Efficacy and safety of zero-fluoroscopy ablation for supraventricular tachycardias. Use of optional contact force measurement for zero-fluoroscopy ablation in a clinical routine setting.

BACKGROUND: Conventional catheter ablation of cardiac arrhythmias is associated with radiation risks for patients and laboratory personnel. Widespread use of zero-fluoroscopic catheter ablation in clinical routine is limited by safety concerns. This study investigated the feasibility of zero-fluoroscopy catheter ablation using a three-dimensional mapping system and optional catheter contact force technology for an all-comers collective. PATIENTS AND METHODS: The study comprised 184 patients; 91 patients, including 29 pediatric patients, underwent a zero-fluoroscopic electrophysiology (EP) study using the EnSite NavX system with real-time visualization of all electrodes. These patients were matched to a control group, which was treated using fluoroscopy in the same period. Inclusion criteria were documented supraventricular tachycardia or a history of symptomatic paroxysmal supraventricular tachycardia. Transseptal access, if necessary, was achieved under transesophageal echocardiographic guidance for ablation of left-sided arrhythmias. Radiofrequency (using optional contact force measurement) or a cryotechnique was used for ablation. RESULTS: We observed no major acute complications. There were no significant differences between the two groups in the follow-up period. CONCLUSION: Zero-fluoroscopic catheter ablation is generally feasible in right-sided cardiac arrhythmias. Safety concerns regarding left atrial substrates or children can be overcome with optional real-time contact force measurement.

[Catheter ablation of paroxysmal atrial fibrillation: extended recommendations considering safety improvements of pulmonary vein isolation with a cryoballoon--Case 11/2011]. / Katheterablation von paroxysmalem Vorhofflimmern: großzügigere Indikationsstellung durch verbesserte Sicherheit der Pulmonalvenenisolation mittels Cryoballon - Fall 11/2011.

HISTORY AND ADMISSION FINDINGS: A 71-year-old, male patient was referred to our clinic for paroxysmal palpitations with dyspnoe and fatigue since four years despite pharmacological treatment with flecainide and bisoprolol. INVESTIGATIONS: A paroxysmal atrial fibrillation was documented in a 24-hour Holter recording. A bicycle ergometry showed a hypertensive reaction during exercise without any sign of coronary insufficiency. Intracardiac thrombi could by excluded by transesophageal echocardiography. DIAGNOSIS, TREATMENT AND COURSE: The diagnosos of a drug-refractory paroxysmal atrial fibrillation was made and cryoballoon pulmonary vein isolation was performed. A follow-up 3 months after the ablation disclosed a freedom from atrial fibrillation documented in 7-day Holter recording. CONCLUSIONS: Compared to pharmacological rhythm control, interventional treatment has been established as more effective therapy for paroxysmal atrial fibrillation. However, patients should be referred to the ablation early enough to avoid structural atrial remodeling and thus transition into persistent or permanent atrial fibrillation. New technical developments e.g. cryoballoon catheter-system simplifies the procedure and has been reported to be effective and safe to use for circumferential pulmonary vein isolation. Should the very promising preclinical data on efficacy and safety of cryothermal energy ablation be confirmed by results of ongoing, controlled trials, the catheter ablation may become the fist-line treatment for all patients with paroxysmal atrial fibrillation.

[Contact force control - the key to safe zero-fluoroscopy catheter ablation of atrioventricular nodal reentrant tachycardia]. / Die Anpresskraftkontrolle als Schlüssel zur sicheren strahlenfreien Katheterablation der AV-Knoten-Reentrytachykardie.

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT) is a frequent supraventricular tachycardia in children and young adults. Despite favourable success rates of catheter ablation, conventional fluoroscopic catheter guidance is associated with risks of low-dose ionizing radiation for the patient and the personnel. Here we describe a technique for zero-fluoroscopy catheter ablation using contact force technology. PATIENTS AND METHODS: Zero-fluoroscopy catheter ablation was attempted in 12 patients with AVNRT (median age 20 years; range 11-75 years). An ablation catheter with integrated contact force sensor and a nonfluoroscopic electroanatomical mapping system was used for visualization of cardiovascular structures. Mean contact forces during mapping and ablation were restricted to an upper limit of 50 g to avoid cardiovascular injuries. RESULTS: Zero-fluoroscopy catheter ablation was performed successfully and uneventfully in all patients. There were no arrhythmia recurrences during a median follow-up of 6.2 months (range 2.7-12.8). CONCLUSION: Zero-fluoroscopy catheter ablation of AVNRT is possible and appears simple yet safe, when a nonfluoroscopic electroanatomical mapping system is used in combination with an ablation catheter with integrated contact force sensor. The presented technique could thus be easily employed in most electrophysiological laboratories.

