[Interventional electrophysiology in cardiac MRI : what is the current status?]. / Interventionelle Elektrophysiologie in der kardialen MRT : Wie ist der aktuelle Stand?

The ablation of simple and complex cardiac arrhythmias has become a first-line therapy in interventional cardiology and is mainly guided by conventional fluoroscopy. Cardiac magnetic resonance imaging (cMRI) allows exact three-dimensional (3D) visualization of complex anatomical structures and serves in the planning and implementation of ablation procedures. Post-procedural lesion visualization using cMRI can assess the success of ablation therapy and may distinguish potential complications. Performing ablation directly in the MRI scanner, with the option of anatomical substrate imagining, exact catheter navigation and real-time lesion visualization, holds the promise of improving success rates and safety in the interventional therapy of simple and complex arrhythmias.

[New developments in the antiarrhythmic therapy of atrial fibrillation]. / Neue Entwicklungen in der antiarrhythmischen Therapie des Vorhofflimmerns.

Atrial fibrillation, which is associated with a worsening of congestive heart failure symptoms, an increased rate of stoke, and increased mortality, is still difficult to treat. New therapies must not only increase effectiveness, but also have to have an improved safety profile, in order to avoid sodium channel block in the ventricle of older patients with atrial fibrillation, and also prevent electrical and morphological remodeling. Dronedarone is less effective compared to amiodarone, but has a better side effect profile which leads to fewer discontinuations of treatment. The atrial ion channels are specifically blocked by a number of prospective antiarrhythmic substances. The most advanced is the testing of vernakalant (RSD1235), which primarily suppresses the I(Kur) current. Ranolazine is a new antianginal substance which influences the atrial ion channels and leads to a significant reduction of atrial and more specifically ventricular tachyarrhythmias. A number of other drugs are in development. They will lead to a better understanding of which form of atrial fibrillation can be best treated with which antiarrhythmic agent.

Chronic effects of early started angiotensin converting enzyme inhibition and angiotensin AT1-receptor subtype blockade in rats with myocardial infarction: role of bradykinin.

OBJECTIVE: The long-term effects and mechanisms of early started angiotensin converting enzyme (ACE) inhibition post myocardial infarction (MI) are not well understood. Chronic effects of early ACE inhibition on hemodynamics, left ventricular diastolic wall stress and remodeling were, therefore, compared to that of angiotensin AT1-receptor subtype blockade in rats with experimental myocardial infarction. The contribution of bradykinin potentiation to both ACE inhibitor and angiotensin AT1-receptor subtype blockade was assessed by cotreatment of rats with a bradykinin B2-receptor antagonist. METHODS: MI was produced by coronary artery ligation in adult male Wistar rats. The ACE inhibitor, quinapril (6 mg/kg per day), or the angiotensin AT1-receptor subtype blocker, losartan (10 mg/kg per day), administered by gavage, and the bradykinin B2-receptor antagonist, Hoe-140 (500 micrograms/kg per day s.c.), administered either alone or in combination with quinapril or losartan, were started 30 min after MI and continued for eight weeks. RESULTS: Quinapril and losartan reduced left ventricular end-diastolic pressure and global left ventricular diastolic wall stress only in rats with large MI. Pressure volume curves showed a rightward shift in proportion to MI size that was not prevented by quinapril or losartan treatment. Only the ACE inhibitor reduced left ventricular weight and this effect was prevented by cotreatment with the bradykinin antagonist. Baseline and peak cardiac index and stroke volume index, as determined using an electromagnetic flowmeter before and after an acute intravenous volume load, were restored by quinapril, whereas losartan had no effects. CONCLUSION: Treatments starting 30 min after coronary artery ligation, with either quinapril or losartan, reduced preload only in rats with large MI. Despite this unloading of the heart, structural dilatation was not prevented by this early treatment. Only quinapril improved cardiac performance and reduced left ventricular weight and this effect was abolished by cotreatment with Hoe-140, suggesting an angiotensin II blockade-independent, but bradykinin potentiation-dependent, mechanism.