Erratum to "Nanocommunication via FRET With DyLight Dyes Using Multiple Donors and Acceptors".

In the above paper [1], an exponent is missing from equations (5) and (6). The correct version of the equations are as follows.

Conflict of interest policies and disclosure requirements among European Society of Cardiology National Cardiovascular Journals.

Disclosure of potential conflicts of interest (COI) is used by biomedical journals to guarantee credibility and transparency of the scientific process. COI disclosure, however, is not systematically nor consistently dealt with by journals. Recent joint editorial efforts paved the way towards the implementation of uniform vehicles for COI disclosure. This paper provides a comprehensive editorial perspective on classical COI-related issues. New insights into current COI policies and practices among European Society of Cardiology national cardiovascular journals, as derived from a cross-sectional survey using a standardised questionnaire, are discussed.

Premature ventricular complex-induced chronic cough and cough syncope.

The present case study reports a case of chronic cough and cough syncope associated with frequent premature ventricular complexes (PVCs). Careful analysis of cough-related symptoms and ECG monitoring led to the suspicion of PVC-induced cough. A coincidence between PVCs and episodes of cough was also documented by a portable multichannel recorder. Moreover, Doppler echocardiography revealed a PVC-induced transient increase in the pulmonary artery blood flow. After exclusion of other possible aetiologies, complete relief of chronic cough and cough syncope was achieved by radiofrequency ablation of the arrhythmogenic focus located in the right ventricular outflow tract. Premature ventricular complexes should be considered as a cause of chronic cough and cough syncope and an interdisciplinary cooperation can lead to successful diagnosis and treatment of this condition.

Influence of mobile phones on accuracy of ECG interpretation algorithm in automated external defibrillator.

BACKGROUND: Automated External Defibrillators (AED) are a recommended tool for out-of-hospital emergency medical services. Mobile phones (GSM) are a potential source of electromagnetic interference which may cause failure of ECG interpretation and subsequent inappropriate action of AED's. METHODS: We evaluated the influence of 900 MHz GSM phones on the accuracy of automatic ECG interpretation with a GSM Mobile Station Tester with adjustable power and mode of transmission (Hewlett-Packard HP5515A), GSM phones (Alcatel, Ericsson, Nokia, Panasonic), ECG simulator (Metron) and four AEDs (Fore Runner-Hewlett-Packard, Heartstart 3000-Laerdal, Cardio-Aid 100-Artema, Heartstream XLT-Agilent). The protocol included 18 different ECG patterns, different ECG voltages, and different power and mode of transmission. RESULTS: The first stage of the protocol included minimal power of signal transmitted from GSM Mobile Station Tester and maximum power of GSM phone's signal--hence maximal potential interference to AED. The protocol was based on close direct contact between the GSM phone and the AED device. Regardless of the ECG pattern, with both 0.5 and 1.0 mV ECG voltage, and the GSM phone placed on various parts of AED device or at the patient cable, no failure of AED algorithm occurred. No detectable noise was seen at AED's ECG display. CONCLUSION: AEDs seems to be well protected against clinically significant failure caused by noise from 900 MHz GSM phones.

Efficacy and safety of dofetilide in the prevention of symptomatic episodes of paroxysmal supraventricular tachycardia: a 6-month double-blind comparison with propafenone and placebo.

