement of nonsustained episode counters occurred in one device, and a set screw and power source cell loosened in another, which was connected to an external power source. No arrhythmias occurred during in vivo procedures, but programmed parameters were reset and elective replacement indicated after one procedure. ESWL can be performed safely in selected patients with ICDs, but testing should be performed afterwards to confirm satisfactory function and component continuity.

Background Direct-current cardioversion remains the gold standard for restoration of sinus rhythm in patients with atrial flutter. Although an initial energy of 50 J is recommended, the optimal energy settings have not been evaluated in a large series of contemporary patients.Methods We compared the outcome of cardioversion with 50 J versus 100 J in 330 consecutive patients with atrial flutter. Initial energy was based on attending physician preference. One hundred sixty patients received 50 J and 170 patients received 100 J.Results Patients in both groups did not differ significantly in age, sex, weight, body mass index, duration of the arrhythmia, postoperative status, presence and type of structural heart disease, or use of antiarrhythmic drugs. Patients in the 100-J group had more first shock conversion (85% vs 70%; P = .001), fewer total shocks (1.2 +/- 0.5 vs 1.4 +/- 0.7, P = .001), and less induction of atrial fibrillation (2% vs 11%; P = .002). There were no significant differences in overall restoration of sinus rhythm, cumulative energy delivered, anesthetic dose, and procedure room time. On multivariate analysis, delivery of 100 J was the strongest predictor of first shock success (odds ratio 2.6, 95% confidence interval 2.13 to 3.16; P < .001).Conclusion An initial energy of 100 J is more efficient For restoration of sinus rhythm in patients with atrial flutter.

Use of IV (Conscious) Sedation/Analgesia by Nonanesthesia Personnel in Patients Undergoing Arrhythmia Specific Diagnostic, Therapeutic, and Surgical Procedures. This article is intended to inform practitioners, payers, and other interested parties of the opinion of the North American Society of Pacing and Electrophysiology (NASPE) concerning evolving areas of clinical practice or technologies or both, that are widely available or are new to the practice community. Expert, consensus documents are so designated because the evidence base and experience with the technology or clinical practice are not yet sufficiently well developed, or rigorously controlled trials are not yet available that would support a more definitive statement. This article has been endorsed by the American College of Cardiology, October 1997.

The new DDDR pacemaker META DDDR utilizes a minute veritilation sensor based on transthoracic impedance measurements. The sensor determines the metabolic indicated interval, the atrioventricular (AV) delay and the postventricular atrial refractory period (PVARP). The baseline PVARP must be carefully selected to define nonphysiological tachycardias. If a Pwave falls within the PVARP the pacemaker will automatically switch to the VVIR mode. This behavior prevents tracking of paroxysmal atrial tachyarrhythmias (PAT). Twenty‐eight patients with sinus node dysfunction (n = 20), AV junction ablation (n = 5), complete or intermittent AV block (n = 3); who received a META DDDR pacemaker were studied. The mean age was 65 ± 13 years. Results: mode switching (reversion) to VVIR was observed in 57% of the patients. Forty‐two percent had episodes of mode switching to VVIR during a stress test four related to PAT, and seven to sinus tachycardia. Fifty percent had episodes of mode switching to VVIR during a 24‐hour Holter, four related to PAT, three to retrograde P wave sensing, and two to sinus tachycardia. At the last follow‐up, 20 of the 26 patients initially programmed to the DDDR mode remained in the DDDR mode, while five were reprogrammed to the DDD and one to the VVIR mode. Mode switching has a high sensitivity but a low specificity for PAT. It appears to be a useful approach to prevent rapid tracking of atrial tachyarrhythmias. Careful PVARP programming is critical to appropriate reversion behavior, but further modifications of the algorithm are needed to improve its performance.

