Search

As the number and complexity of fluoroscopically guided interventions increase, a serious effort has to be put on the optimisation of the X-ray dose delivered to the patient. In order to set up this optimisation process, the clinical practice for a given cardiology centre has to be analysed with relevant statistical power and compared with the data at local or national level. Data from 8 Swiss cardiology centres for 10 different vascular and heart rhythm procedures have been collected. The collected dose indicators were, when available, cumulated air kerma, cumulated dose-area product, fluoroscopy time and the number of images per procedure. Data analysis was performed using an in-house software solution in terms of the first, second and third quartiles. This kind of large-scale analysis could yield some onsets towards local practice optimisation based on anonymous dose indicator cross-comparison. Further effort should nevertheless be made in order to proceed towards an operator-based data analysis, thus allowing for an individual practice optimisation., (© The Author 2016. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Atrial flutter in the donor part of orthotopic heart transplants has been reported and successfully treated by radiofrequency ablation of the cavotricuspid isthmus, but mapping and ablation of atypical flutter circuits may be challenging.(1) Entrainment mapping has been used in combination with activation mapping to define the mechanism of atypical atrial flutter. Here, we report a case where colour-coded three-dimensional (3D) entrainment mapping allowed us to accurately determine and visualize the 3D location of the reentrant circuit and to plan the ablation of a left atrial flutter without the need for activation mapping.

Current treatments of heart transplantation are limited by incomplete effectiveness, significant toxicity, and failure to prevent chronic rejection. Genetic manipulation of the donor heart at the time of removal offers the unique opportunity to produce a therapeutic molecule within the graft itself, while minimizing systemic effects. Cytoprotective approaches including gene transfer of heme oxygenase (HO)-1, endothelial nitric oxide synthase, and antisense oligodeoxynucleotides specific for nuclear factor (NF)-kappa B or intercellular adhesion molecule (ICAM)-1 reduced ischaemia-reperfusion injury and delayed cardiac allograft rejection in small animals. Exogenous overexpression of immunomodulatory cytokines such as interleukin (IL)-4, IL-10 and transforming growth factor-beta, as well as gene transfer of inhibitors of pro-inflammatory cytokines also delayed graft rejection. Gene transfer-based blockade of T-cell costimulatory activation with CTLA4-Ig or CD40-Ig resulted in long-lasting graft survival and donor-specific unresponsiveness, as manifested by acceptance of a second graft from the original donor strain but rejection of third-party grafts. Similar results were obtained with donor major histocompatibility complex class I gene transfer into bone marrow cells. Gene therapy approaches to chronic rejection included gene transfer of HO-1, soluble Fas, tissue plasminogen activator and antisense oligodeoxynucleotides specific for the anti-apoptotic mediator Bcl-x or the E2F transcription factor. Despite major experimental advances, however, gene therapy for heart transplantation has not entered the clinical arena yet. Fundamental questions regarding the most suitable vector, the best gene, and safety issues remain unanswered. Well-controlled studies that compare gene therapy with established treatments in non-human primates are needed before clinical trials can be started.

Graft vasculopathy is an accelerated form of coronary artery disease that occurs in transplanted hearts. Despite major advances in immunosuppression, the prevalence of the disease has remained substantially unchanged during the last two decades. According to the 'response to injury' paradigm, graft vasculopathy is the result of a continuous inflammatory response to tissue injury initiated by both alloantigen-dependent and independent stress responses. Experimental evidence suggests that these responses may become self-sustaining, as allograft re-transplantation into the donor strain at a later stage fails to prevent disease progression. Histological evidence of endothelitis and arteritis, in association with intima fibrosis and atherosclerosis, reflects the central role of alloimmunity and inflammation in the development of arterial lesions. Experimental results in gene-targeted mouse models indicate that cellular and humoral immune responses are both involved in the pathogenesis of graft vasculopathy. Circulating antibodies against donor endothelium are found in a significant number of patients, but their pathogenic role is still controversial. Alloantigen-independent factors include donor-transmitted coronary artery disease, surgical trauma, ischaemia-reperfusion injury, viral infections, hyperlipidaemia, hypertension, and glucose intolerance. Recent therapeutic advances include the use of novel immunosuppressive agents such as sirolimus (rapamycin), HMG-CoA reductase inhibitors, calcium channel blockers, and angiotensin converting enzyme inhibitors. Optimal treatment of cardiovascular risk factors remains of paramount importance.

