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DOI: 10.1055/a-2666-3061
Wirkt die moderne pharmakologische Herzinsuffizienztherapie antiarrhythmisch?
Is There an Antiarrhythmic Effect Inherent to Modern Heart Failure Medication?Authors

Zusammenfassung
Das Vorliegen einer Herzinsuffizienz erhöht die Wahrscheinlichkeit für das Auftreten ventrikulärer Arrhythmien und erhöht darüber unmittelbar die Mortalität betroffener Patientinnen und Patienten. Die mit einer Herzinsuffizienz verbundenen Arrhythmien entstehen durch das Zusammenspiel struktureller, elektrischer und autonomer Veränderungen des Myokards. Während für Patientinnen und Patienten mit Herzinsuffizienz und reduzierter Ejektionsfraktion (HFrEF) durch die medikamentöse Therapie aus Betablockern, Angiotensin-Rezeptor-Neprilysin-Inhibitoren, Mineralokortikoidrezeptor-Antagonisten und Natrium-Glukose-Kotransporter 2-Inhibitoren (SGLT2) sowohl prognoseverbessernde als auch antiarrhythmische Effekte nachgewiesen werden konnten, ist die Datenlage bei Herzinsuffizienz mit mäßiggradig reduzierter oder erhaltener Ejektionsfraktion limitiert. Hier konnten bislang lediglich SGLT2i und Finerenon eine prognostische Verbesserung zeigen, wobei Daten zum antiarrhythmischen Potenzial in diesen Subgruppen bisher fehlen. Die bei HFrEF beobachteten antiarrhythmischen Effekte beruhen auf einer positiven Beeinflussung des strukturellen myokardialen Remodelings, des Kalziumhaushalts und der autonomen kardialen Funktion. Eine leitliniengerechte Anwendung der medikamentösen Vierfachkombination führt dabei zu einer inkrementalen Risikoreduktion für ventrikuläre Arrhythmien und plötzlichen Herztod.
Abstract
The presence of heart failure increases the likelihood of ventricular arrhythmias and thereby directly contributes to the elevated mortality observed in affected patients. These arrhythmias result from the interplay of structural, electrical, and autonomic alterations of the myocardium. In heart failure with reduced ejection fraction (HFrEF), pharmacological therapy with beta-blockers, angiotensin receptor–neprilysin inhibitors, mineralocorticoid receptor antagonists, and sodium-glucose co-transporter 2 inhibitors (SGLT2i) has been shown to confer both prognostic and antiarrhythmic benefits. In contrast, evidence for patients with mildly reduced or preserved ejection fraction remains limited. In these subgroups, only SGLT2i and finerenone have thus far demonstrated prognostic improvement, while data on their antiarrhythmic potential are still lacking. The antiarrhythmic effects observed in HFrEF are thought to result from favorable modulation of structural myocardial remodeling, calcium homeostasis, and autonomic cardiac function. Guideline-directed implementation of the quadruple pharmacological therapy is associated with incremental risk reduction for ventricular arrhythmias and sudden cardiac death.
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Die Mortalität von Patientinnen und Patienten mit Herzinsuffizienz mit reduzierter Ejektionsfraktion (HFrEF) ist im Vergleich zur Allgemeinbevölkerung signifikant erhöht. Über 80% dieser Todesfälle sind kardiovaskulär mit einem hohen Anteil plötzlicher Herztode.
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Eine leitliniengerechte HFrEF-Therapie, bestehend aus Betablockade, Angiotensin-Rezeptor-Neprilysin-Inhibition, Mineralokortikoidrezeptor-Antagonismus und SGLT-2-Inhibition, kann die Gesamtmortalität, den plötzlichen Herztod und ventrikuläre Arrhythmien effektiv reduzieren.
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Um das volle Potenzial der HFrEF-Therapie auszuschöpfen, sollte diese unabhängig von einer möglicherweise bestehenden klinischen Beschwerdefreiheit in der entsprechenden Vierfachkombination und Zieldosierung angewendet werden.
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Patientinnen und Patienten mit Herzinsuffizienz mit mäßig reduzierter (HFmrEF) und erhaltener (HFpEF) Ejektionsfraktion profitieren von einer Therapie mit SGLT-2-Inhibition und Finerenon, wobei Daten zum antiarrhythmischen Potenzial der Substanzen bisher limitiert sind.
Publikationsverlauf
Artikel online veröffentlicht:
08. Oktober 2025
© 2025. Thieme. All rights reserved.
Georg Thieme Verlag KG
Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany
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