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Despite different causes, ischemic and hypertensive heart disease result in the common pathophysiological end of fibrosis formation and myocardial pumping loss. Currently available pharmacological therapies increase the survival time of the diseased patients, but they can not stop the fibrosis of the myocardium and the associated "remodeling". For the first time the causal therapy appears now possible by inhibition of a specific micro-RNA, which is greatly increased in the affected tissue,via antagomirs. This therapeutic strategy will be investigated in preclinical large animal models. To this end, an attempt is made, in animal models of ischemic cardiomyopathy and hypertensive heart failure, by retroinfusion of regional antagomir in the affected working myocardium to inhibit the development of fibrosis and the associated loss of function.