BACKGROUND: Existing drug therapies for paroxysmal supraventricular tachycardia (PSVT) have potentially serious adverse effects. Dofetilide, a pure class III antiarrhythmic agent, may offer an effective and safe alternative for treating PSVT. This study compared the efficacy and safety of dofetilide with that of propafenone and placebo in the prevention of PSVT. METHODS: This multicenter, randomized, placebo-controlled, parallel-group study compared the effectiveness of oral dofetilide 500 microg given twice daily with that of propafenone 150 mg given 3 times a day and placebo in preventing the recurrence of PSVT in 122 symptomatic patients. Episodes of PSVT were documented by symptom diaries and Hertcard (Hertford Medical, Hertfordshire, UK) event recorders. RESULTS: After 6 months of treatment, patients taking dofetilide, propafenone, and placebo had a 50%, 54%, and 6% probability, respectively, of remaining free of episodes of PSVT (P <.001 for both dofetilide and propafenone vs placebo). Both dofetilide and propafenone also decreased the frequency of episodes of PSVT; the median numbers of episodes in the dofetilide- and propafenone-treated groups were 1 and 0.5, respectively, compared with 5 in the placebo-treated group. Dofetilide was well tolerated; no proarrhythmia occurred. Three patients taking propafenone had serious treatment-related adverse effects that required drug discontinuation. CONCLUSIONS: Dofetilide and propafenone were equally effective in preventing the recurrence of or decreasing the frequency of PSVT.

QT interval dispersion in ventricular beats: a noninvasive marker of susceptibility to sustained ventricular arrhythmias.

Increased QT dispersion (QTd) calculated from sinus beats has been shown to identify patients prone to sustained VT. However, predictive accuracy of this parameter is limited. Electrophysiological properties of the myocardium may be altered by a premature ventricular beats, which is a well-established trigger for sustained VT. Therefore, the author hypothesised that QTd in spontaneous or paced ventricular beats may improve identification of patients with inducible sustained VT. In 28 consecutive patients (men, mean age 61 +/- 13 years) who underwent programmed ventricular stimulation, the values of QTd calculated in sinus and ventricular beats were compared between inducible and noninducible patients. The mean QTd values obtained using three different methods differed significantly, QTd in paced ventricular beats being the highest, QTd in spontaneous ventricular beats was intermediate, and QTd in sinus beats was the lowest (83.9 +/- 30 vs 63.0 +/- 29 ms vs 53.9 +/- 27 ms, P < 0.0001 and P < 0.004, respectively). In 13 (46%) patients sustained VT was induced. QTd values were significantly higher in inducible than noninducible patients (QTd sinus beats: 67.5 +/- 31 vs 42.1 +/- 11 ms, P = 0.02; QTd spontaneous ventricular beats: 79.3 +/- 35 vs 46.7 +/- 13 ms, P = 0.008, and QTd-paced ventricular beats: 104.8 +/- 32 vs 65.9 +/- 9 ms, P = 0.0009). The receiver operator characteristic curves showed that at a sensitivity level of 100%, the highest specificity for identification of inducible patients had QTd measured in paced ventricular beats (87%) followed by QTd in spontaneous ventricular beats (45%), and QTd in sinus beats (40%). In conclusion, (1) QTd in ventricular beats is greater than in sinus beats, and (2) QTd calculated from paced ventricular beats identifies patients with inducible sustained VT better than QTd measured during sinus rhythm.

Extrasystolic beats affect transmural electrical dispersion during programmed electrical stimulation.

BACKGROUND: Experimental studies suggest that the electrocardiographic Tpeak-Tend (TpTe) interval reflects transmural dispersion of repolarization (TDR). The genesis and role of the TpTe interval in a clinical setting have not been established. This study aimed to assess the clinical usefulness of the TpTe interval as an index of TDR and a pro-arrhythmic marker. MATERIALS AND METHODS: Endocardial monophasic action potential (MAP) duration and electrocardiographic QTp, QTe and TpTe intervals were assessed in 13 patients undergoing an electrophysiological study. Surface electrocardiograms were recorded during right ventricular pacing (Basic Cycle Length = 600 ms) before and after single extrastimuli. RESULTS: Ventricular arrhythmia was induced in six patients. During ventricular pacing, MAP duration and QTp intervals shortened in response to extrastimuli applied at progressively shorter coupling intervals. In contrast, QTe intervals increased in response to premature stimulation and QTe dispersion increased at short coupling intervals. During sinus rhythm, the TpTe interval was greater in the inducible group in leads V3-V4. Premature stimulation increased the duration of TpTe intervals, suggesting an increase in TDR. The maximum TpTe interval was greater in the inducible than in the noninducible group, both during baseline ventricular drive pacing (163 +/- 22 vs. 130 +/- 27 ms, respectively, P < 0.03) and after application of shortly coupled extrastimuli (263 +/- 66 vs. 200 +/- 47 ms, respectively, P < 0.05). CONCLUSIONS: The TpTe interval of surface ECG is likely to represent TDR. TDR is increased by premature ventricular stimulation and the magnitude of the maximum TpTe interval (i.e. maximum TDR) during ventricular pacing is greater in patients with inducible arrhythmias.

