Stem Cells for Cardiovascular Diseases Revisited in 2019

cardiovascular diseases, such as refractory angina and myocardial failure, caused a frenzy in clinical research in the late 1990’s and early 2000’s. Experimental reports have shown marked improvements in myocardial contractility in heart failure models, and increased myocardial perfusion or even myocardial replacement after necrosis in ischemic models. More than 200 clinical trials were produced, but the experimental effects could not be reproduced. Indeed, an improvement in cardiac function as well as some angiogenic reperfusion have been observed at the clinical level, but those effects were light and temporary, not sufficient to represent a usable therapeutic tool. The reasons for that are an actual challenge to researchers. There are many hypotheses for stem cell therapy failure in clinical therapy. Animal experiments are done in young individuals and outcomes are evaluated invariably at short term. Cardiac diseases are present in older patients, in whom stem cells are also old and submitted to pharmacological effects of therapeutic drugs. Potent and prolonged improvements are necessary to influence clinical outcomes, differently from what can be achieved in animal research. Those could be some of several explanations. The mechanism of action of stem cell therapy is also under exploration. The elements responsible for the effects need to be better understood. Cellular proliferation, paracrine effects, and delivery of cell elements or components are theories to be studied. Proliferation has been demonstrated as not feasible in clinical level. Some considerations should be brought to mind. There are two main types of stem cells. Pluripotent stem cells, capable of differentiating in any type of mature cells, of EDITORIAL