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Novel Therapeutic Strategies

Research within this program aims to bring the wealth of novel targets to clinical application as well as to define new indications for known drugs. The focus is set on the development of therapies that interfere with CVD-induced vascular and myocardial damage.

Therapeutic measures targeting vascular damage

The new generation of drug-eluting stents (DES) has drastically improved the management of patients with cardiovascular disease (CVD). Currently, all DES patients are uniformly treated with a protracted dual anti-platelet (DAP) therapy. However, the current DAP therapy impairs also normal hemostasis and may cause severe bleeding complications. Therefore, a major task of the Munich Heart Alliance is to develop strategies that prevent CVD manifestation and/or progression without compromising essential processes such as immune defense, vascular healing and arrest of bleeding. 
One focus will be on the evaluation of novel stent designs with improved anti-proliferative, pro-healing and anti-inflammatory characteristics. A second major focus will be to develop and evaluate novel antithrombotic strategies that interfere with platelet adhesion and/or coagulation in diseased (or stented) coronary arteries but have a minor effect on normal hemostasis. New antithrombotic concepts will be evaluated by Munich Heart Alliance members in phase I/II trials and in the large phase III/IV ISAR BRAVE and the ISAR REACT trials.

Targeting fibrosis as a key mechanism linked to arrhythmias and impaired contractile function

Cardiac fibrosis is a key structural alteration of post myocardial infarction and a critical element of cardiac remodeling and of cardiac arrhythmias.
In a preclinical study, scientists of the Munich Heart Alliance have recently shown that interfering with a cardiac fibroblast-specific signaling mechanism (miR-21-mediated control of fibroblast ERK activity) prevents and even cures structural and functional deterioration in a mouse model of cardiac damage. This study represents the first example of microRNA therapeutics in a cardiovascular disease model and suggests a new therapeutic entry point for cardiac disease. Based on this expertise, the Munich Heart Alliance aims to employ RNA-based therapeutics to target cardiac fibrosis to cure myocardial infarction-induced myocardial damage and arrhythmias. An especially powerful facet of microRNA biology is the ability of individual microRNAs encoding proteins with related functions (e.g. cell growth, contractility, etc.), in contrast to classical drugs, which act on specific cellular targets.

Preventing sudden cardiac death after myocardial infarction

Despite the general improvement in outcomes among survivors of acute myocardial infarction the rate of death remains highest in the weeks after the event. Sudden cardiac death accounts for approximately 20-50% of all deaths in this population. Combining the expertise of partners of the Munich Heart Alliance we aim to improve the prevention of sudden cardiac death on post myocardial infarction patients by testing a novel strategy for implantable cardioverter-defibrillator therapy for the reduction of total mortality in a large-scale prospective randomized trial.


The MHA bioimaging expertise is essential for all of the above efforts to monitor the proposed translation of new therapeutic concepts into clinical application. Within the Munich research area, scientists have focused on developing imaging methods to assess the beneficial effect of cardiovascular interventions (myocardial perfusion, infarct size, area of risk etc.). Current imaging research addresses the quantitative visualization of biological processes in order to longitudinally evaluate the natural history of disease and its modification by therapeutical interventions.