Susceptibility to neuromediated syncope after acute myocardial infarction.

BACKGROUND: Syncope after acute myocardial infarction (AMI) is a common clinical problem. It may be hypothesised that remodelling and neurohormonal changes following AMI may predispose to neuromediated syncope. DESIGN: To address this issue we prospectively evaluated the incidence of positive results of head-up tilt-table testing in 40 patients following AMI and 40 age and sex matched controls without a history of syncope. The mechanisms of tilt-induced changes in autonomic tone were assessed using spectral analysis of heart rate variability. The patients were followed-up for one year. RESULTS: Positive results of tilt-test occurred in 4 (10%) controls and 13 (33%) AMI patients (P = 0.01). No significant differences in sympathovagal interaction (assessed by a low frequency/high frequency ratio) were detected between the groups before tilting (2. 9 +/- 1.9 vs. 3.1 +/- 2.2; NS). However, dynamic changes of this parameter differed significantly during the first 5 symptomless minutes of the active phase of tilt-test. The ratio increased in the majority of controls (87%) and decreased in the majority of patients (62%) (P < 0.0001). During one year follow-up, syncope or presyncope occurred in 10 (25%) AMI patients but did not occur in any control subject (P < 0.001). The sensitivity, specificity and predictive accuracy of an early tilt-test after AMI for the prediction of syncope or presyncope was 70%, 80% and 78%, respectively. CONCLUSION: Patients after AMI are prone to neuromediated reactions. Sympathetic withdrawal seems to be the most likely mechanism of syncope. The role of tilt testing for identification of patients susceptible to syncope or presyncope after AMI needs further investigation.

Passive-fixation J-shaped versus straight leads in atrial position: comparison of efficacy and safety.

To compare the efficacy and safety of straight and J-shaped passive-fixation atrial leads we retrospectively analyzed the results of 100 consecutive implantations of atrial leads at one institution. There were seven cases of upgrades of VVIR to DDDR systems and in one case an active-fixation lead was chosen as a primary approach. These eight patients were excluded from the analysis. The final study group consisted of 92 cases (69 DDDR, 23 AAIR), 69 were J and 23 straight leads. The stimulation threshold, slew rate, impedance, P wave amplitude, and procedural time did not differ significantly between the two types of leads used. During the long-term follow-up of 6-53 months (30 +/- 11.9 months), replacements using active-fixation leads were required in two patients with straight leads and three patients with J leads (P = NS). In addition, one J lead showed signs of damage (impedance > 3,000 Ohm). Long-term follow-up values of the stimulation thresholds and P wave amplitudes did not differ between the groups (P = NS). Transesophageal echocardiography performed in 13 patients revealed a trend toward more distal placement of straight leads within the right atrial appendage. In conclusion, J-shaped leads do not seem to be superior to the straight leads for atrial implantations.

Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction.