[Risk stratification in non ischemic cardiomyopathy: a case report--Case 5/2010]. / Risikostratifizierung bei nichtischämischer Kardiomyopathie: Eine Kasuistik - Fall 5/2010.

HISTORY AND ADMISSION FINDINGS: A 65-year-old male patient with rapid increasing shortness of breath and newly diagnosed atrial fibrillation was admitted to our hospital. INVESTIGATIONS: The ECG revealed atrial fibrillation. Echocardiography showed severe decreased left ventricular function. The magnetic resonance imaging (MRI) scan confirmed the severe reduced left ventricular function with a two graded mitral regurgitation as well as a pronounced late enhancement in the posterobasal area of the interventricular septum. Cardiac catheterisation showed mild diffuse atherosclerosis of the coronary arteries without stenotic lesions. Multiple myocardial biopsies of the right ventricle revealed extensive remodelling processes with focal fibrosis in presence of mononuclear cell infiltrates, T-wave alternans and the heart rate variability were positive. DIAGNOSIS, TREATMENT AND COURSE: Nonischaemic cardiomyopathy (NICM) with severe reduced left ventriucular function was diagnosed. After successful electrical cardioversion and initiation of a sufficient heart failure treatment, the clinical symptoms as well as left ventricular function improved significantly. CONCLUSION: Risk stratification of sudden cardiac death remains a clinical challenge especially in NICM. Significantly predictors in ischaemic cardiomyopathy, such as heart rate turbulance (HRT) and T-wave alternans, are not useful or have no importance in NICM. However, the prognosis does not correlate with restricted left ventricular function in NICM. Cardiac MRI or marker of autonomic dysfunction could be helpful in risk stratification. How far late enhancement is a surrogate parameter or the real substrate for life threatening arrhythmias is still unclear. Non-invasive risk stratification could be helpful in borderline decisions, however, it should not be taken mandatory. Close-meshed control intervals of the clinical status under optimal medication are recommended, followed by a implantation of an implantable cardioverter-defibrillator (ICD) if needed. ICD implantation is superior to medical treatment in persistent depressed left ventricular function. The ideal time for ICD implantation in newly diagnosed NICM remains unclear at the moment.

Dissimilar atrial rhythms: coexistence of reentrant atrial tachycardia, atrioventricular nodal reentrant tachycardia and interatrial conduction block.

We report a patient in whom mapping of the right atrium with multipolar catheters and electroanatomic mapping revealed the presence of three dissimilar rhythms: a reentrant atrial tachycardia in the antero-lateral wall of the right atrium and an atrioventricular nodal reentrant tachycardia (AVNRT) isolated from each other and a conduction disturbance at the interatrial septum resulting in a rate-related interatrial block and a slow left atrial rhythm. The AVNRT was stopped with intravenous adenosine (6 mg) and induced repeatedly by atrial extrastimuli associated with a critical atrioventricular delay and dual atrioventricular nodal pathways. Electroanatomic mapping disclosed extensive fibrosis isolating viable myocardium of the antero-lateral wall from the rest of the right atrium. The viable myocardium in the antero-lateral wall was activated by a reentrant rhythm circulating around an islet of fibrosis located in the middle of the viable tissue. The AVNRT was ablated by a standard approach and the reentrant atrial tachycardia by producing a linear lesion bridging the central islet of fibrosis with the anterior tricuspid annulus. This case highlights the complicated nature of some dissimilar atrial rhythms and the power of electroanatomic mapping tools to reveal the exact mechanism and guide radiofrequency ablation.

Altered transient outward current in human atrial myocytes of patients with reduced left ventricular function.

INTRODUCTION: Electrophysiologic remodeling is involved in the self-perpetuation of atrial fibrillation. To define whether differences in atrial electrophysiology already are present in patients with increased susceptibility for atrial fibrillation, we compared patients in sinus rhythm with and without heart failure. METHODS AND RESULTS: Atrial specimens were obtained from patients with reduced left ventricular ejection fraction (LVEF; n = 10) and normal LVEF (n = 16) who were undergoing aortocoronary bypass surgery and from donor hearts (n = 4). Enzymatically isolated atrial myocytes were investigated by whole cell, patch clamp techniques. Total outward current was significantly larger in myocytes of hearts with low LVEF than normal LVEF (19.4 +/- 1.3 vs 15.1 +/- 1.2 pA/pF at pulses to +60 mV, respectively). Analysis of inactivation time courses of different outward current components revealed that the observed current difference is due to the transient calcium-independent outward current I(to1) which is twice as large in the low LVEF group than in the normal LVEF group (9.4 +/- 0.9 vs 4.7 +/- 0.4 pA/pF at pulses to +60 mV, respectively). I(to1) recovery from inactivation was significantly more rapid in myocytes of hearts with low LVEF, and action potential plateau in these cells was significantly shorter. The results of I(to1) and action potential measurements in atrial myocytes of donor hearts were very similar to the results of patients with preserved heart function. CONCLUSION: I(to1) in human atrial myocytes of patients with reduced LVEF has an increased density and altered kinetics in sinus rhythm. These differences in outward current may explain the reduced plateau phase of action potentials.

