Localization of cardiac arrhythmias: conventional noninvasive methods

Noninvasive localization of the accessory pathway (AP) in patients with the Wolff-Parkinson-White syndrome and of the site of origin of ventricular tachycardia (VT) is reviewed. 12-lead electrocardiography (ECG) is the most readily available method for localization of both the AP and the site of VT origin. Many published ECG criteria are introduced. The application of body surface potential mapping, vectocardiography, nuclear phase imaging, echocardiography, computed tomography, nuclear magnetic resonance, and signal-averaged ECG in the localization of these arrhythmogenic substrates is also described. We believe that ECG is the most sensitive noninvasive method for AP localization as well as being convenient and simple; it may be used as the only noninvasive method for the initial evaluation. The left lateral AP, which occurs with an incidence of more than 40%, could be localized preoperatively by noninvasive methods only. For localization of the site of VT origin, none of the noninvasive methods is accurate enough for guiding the surgical and catheter-mediated ablative therapies so far.Abbreviations AP accessory pathway - ARVD arrhythmogenic right ventricular dysplasia - BSPM body surface potential mapping - LFW left free wall - LAW left anterior wall - LLW left lateral wall - LPW left posterior wall - LPS left posteroseptal - NMR nuclear magnetic resonance - PS posteroseptal - RFW right free wall - RAS right anteroseptal - RAW right anterior wall - RLW right lateral wall - RPW right posterior wall - RPS right posteroseptal - VPB ventricular premature beats     

Entrapment of circular mapping catheter in the mitral valve

BACKGROUND: Ablation procedures in the left atrium for treatment of atrial fibrillation are becoming increasingly common. The procedure often involves placing one or two circular mapping catheters in the left atrium. Entrapment of an ablation catheter in the mitral valve during ablations of left-sided accessory pathways by the retrograde approach has been described in two earlier published reports. More recently, several reports describe similar entrapment of a mapping catheter. In a recently published review, however, only one case of unspecified valve damage was registered among 8745 atrial fibrillation procedures. OBJECTIVE: The purpose of this study was to evaluate patients with entrapment. METHODS: Retrospective analysis of electrophysiological results. RESULTS: We describe three patients with entrapment during ablations for atrial fibrillation. The entrapments occurred with three different operators at three different electrophysiological laboratories within 2 years. The complication described here may be more common than is widely appreciated. CONCLUSIONS: From our figures, we estimate the incidence of the complication to 0.9% (95% confidence interval, 0.2-2.5%).     

Bedside Coagulometry During Intravenous Heparin Therapy after Coronary Angioplasty

In order to assess the applicability of a bedside coagulometer for measurement of b-APTT, serial blood samples were obtained from 20 patients receiving intravenous heparin treatment following PTCA, and from 5 healthy volunteers. B-APTT was analysed bedside on the Hemochron® coagulometer; p-APTT and p-heparin, measured asfactor anti-Xa activity, were analysed ex-vivo in the laboratory. B-APTT values, determined by the Hemochron coagulometer, were closely correlated to p-heparin (r=0.83, p<0.001, SD=52 seconds (sec), n=89), and duplicate determinations of b-APTT on the Hemochron coagulometer showed an acceptable repeatability. However, an APTT ratio of 1.5–2.5 was not related to a therapeutic p-heparin level, neither as measured by the Hemochron device nor in the laboratory. Abstract. Background: When administering intravenous heparin during angioplasty procedures, a quick and reliable method for safe and effective monitoring of anticoagulation is necessary. Objective: To assess the applicability of a bedside coagulometer, measuring the activated partial thromboplastin time (APTT) in patients receiving intravenous heparin treatment after percutaneous transluminal coronary angioplasty (PTCA). Methods: In patients with stable angina pectoris, receiving intravenous heparin treatment following PTCA, serial blood samples were obtained by venipuncture and from the arterial sheath for analysis of whole blood APTT (b-APTT), and plasma heparin concentration (p-heparin). Additionally, in healthy volunteers blood samples were obtained after a single bolus injection of heparin. B-APTT was analysed bedside on the Hemochron® coagulometer; p-APTT and p-heparin, measured as factor anti-Xa activity, were analysed ex-vivo in the laboratory using conventional analytical methods. Results: In 20 patients a total of 94 venous and 69 arterial blood samples were analysed, and in five healthy volunteers analyses were performed in 20 venous blood samples. B-APTT values, determined by the Hemochron coagulometer, were closely correlated to p-heparin (r=0.83, p<0.001, SD=52 seconds (sec), n=89). An APTT ratio of 1.5–2.5 was not related to a therapeutic p-heparin level, however, neither when using APTT assessed by the Hemochron device nor APTT measured in the laboratory. Duplicate determinations of b-APTT on the Hemochron coagulometer showed an acceptable repeatability; the mean difference between duplicate measurements was 4[emsp4 ] sec (coefficient of variation (c.v.)=6%, p<0.05, n=163). Conclusions: In patients receiving intravenous heparin after PTCA treatment, b-APTT values measured by the Hemochron method showed an acceptable repeatability and were significantly correlated to p-heparin.     