AIMS: Intravenous amiodarone has recently emerged as an important drug for the acute treatment of ventricular tachyarrhythmias. However, electrophysiological actions and the efficacy of the drug in the suppression of ventricular tachycardia inducibility have not yet been fully established. The present study was designed to address these issues. METHODS AND RESULTS: The study group consisted of 18 patients (all males, mean age 75 +/- 14 years), who underwent electrophysiological study due to a history of sustained ventricular tachyarrhythmia or syncope with non-sustained ventricular tachycardia detected on ambulatory ECG monitoring. The effects of 5 mg.kg(-1) or 10 mg.kg(-1) of intravenous amiodarone on (1) ventricular refractoriness (QTc interval, right ventricular effective refractory period and monophasic action potential duration), (2) intraventricular conduction (paced-QRS and signal-averaged QRS duration), and (3) ventricular tachycardia inducibility, were examined. The drug had no significant effect on ventricular refractoriness. However, a relatively small but significant slowing of intraventricular conduction was seen (paced-QRS duration: 182 +/- 27 ms vs 191 +/- 28 ms, P<0.0007; 183 +/- 32 ms vs 195 +/- 33 ms, P<0.0007; and 177 +/- 21 ms vs 192 +/- 24 ms, P<0.003, at the cycle lengths of 600, 500 and 400 ms, respectively). This effect was more evident during extrasystolic beats than during stable pacing (for example, at the cycle length of 600 ms, the magnitude of amiodarone-induced lengthening of QRS duration was 23.9 +/- 17.6 ms vs 9.7 +/- 7.2 ms, P<0.009, respectively). Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion. CONCLUSION: Intravenous amiodarone does not prolong ventricular refractoriness, slows intraventricular conduction and may facilitate inducibility of sustained ventricular arrhythmias.

Wavelet decomposition analysis of the signal averaged electrocardiogram used for risk stratification of patients with hypertrophic cardiomyopathy.

AIMS: To study the predictive value of wavelet decomposition, as demonstrated by the signal-averaged ECG, in order to identify patients with hypertrophic cardiomyopathy at increased risk for malignant ventricular arrhythmias or sudden death. METHODS AND RESULTS: Two hundred and forty-six patients with hypertrophic cardiomyopathy were studied. During a mean follow-up of 68 +/- 17 months 32 patients died, of whom 17 died suddenly. Patients with sudden death, together with eight patients with a history of ventricular fibrillation (sudden death/ventricular fibrillation group) were analysed and compared to the other 221 patients as well as to a subgroup of 82 patients without a history of syncope, ventricular arrhythmias on a long-term ECG recording or a family history of sudden death. There were no differences in mean values of the four wavelet decomposition parameters among patients in the sudden death/ ventricular fibrillation group, those without sudden death/ ventricular fibrillation or patients in the low risk group. There were, however, significant differences between patients dying non-suddenly and patients being alive at the end of follow-up. Eighty-seven patients (35%) demonstrated evidence of non-sustained ventricular tachycardia on a long-term ECG. Analysis of wavelet decomposition resulted in abnormal findings in these patients more often than in those without ventricular arrhythmias. CONCLUSION: The usefulness of wavelet decomposition analysis in predicting sudden death or ventricular fibrillation is limited in patients with hypertrophic cardiomyopathy. It may, however, play a role in identifying patients at risk of dying non-suddenly and of patients with non-sustained ventricular tachycardia.

Use of spectral turbulence analysis for the identification of patients at high risk for ventricular fibrillation and sudden death in patients with hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy carries an increased risk of sudden death. The aim of the present study was to assess the predictive value of the signal-averaged ECG, analysed in the time domain and using a new method, spectral turbulence analysis, for the identification of high-risk patients. Two-hundred and forty-six patients with hypertrophic cardiomyopathy were studied. During a mean follow-up of 68 +/- 17 months, 17 patients died suddenly. Patients with sudden death (SD) and/or a history of ventricular fibrillation (VF; n = 25) were compared to patients without SD/VF (n = 221) and to patients without any recognised risk factors for SD (n = 82). There were no differences in mean values of the time domain or spectral turbulence parameters analysed between patients in the SD/VF group and the patients without SD/VF or in the low-risk group. It is concluded that the clinical usefulness of the signal-averaged ECG, analysed in the time domain or as spectral turbulence analysis, is limited in identifying high-risk patients with hypertrophic cardiomyopathy.

