Cardiovascular diseases are still one of the leading causes of death in industrialized nations, despite numerous drug and device therapies. Heart failure (HF) is the final stage of many cardiac diseases and describes the inability of the heart to maintain constant blood circulation in the body at normal ventricular pressure. Regardless of its etiology, such as coronary diseases, long-standing hypertension, or cardiomyopathies, HF is characterized by structural changes (remodeling), endothelial dysfunction with vasoconstriction, and a generalized neurohumoral activation, in addition to a reduction in function of the left and/or right ventricle. Therefore, the search for new and alternative treatment methods to improve the symptoms and prognosis of affected patients is necessary. One of the most important mediators for the regulation of vascular resistance is nitric oxide (NO), which is synthesized by NO synthases. NO activates the soluble guanylate cyclase (sGC), resulting in an increased production of the second messenger cGMP (cyclic guanosine monophosphate). Impairment of the NO-sGC-cGMP pathway and consequent deficiency of cGMP contributes to the processes of myocardial and endothelial dysfunction in the development and progression of HF. The development of pharmacologically active molecules that can directly stimulate the sGC is of particular interest in this regard, as there is, for example, no development of tolerance during long-term medication or other negative side ...