Efficacy of oral mexiletine therapy at a 12-h dosage interval.

The antiarrhythmic effectiveness and safety of 12-h oral administration of mexiletine were evaluated in adult outpatients with a baseline hourly rate of PVCs of 30 or higher who had initially shown at least a 50 percent reduction of this rate when treated with mexiletine at an 8-h dosage interval. Doses were titrated on the basis of 24-h Holter monitoring for both 8- and 12-h intervals. Seventeen of 26 patients showed PVC reductions after 8-h treatment. Fifteen of these 17 patients reached the goal reduction of greater than or equal to 50 percent in the hourly PCV rate with 12-h dosing. Hour-by-hour analysis disclosed a consistent degree of PVC suppression throughout both 8- and 12-h dose intervals. No increase in the incidence of adverse effects was associated with conversion to the 12-h regimen.     

Intestinal ischemia due to vascular elastosis caused by metastasizing carcinoid tumor of Meckel's diverticulum

A case of a carcinoid tumor arising in a Meckel's diverticulum is reported. By the time of detection, the tumor had spread to the mesentery causing ischemia of the small intestine due to the associated vascular elastosis.     

Effects of resveratrol in experimental and clinical non-alcoholic fatty liver disease

The prevalence of obesity and related conditions like non-alcoholic fatty liver disease(NAFLD) is increasing worldwide and therapeutic options are limited.Alternative treatment options are therefore intensively sought after.An interesting candidate is the natural polyphenol resveratrol(RSV) that activates adenosinmonophosphate-activated protein kinase(AMPK) and silent information regulation-2 homolog 1(SIRT1).In addition,RSV has known anti-oxidant and anti-inflammatory effects.Here,we review the current evidence for RSVmediated effects on NAFLD and address the different aspects of NAFLD and non-alcoholic steatohepatitis(NASH) pathogenesis with respect to free fatty acid(FFA) flux from adipose tissue,hepatic de novo lipogenesis,inadequate FFA β-oxidation and additional intra- and extrahepatic inflammatory and oxidant hits.We review the in vivo evidence from animal studies and clinical trials.The abundance of animal studies reports a decrease in hepatic triglyceride accumulation,liver weight and a general improvement in histological fatty liver changes,along with a reduction in circulating insulin,glucose and lipid levels.Some studies document AMPK or SIRT1 activation,and modulation of relevant markers of hepatic lipogenesis,inflammation and oxidation status.However,AMPK/SIRT1-independent actions are also likely.Clinical trials are scarce and have primarily been performed with a focus on overweight/obese participants without a focus on NAFLD/NASH and histological liver changes.Future clinical studies with appropriate design are needed to clarify the true impact of RSV treatment in NAFLD/NASH patients.     

Cerebrospinal fluid asparagine depletion during pegylated asparaginase therapy in children with acute lymphoblastic leukaemia

L‐asparaginase is an important drug in the treatment of childhood acute lymphoblastic leukaemia (ALL). Cerebrospinal fluid (CSF) asparagine depletion is considered a marker of asparaginase effect in the central nervous system (CNS) and may play a role in CNS‐directed anti‐leukaemia therapy. The objective of this study was to describe CSF asparagine depletion during 30 weeks of pegylated asparaginase therapy, 1000 iu/m² i.m. every second week, and to correlate CSF asparagine concentration with serum L‐asparaginase enzyme activity. Danish children (1–17 years) with ALL, treated according to the Nordic Society of Paediatric Haematology and Oncology ALL2008 protocol, standard and intermediate risk, were included. CSF samples were obtained throughout L‐asparaginase treatment at every scheduled lumbar puncture. A total of 128 samples from 31 patients were available for analysis. Median CSF asparagine concentration decreased from a pre‐treatment level of 5·3 μmol/l to median levels ≤1·5 μmol/l. However, only 4/31 patients (five samples) had CSF asparagine concentrations below the limit of detection (0·1 μmol/l). In 11 patients, 24 paired same day serum and CSF samples were obtained. A decrease in CSF asparagine corresponded to serum enzyme activities above 50 iu/l. Higher serum enzyme activities were not followed by more extensive depletion. In conclusion, pegylated asparaginase 1000 iu/m² i.m. every second week effectively reduced CSF asparagine levels.