Endogenous adenosine reduces the occurrence of ischemia-induced ventricular fibrillation in rat heart.

The aim of this study was to determine whether endogenous adenosine has antiarrhythmic effects on ischemia-induced ventricular tachyarrhythmias. We therefore modulated the effect of endogenous adenosine in isolated rat hearts using four different approaches. First, interstitial adenosine was elevated by metabolic inhibition with either EHNA (erythro-9-(2-hydroxy-3-nonly)adenine) or acadesine [5-amino-1-beta-D-imidazole-4-carboxamide). Second, cardiac effects of A1 adenosine receptors were allosterically enhanced with PD81,723 (2-amino-4,5-dimethyl-3-thienyl)[3-(trifluoromethyl)phenyl]-methanone . Third, endogenous adenosine release was suppressed with NBMPR (S-(4-nitrobenzyl)-6-thioinosine), and fourth, adenosine receptor subtypes were blocked with antagonists of different selectivity. Regional ischemia, induced by coronary artery ligation, caused ventricular fibrillation of a reproducible kind in about 20% of untreated hearts with a low calcium concentration in the perfusion medium (0.80 mmol/l CaCl2) and in about 75% with high calcium (1.85 mmol/l) within an observation period of 30 min. At high calcium, EHNA (1 and 10 micromol/l) and acadesine (500 micromol/l) suppressed the occurrence of ventricular fibrillation from 68% (controls) to 47%, 33% and 38%, respectively. Conversely, PD81,723 (10 micromol/l) did not influence the occurrence of ventricular fibrillation. At low calcium, NBMPR (0.1 and 1 micromol/l) resulted in a concentration-dependent rise of ventricular fibrillation from 13% (controls) to 40% and 57%, respectively. The adenosine receptor antagonists theophylline (100 micromol/l), XAC (Xanthine Amine Congener; 1 micromol/l) and 8-PT (8-phenyltheophylline; 1 micromol/l) caused a rise in the occurrence of ventricular fibrillation from 25%, 15% and 18% (controls) to 57%, 39% and 44%, respectively, and the selective A2a receptors antagonist CSC (8-(3-chlorostyryl)caffeine; 5 micromol/l) from 20% to 56%. Conversely, the selective A1 receptor blocker DPCPX (8-cyclopentyl-1,3-dipropyl-xanthine; 1 micromol/l) was ineffective. NBMPR or EHNA concentration-dependent suppressed or increased ischemia-induced adenosine overflow, respectively, in a concentration-dependent manner, whereas the adenosine receptor antagonists did not influence adenosine overflow. We conclude that endogenous adenosine is an antiarrhythmic mediator accumulating in acute ischemic myocardium to a level which effectively decreases the occurrence of ventricular fibrillation by an A2 adenosine receptor activation in the isolated rat heart.

On the regulation of the expressed L-type calcium channel by cAMP-dependent phosphorylation.

The Ca2+ channel subunits alpha 1C-a and alpha 1C-b were stably expressed in Chinese hamster ovary (CHO) and human embryonic kidney (HEK) 293 cells. The peak Ba2+ current (IBa) of these cells was not affected significantly by internal dialysis with 0.1 mM cAMP-dependent protein kinase inhibitor peptide (mPKI), 25 microM cAMP-dependent protein kinase catalytic subunit (PKA), or a combination of 25 microM PKA and 1 microM okadaic acid. The activity of the alpha 1C-b channel subunit expressed stably in HEK 293 cells was depressed by 1 microM H 89 and was not increased by superfusion with 5 microM forskolin plus 20 microM isobutyl-methylxanthine (IBMX). The alpha 1C-a.beta 2.alpha 2/delta complex was transiently expressed in HEK 293 cells; it was inhibited by internal dialysis of the cells with 1 microM H 89, but was not affected by internal dialysis with mPKI, PKA or microcystin. Internal dialysis of cells expressing the alpha 1C-a.beta 2.alpha 2/delta channel with 10 microM PKA did not induce facilitation after a 150-ms prepulse to +50 mV. The Ca2+ current (ICa) of cardiac myocytes increased threefold during internal dialysis with 5 microM PKA or 25 microM microcystin and during external superfusion with 0.1 microM isoproterenol or 5 microM forskolin plus 50 microM IBMX. These results indicate that the L-type Ca2+ channel expressed is not modulated by cAMP-dependent phosphorylation to the same extent as in native cardiac myocytes.