Intravenous amiodarone is safe and seems to be effective in termination of paroxysmal supraventricular tachyarrhythmias.

BACKGROUND: Paroxysmal atrial fibrillation (PAF) and paroxysmal supraventricular tachycardia (PSVT) leading to hemodynamic compromise are among the most common reasons for admission to the coronary care unit (CCU) and need prompt and efficient therapy. Direct current cardioversion is the therapy of choice, but if found contraindicated or unavailable some antiarrhythmic agents are usually given to restore sinus rhythm. Many of these drugs have obvious limitations, especially in patients with acute myocardial infarction and/or heart failure. HYPOTHESIS: The aim of the present study was to assess the safety and efficacy of intravenous amiodarone in the acute termination of PAF or PSVT refractory to other antiarrhythmic agents in a large group of patients consecutively admitted to our CCU. METHODS: In the present study, we evaluated the safety and efficacy of amiodarone given intravenously in 142 consecutive patients with PAF or PSVT lasting < 24 h. In 37% of patients no evidence of underlying heart disease which may have caused arrhythmias were defined. A median of two other antiarrhythmic agents given prior to the first amiodarone injection had been ineffective. RESULTS: Sinus rhythm was restored in 91 patients (64%) (65% in the PAF group and 61% in the PSVT group). The mean time to rhythm conversion was 5.5 +/- 6.1 h for patients with PAF and 1.2 +/- 1.2 h for patients with PSVT. The mean dose of amiodarone administered up to conversion was 340 +/- 220 mg for PAF and 220 +/- 105 mg for PSVT. Except for transient first-degree atrioventricular block in two patients, no adverse effects possibly related to amiodarone were observed (including proarrhythmia and incidence or aggravation of heart failure symptoms). CONCLUSION: Amiodarone given intravenously for acute termination of supraventricular tachyarrhythmias is completely safe and seems effective. The results of this study, which is the largest ever made, indicate a need of randomized, controlled trials for the ultimate assessment of the efficacy of amiodarone in this clinical setting.

The incidence of asymptomatic paroxysmal atrial fibrillation in patients treated with propranolol or propafenone.

Anti-arrhythmic therapy for paroxysmal atrial fibrillation leads to complete symptomatic relief in a number of patients. The elimination of symptoms may be associated either with a complete elimination of arrhythmia or with a conversion of symptomatic atrial fibrillation into asymptomatic episodes of arrhythmia. The aim of the study was to evaluate the occurrence of asymptomatic paroxysmal atrial fibrillation in 52 patients treated with propafenone (35 drug trials) or propranolol (34 drug trials) by means of ambulatory ECG Holter monitoring. Propafenone was clinically effective (complete relief of symptoms) in 26 (74%) patients. However, in 7 cases (27%) asymptomatic episodes of arrhythmia were still recorded when awake. In patients treated with propranolol clinical symptoms were absent in 18 (53%). However, in 4 (22%) patients attacks of paroxysmal atrial fibrillation were present. The mechanism of drug-induced conversion of symptomatic episodes of atrial fibrillation into asymptomatic spells of arrhythmia was a marked shortening in duration of episodes in 7 patients (from 2215 +/- 3843 s to 16 +/- 10 s, N.S.) or by a significant slowing of ventricular response during atrial fibrillation in 4 patients (from 125 +/- 27 to 84 +/- 8 beats/min, P = 0.05). In conclusion, in a significant proportion of patients with symptomatic paroxysmal atrial fibrillation asymptomatic episodes of arrhythmia may occur while on anti-arrhythmic drug therapy. Some of these patients, particularly those with other risk factors for stroke such as advanced age or the presence of organic heart disease, may require anti-coagulant therapy or change in anti-arrhythmic treatment, and can be selected on the basis of ambulatory ECG monitoring.