| Abstract | Cardiac remodeling, currently defined as a group of molecular, cellular and interstitial changes that manifest clinically as changes in size, mass, geometry and function of the heart after injury. This results in poor prognosis because of its correlation with ventricular dysfunction and malignant arrhythmias. In spite of worldwide progression made in investigatory properties and treatment of cardiac remodeling, no advancement has been seen in clinical settings for different treatment strategies apart from targeting the RAAS. The importance of investigating further options for the pharmacological treatment against CR lies behind the fact that while angiotensin converting enzyme inhibitor, angiotensin receptor blockers and beta-blockers are the mainstay of pharmacologic therapy directed at limiting adverse remodeling, the benefits are most often seen in patients with large infarcts and individuals who are not candidates for reperfusion therapies, nor in patients with different pathological processes such as diabetic cardiomyopathy. Moreover, their use is associated with no more than a 20–25% reduction in major adverse cardiac events. Apart from LCZ696 there have been no new treatments introduced clinically for the past three decades that specifically target adverse LV remodeling. Active research has been done to investigate promising and potential drugs to induce a better result with less side effects and maximal positive outcomes. Apart from LCZ696, anti-diabetics such as anti-glucagon peptides or SGLT2 inhibitors, and even an extremely promising and potential natural herbal drug called Qiliqiangxin, currently used for the treatment of heart failure in several patients across China. Current investigations on new efficient therapy agents are hampered by the broad spectrum of changes in cardiac remodeling, given the fact that when speaking of said topic, hypertrophy, fibrosis and cardiomyocyte apoptosis are some of the cellular changes that occur. Furthermore, the heterogeneity between the patients as well as the many different pathological processes that give rise to cardiac remodeling limits the applicability of some promising and potential therapeutic drugs on improving cardiac function. Studies conducted on potential therapeutic drugs are currently focused on animal models with the aspiration of progressing into human clinical trials. Therefore, the focus should be on aiming to advance into clinical trials while stratifying the current data available to us. |
| Abstract (croatian) | Srčano remodeliranje je definirano kao skupina molekularnih, staničnih i intersticijskih promjena, koje se manifestiraju klinički kao promjene u veličini, težini, geometriji i funkciji srca nakon ozljede. Završava nepovoljnom prognozom zbog povezanosti s ventrikularnom disfunkcijom i malignom aritmijom. Unatoč napretku u istraživanju svojstava i načina liječenja srčanog remodeliranja u cijelom svijetu, nema napredovanja u kliničkom okruženju za različite strategije liječenja, osim ciljanja na RAAS. Važnost daljnjeg istraživanja opcija za farmakološko liječenje srčanog remodeliranja, leži u činjenici da, dok su ACEI, ARB i BB glavni oslonac farmakološke terapije usmjerene na ograničavanje nepovoljnog remodeliranja, najveća korist je viđena u pacijentima s velikim infarktima, pacijentima koji nisu kandidati za reperfuzijsku terapiju, a ne u pacijenata s različitim patološkim procesima, kao dijabetička kardiomiopatija. Štoviše, njihova upotreba je povezana s ne više od 20-25% smanjenja u većim nepoželjnim srčanim događajima. Osim LCZ696, nije bilo novih kliničkih načina liječenja unazad 30 godina koji bi specifično ciljali lijevo ventrikularno remodeliranje. Vrše se aktivna istraživanja nad obećavajućim potencijalnim lijekovima koji bi dali bolje rezultate, s manjim posljedicama i maksimalnim pozitivnim učinkom. Osim LCZ696, antidijabetički lijekovi kao anti glukagonski peptidi ili SGLT2 inhibitori, čak i vrlo obećavajući prirodni biljni lijek Qiliqiangxin, koji se trenutno koristi za liječenje srčanih zatajenja u Kini. Trenutna istraživanja na novim efikasnim terapijskim agentima su otežana širokim spektrom promjena u srčanom remodeliranju na staničnoj razini, kao što su hipertrofija, fibroza i kardiomiocitna apiptoza. Nadalje, heterogenost pacijenata i raznih patoloških procesa koji povećavaju srčano remodeliranje, ograničava primjenjivost nekih obećavajućih potencijalnih lijekova koji bi poboljšali funkciju srca. Studije napravljene na tim lijekovima su trenutno u fazi ispitivanja na životinjama, s nadom prelaska na klinička ispitivanja na ljudima. Trenutni fokus bi trebao biti na cilju prelaska na klinička ispitivanja i raslojavanju trenutnih podataka. |
