Resumen de Marcadores inflamatorios y de disfunción endotelial en la insuficiencia cardíaca
The incidence and prevalence of heart failure (HF) is increasing, mainly to the better treatment of ischaemic cardiopathy and the aging of the general population. It¿s known since many years that HF is not only a pump failure, but also a disease where the neurohormonal and inflammatory system play a key role. It is well known that inflammation has a key role in HF. Inflammation has been involved mainly in the maintenance of the disease. Since the first inflammatory markers (IM) were discovered (RCP and TNF-¿) many others IM have been implicated in the development of HF. The use of the different IM is very wide, and they are used as diagnostic tools, as prognosis markers and to overview the treatment of HF. Endothelial dysfunction (ED) and coagulation, althoughl later, have been also implicated in the development of HF. Many advances have been made in the last years, but there are also areas involving inflammation and HF not explored. The doctoral thesis that here is presented like ¿compendium of publications¿, analyse different aspects of inflammation, ED and coagulation in HF. One of the facts not elucidated until know, was if it were any difference in IM according to the etiology of heart failure. As published in the first article of this thesis, there is no such a difference, even in those IM more specifics of ischaemic cardiomyopathy. These data point out that once HF is established, the neurhormonals and inflammatory pathways are not different according to the HF etiology. Another interesting result was that a correlation between the functional class and the levels of IM was found, but not with ejection fraction. Circulating endotelial cells (CEC) are lately on the best methode to determine the ED in any disease. In the second article of this thesis it is shown that CEC correlate properly with other ED markers already known, like von Willebrand factor. In this article was also observed the evolution of the CEC in patients with acute HF to the chronic and steady phase, where the CEC are still elevated compare to healthy controls. HF is tipically divided in two groups. On group is HF with systolic dysfunction (SHF) and the other HF with ejection fraction preserved (SFPHF). Until recently, only SHF was of interest and therefore analyzed, leaving SFPHF without scientific evidence. In the area of IM it is similar. In the third article of this thesis, several IM were analyzed in patients with acute HF, and thereafter divided according to the ejection fraction. The results show no differences between both groups in this phase. This results correlate with the clinical perception where although etiology and the disease pathway are different, the clinical onset and treatment in the acute phase is similar. Finally, in every article there are data regarding the coagulation in HF. In all the evidence showed, patients with HF have higher levels of procoagulation markers than healthy controls, and more in the acute phase than in the chronic. This activation could explain the higher risk of thromoboembolic events that these patients have.
