Researchers from the universities of Würzburg and Duisburg-Essen have shown that after a stroke, there is an increased risk of developing a chronic heart defect. They report this in the specialist magazine “Annals of Neurology”.
People with cardiac insufficiency often suffer from stroke. Scientists from the Julius Maximilian University of Würzburg (JMU) and the University of Duisberg-Essen (UDE) have now been able to demonstrate for the first time that the reverse course of the disease often occurs: after a stroke a heart failure can develop over months.
The discovery may have an impact on the treatment of stroke patients. “Brain function can not be considered for stroke alone; long-term cardiac diagnosis must also be considered,” says Professor Christoph Kleinschnitz of the Department of Neurology at the Essen University Hospital.
Heart and brain
There have already been indications that heart failure (HI) may develop through a disorder of the autonomic nervous system. However, the exact mechanism behind this was unknown. Previous studies on stroke patients only showed that, up to several weeks after a stroke, cardiac arrhythmias, the death of heart muscle cells and functional disturbances of the heart can occur.
Within the first three months after a stroke, 19% of all patients experience severe cardiac events: a heart attack or a sudden cardiac death. But so far little is known about the long-term consequences of a stroke on the development of a chronic heart defect.
SICFAIL Study Closes Gap
The project “SICFAIL” (a functional impairment of the heart caused by a stroke) has now been evaluated by the close collaboration between neurologists, cardiologists and clinical epidemiologists of the university clinics and the German Center for Cardiac Insufficiency in Würzburg (DZHI) and also develop new treatment strategies. SICFAIL consists of an experimental and a clinical part that has not yet been completed.
“The basic hypothesis is that an IS (Ischemic stroke caused by a sudden hypotension of the brain) induces chronic heart failure (HI), and that this is basically accessible to a pharmacological intervention,” explains Michael Bieber from the University Hospital Würzburg.
An important milestone for this was the demonstration that an actual functional disorder of the heart develops after an experimental stroke. For example, stroke function was significantly reduced eight weeks after stroke induction. This neurocardial damage is caused by a chronic overactivation in a part of the nervous system, the sympathetic nervous system. This problem also leads to increased collagen formation at the heart.
The scientists tested a pharmacological strategy to prevent HI after stroke. The Metoprolol betaine was administered, as is also the case with HI patients. This decreased the sympathetic activation, improved the heart function significantly and the morphological changes at the heart remained.
“If the experimental results can be confirmed in the clinical part of the SICFAIL study, this drug therapy with a betablocker could also be a useful starting point in patients after a stroke,” says Professor Stefan Frantz, cardiologist and director of the Medical Clinic and Polyclinic I at the University Hospital Würzburg.
“The recruitment and basic examinations for the clinical part were successfully completed in the middle of the year, and the annual follow – up is still ongoing, and the results of the first analyzes are expected early next year”, adds Professor Peter Heuschmann, Head of the Department of Clinical Epidemiology and Biometrics at the JMU.
Source : University of Würzburg