CardioSomatics

Aim. To study a contribution of polymorphism A-8202G (rs11697325) of a gene of matrix metalloproteinase-9 (MMP-9) in development of arterial hypertension (AH) in patients with the rheumatoid arthritis (RA).

Materail and methods. 143 patients with RA were examined, among which a group of patients with RA without AH (n=50) and a group of patients with RA in association with AH (n=93) were identified. Healthy volunteers (n=151) were also divided into 2 groups comparable in age, sex and number with the main groups (control group 1 – n=54, control group 2 – n=97). The work used a range of clinical, laboratory, instrumental methods. A molecular genetic study was also performed. Blood samples were taken from all study participants. DNA isolation was carried out by the standard phenol-chloroform method. Genotyping for the MMP-9 gene was performed by PCR-RFLP analysis (polymerase chain reaction – restriction fragment length polymorphism). PCR was carried out with a set of primers to the corresponding regions of the genome. PCR products were analyzed by electrophoresis in 4% polyacrylamide gel followed by staining with ethidium bromide.

Results. In the course of a molecular genetic study, a statistically significant predominance of the homozygous AA genotype and the A allele of the MMP-9 (rs11697325) gene polymorphism was observed in the group of patients with RA, both separately and in association with AH, in comparison with the data of control groups. The risk of developing RA estimated by the odds ratio (OR) in carriers of the AA genotype of the MMP-9 gene is 1.8 times higher (95% confidence interval – CI – 1.136–2.950; p=0.02) than in carriers of the GG and GA genotypes; in carriers of the A allele, the risk of developing RA is 1.6 times higher compared to the G allele (95% CI 1.119–2.578; p=0.01). The OR risk of developing RA in association with hypertension in carriers of the AA genotype of the MMP-9 gene is 2.8 times higher (95% CI 1.283–6.54; p=0.04) compared to GA and GG genotypes, 2.1 times higher in carriers of the A allele (95% CI 1.113–4.127; p=0.02) compared to the G allele.

Conclusion. Thus, the results of the study indicate that the homozygous AA genotype and the A allele of the MMP-9 (rs11697325) gene polymorphism are the predictors of the development of RA both as a separate nosological unit and in association with AH.

Aim. To study the relationship between serum levels of aldosterone, tissue inhibitor of matrix metalloproteinases-1 (TIMP-1), tumor necrosis factor-alpha (TNF-α) and structural and functional changes in the heart during the progression of chronic heart failure (CHF) with a moderately reduced ejection fraction (CHFunEF) in patients with type 2 diabetes mellitus (DM).

Material and methods. 58 patients were examined – 30 (51.7%) men and 28 (48.3%) women – diagnosed with DM and CHFunEF (EF=41–49%), with functional class (FC) I, II and III of CHF according to New York Heart Association (NYHA). The control group consisted of 16 people. Patients underwent echocardiography, determination of serum levels of aldosterone, TIMP-1 and TNF-α by ELISA. The patients were divided into 2 groups: 1st group – patients with DM and CHFunEF who had a myocardial infarction (MI) – 27 people (46.6%), 2nd group – patients with DM and CHFunEF – 31 people (53.4%). Statistica v. 10.0 software (USA) was used for statistical analysis. Differences were considered statistically significant at р<0.05.

Results. Serum levels of aldosterone, TIMP-1 and TNF-α were significantly higher than those of the control group and increased with an increase in CHF FC. In patients of the 1st group, the volume and index values of the left parts of the heart and serum levels of biomarkers significantly exceeded those of the 2nd group.

Conclusion. Activation of the aldosterone system, increased profibrotic and immuno-inflammatory processes with the progression of CHFunEF in patients with DM lead to an increase in serum levels of aldosterone, TIMP-1 and TNF-α with an increase in CHF FC. Patients with DM and CHFunEF who have undergone MI have more pronounced structural and functional changes in the heart and greater values of volumetric and index parameters of the left heart than patients with DM and CHFunEF. Serum levels of aldosterone, TIMP-1 and TNF-α in patients with DM and CHFunEF who have undergone MI exceed those in patients with DM and CHFunEF, these biomarkers can be used to diagnose the progression of CHFunEF in patients with DM.

Systemic amyloidosis is a group of diseases associated with extracellular deposition of fibrillar proteins, resulting in the loss of normal organ structure and function. AL-amyloidosis occurs when amyloid is deposited, consisting of full-length lambda or kappa immunoglobulin light chains, or fragments thereof. This article describes the complexity of timely diagnosis of systemic AL-amyloidosis with a predominant heart lesion in the absence of myocardial «hypertrophy» on the example of an elderly patient in whom the leading manifestation of the disease was heart failure with a preserved left ventricular ejection fraction.

The review discusses the relationship between chronic heart failure and diabetes mellitus type 2, metabolic phenotypes of patients w ith chronic heart failure with preserved left ventricular ejection fraction (HFpEF), features of the pathophysiological interaction between diabetes mellitus and HFpEF. Chronic inflammatory condition, metabolic disorders and comorbidities are the pathophysiological basis of HFpEF. The review discusses the concept of diabetic cardiomyopathy, its molecular mechanism and current possibilities of treating this pathology, considering the impact on the prognosis.