Confirmation of protection and integrity of personal and clinical data of the included patients was also provided

Confirmation of protection and integrity of personal and clinical data of the included patients was also provided. rs4646174, homozygotes for the C allele offered a dilated LV with indicators of LVH with statistical significance and experienced a tendency towards a lower ejection portion. rs1024611 AA variant service providers had a significant LVH in the dominant model. In conclusion, our study showed a strong association between echocardiographic parameters of cardiac remodeling and SNPs rs4646156, rs4646174 of and rs1024611 of polymorphism, rs4646156, rs4646174, polymorphism, rs1024611, heart failure, echocardiography Introduction Heart failure still represents the leading cause of hospital admission in patients over 65 years of age. It is defined as a multifactorial disease, which involves environmental factors and genetic predispositions and severely affects the quality of life of these patients (1). Genetic polymorphisms are involved in the pathogenesis of heart failure, but also in disease progression, and they may influence clinical outcomes or therapeutic responses (2-10). It is well known that this renin-angiotensin system (RAS) plays an important role in heart failure progression. Angiotensin transforming enzyme (ACE) converts angiotensin I (Ang I) to angiotensin II (Ang II), and angiotensin transforming enzyme 2 (ACE2) cleaves Ang I into Ang-(1-9) and Ang II into Ang-(1-7). Ang II has pro-inflammatory and pro-atherosclerotic effects, and promotes hypertrophy and fibrosis, while Ang-(1-7) reduces left ventricular remodeling and the infarcted area, protects against cardiac hypertrophy, therefore using a cardioprotective effect. By having an opposite effect on the cardiovascular system, ACE and ACE2 counteract each other to regulate heart function (1,3,11-16). The gene is located on chromosome Xp22. ACE2 is mainly expressed in cardiac tissue, the renal endothelium and in the blood vessels, Hydroxyflutamide (Hydroxyniphtholide) and is widely expressed in human tissues and cells, except for reddish blood cells. Soluble ACE2 activity is usually a biomarker for heart failure and arterial hypertension (4,17-19). genetic variants are associated with essential hypertension (20-23), coronary artery disease (20), heart failure (13), atrial fibrillation or left atrial remodeling (20). Research studies have confirmed that gene polymorphism rs4646156 is usually associated with higher left ventricular mass and septal wall thickness, left ventricular hypertrophy (LVH) in men, diabetic-related cardiovascular complications, and a higher risk for severe pectoris angina in women (20,21,24-29). gene polymorphism rs4646174 is usually associated with arterial hypertension and is found frequently in patients diagnosed with pectoris angina without significant stenosis of the circumflex artery (25,27). The molecular mechanism of chronic inflammation associated with cardiac-specific expression of MCP-1 and its role in heart failure has been described in previous research studies. Experimental studies showed a correlation between expression and increased mortality in congestive heart failure. -2518 A G (rs1024611) polymorphism is frequently associated with coronary artery disease, non-familial dilated cardiomyopathy, myocardial infarction, ischemic heart disease, ischemic stroke, arterial hypertension and carotid atherosclerosis in patients with type 2 diabetes, underlying the role of MCP-1 in atherosclerosis initiation, coronary artery disease and myocardial infarction (30-35). Identifying additional components of RAS and molecular pathways involved in the pathogenesis of heart failure may lead to novel molecular biomarkers which could represent the basis in developing novel Hydroxyflutamide (Hydroxyniphtholide) therapeutic strategies for these patients, individualized therapeutic options which might improve therapy response, clinical outcomes, survival rates and quality of life of these patients. Based on current data regarding the association of and polymorphisms with heart failure and the importance of understanding molecular pathways underlying heart failure and targeting different genes in defining novel therapeutic strategies, our study aimed to evaluate three SNPs, polymorphisms (rs4646156, rs4646174) and (rs1024611) and their potential correlation with echocardiography parameters involved in cardiac remodeling in patients diagnosed with heart failure. Patients and methods The study was observational, prospective, cohort type. The current study included 116 patients diagnosed with heart failure and admitted to the Departments of Cardiology from Niculae Stancioiu Heart Institute, Clinical Rehabilitation Hospital and Municipal Clinical Hospital of Cluj-Napoca, Romania, between November 2017 and March 2019. The inclusion criteria were: Hydroxyflutamide (Hydroxyniphtholide) Patients aged at least 18 years with symptomatic heart failure of New FGFR2 York Heart Association (NYHA) functional classes II to IV, high pro-BNP values (over 300 pg/ml in an acute setting and over 125 pg/ml in a non-acute setting). Our study excluded patients with congenital heart disease, primary pulmonary hypertension, secondary arterial hypertension, pericardial disease, sepsis, malignancies, recent coronary bypass surgery and severe valvular heart disease. Written consent was obtained from each participant after they were provided information concerning genetic testing and the study design. Confirmation of protection and integrity of personal and clinical data of the included patients.