. A unique mechanism of “cross‐talk” has recently been described in the Gemini 4J5A DDD pacemaker in which cross‐inhibition of the ventricular output stimulus may occur in the early Gemini 415A models which were manufactured with dual anodal rings interconnected by a wire. The Gemini 415A units with dual anodal rings were implanted under investigational protocol in 53 patients from September 1982 to August 1984. To date, cross‐talk has been discovered in six patients during clinical follow‐up, manifesting as inappropriate ventricular inhibition. Syncope was documented in one patient. Non‐Cordis atrial and ventricular leads were present in all six patients and five patients had at least one chronic lead. Cross‐talk was neither evident nor provokable in Gemini 415A units which had compatible Cordis lead systems. Reduction of the atrial output and/or the ventricular sensitivity prevented cross‐inhibition in three patients. Cross‐talk persisted in three patients despite programming to the lowest atrial output and/or ventricular sensitivity parameters. Cross‐talk, spontaneous or provoked, has not occurred in 36 patients having currently designed 415A pulse generators manufactured with a single anodal ring in the ventricular connector channel. We conclude that: (1) this unique form of cross‐talk is “design‐dependent” and occurs only in Gemini 415As with dual interconnected anodal rings and cannot occur in 415As manufactured with a single anodal ring; (2) this form of cross‐talk has occurred only in 415As with non‐Cordis leads and appears to be a time dependent development; (3) reduction of the atrial output or use of pacing modes without atrial pacing or ventricular sensing can prevent cross‐talk; (4) patients with Gemini 415As having dual anodal rings, which can be identified radiographically. are at risk for this design‐dependent cross‐talk and merit close observation.

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTHigh-resolution electrophoretic fractionation and partial characterization of the mitochondrial translation products from HeLa cellsEdwin Ching and Giuseppe AttardiCite this: Biochemistry 1982, 21, 13, 3188–3195Publication Date (Print):June 22, 1982Publication History Published online1 May 2002Published inissue 22 June 1982https://pubs.acs.org/doi/10.1021/bi00256a024https://doi.org/10.1021/bi00256a024research-articleACS PublicationsRequest reuse permissionsArticle Views63Altmetric-Citations34LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts

It has become increasingly clear in the last few years that the segregation of the mitochondrial genetic system in the unique environment of mitochondria has caused it to evolve in a way distinct in many respects from both prokaryotic and eukaryotic genetic systems. The most dramatic evidence of this evolutionary individuality of the mitochondrial system has been recently provided by the discovery of unusual features in the genetic code and in the codon recognition pattern in mitochondria from mammalian cells, yeast and Neurospora crassa (Barrell et al. 1979; Macino et al. 1979; Fox 1979; Barrell et al. 1980; Heckman et al. 1980; Bonitz et al. 1980). There may be a question as to whether these unusual features are vestiges of a primitive genetic code and decoding mechanism or, on the contrary, highly evolved characteristics which have emerged under the particular selective pressures operating in mitochondria.

Cytochrome c oxidase (ferrocytochrome c:oxygen oxidoreductase, EC 1.9.3.1), the terminal oxidase of the respiratory chain in eucaryotic cells, has been purified from human placenta mitochondria. Seven polypeptides have been identified reproducibly by high-resolution electrophoresis of the enzyme complex through sodium dodecyl sulfate (Na-DodSO4)--urea polyacrylamide gels; these correspond closely in size to the subunits of beef heart cytochrome c oxidase. When HeLa cells, grown in suspension culture, were pulse-labeled with [35S]methionine in the presence of cycloheximide to inhibit cytoplasmic protein synthesis and chased with an excess of unlabeled methionine in the absence of the drug, the mitochondrially synthesized polypeptides were resolved into at least 17 components by NaDodSO4--urea polyacrylamide gel electrophoresis. After labeled HeLa mitochondria were mixed with human placenta mitochondria and the cytochrome c oxidase was isolated, three of the labeled components were found to copurify with the three largest subunits of the complex. We conclude that human cytochrome c oxidase contains seven subunits, the three largest of which are synthesized on mitochondrial ribosomes, while the other four are synthesized in the cytoplasm.