Aims: In Europe, no written official guidelines on indications for coronary stent placement are available. We therefore assessed the opinions of European interventional cardiologists on these indications., Methods and Results: In April 1997, a questionnaire was sent to the members of the Working Group on Coronary Circulation of the European Society of Cardiology with interventional cardiology as the main activity. A total of 165 questionnaires were returned and analysed. For the treatment of acute or threatened vessel closure during PTCA, the threshold for stenting is set at the level of a type C dissection by 42% of the cardiologists, while 22% stent any form of dissection and 13% require an impaired TIMI flow. A suboptimal PTCA result necessitating stenting is defined as a residual stenosis of >50% by 35% or of 30 >30% by 55% of the respondents. When considering primary prevention of restenosis, only 2% unconditionally stent focal, new-onset lesions in native coronary arteries, 44% refrain from stenting in a case of a stent-like PTCA result (

Two cases with drug refractory ectopic atrial tachycardia are described. A map-guided partial resection of the right atrium (RA) was done after preoperative endocardial catheter mapping had shown well-defined areas of fractionated RA potentials. Intraoperatively, there were no aneurysmal formations present as described by other authors. Histopathologic examination of the resected tissue showed atrial myocarditis in both patients. Postoperative right ventricular myocardial biopsies revealed no inflammatory tissue. A minor elevation of antibodies against echoviruses was found in one case. Postoperative electrophysiologic studies were negative. We conclude: focal RA myocarditis without concomitant ventricular myocarditis may represent one cause of drug-resistant ectopic atrial tachycardia. Map-guided surgical intervention may cure the disease.

Balloon angioplasty fails to provide acceptable long-term results for a significant proportion of patients. An intravascular mechanical support, developed with the aim of preventing restenosis and acute closure of diseased arteries after transluminal angioplasty, was implanted in 44 patients (39 male and five female), aged from 35 to 70 years (mean 56 years) with documented restenosis of native coronary artery (41 stents) and bypass grafts (12 stents). In the group of bypass graft patients there was no local restenosis and no major complication. In patients in whom stents were placed in native coronary arteries, the complication rate was higher (two patients died after coronary bypass surgery). One patient died suddenly at home. Except for one patient, in whom a new lesion developed proximally with extension into the stent, no case of restenosis could be observed. Despite the still relatively high complication rate, we feel that stenting may present a rational approach to the unresolved problem of restenosis after coronary angioplasty.

We evaluated the efficacy of flecainide acetate (given intravenously to a maximal dose of 2 mg kg-1 and then orally in a dose of 100 mg b.d. or 100 mg t.d.s.) in the conversion to sinus rhythm of 50 patients exhibiting supraventricular arrhythmias (39 with atrial fibrillation, 6 with atrial flutter, 4 with supraventricular tachycardia and one with supraventricular tachycardia in association with the Wolff-Parkinson-White syndrome). Conversion was achieved in 36 patients (72%) (29 cases with atrial fibrillation, 4 cases with supraventricular tachycardia, 2 cases with atrial flutter and one case with Wolff-Parkinson-White syndrome), over a mean period of 7.4 +/- 9 h. The patients in which conversion was achieved had arrhythmias which had been in existence for a shorter time (5.3 +/- 9.8 days) than those in which conversion was not achieved (16.7 +/- 26.2 days) (P less than 0.01). The mean dosage of flecainide used to achieve conversion was 2.5 +/- 2.36 mg kg-1. Flecainide appears to be an effective agent for the conversion to sinus rhythm of atrial fibrillation and supraventricular tachycardias. Its efficacy in cases of atrial flutter has not yet been demonstrated.