Vol 13, No 3 (2022)

Objective. This study evaluates the severity of chronic heart failure (CHF), ejection fraction (EF), and global contractility of the left ventricle (LV) using Speckle–tracking (STE) in patients with takotsubo syndrome (TS) in the early and late disease stages of the disease and compares these data with an assessment of the quality of life (QoL) of patients.

Material and methods. The study included 60 patients with TS, with a mean age of 65.5±13.4 years. The severity of CHF symptoms was assessed using the SHOKS scale (assessment of the clinical condition in CHF). The Minnesota Questionnaire and the HeartQol questionnaire were used to study QoL. Echocardiography data (ECHOCG) were recorded during the acute period and at discharge from the hospital. In the late disease period, ECHOCG was performed using the STE method. After 1 year, endothelial function was studied using the EndoPAT 2000 device to determine the reactive hyperemia index.

Results. According to the SHOKS scale, the severity of CHF symptoms corresponded to 1–2 functional class (FC) in all patients with TS in the long-term disease; however, before the development of TS, only 15 people had signs of CHF at the level of 1–2 FC. According to ECHOCG, LVEF in patients with TS was 44.5±9.7% at admission, 60.2±7.6% at discharge, 61.6±9.2% after a year, and 60.0±9.0% after 2 years. The average values of global longitudinal and global circular deformation of the left ventricle in patients with TS were 14.0±3.1 and 15.0±4.1%, respectively, after 1 year from disease onset and 12.3±1.9 and 13.1±1.9%, respectively, after 2 years. When comparing the data of the Minnesota Questionnaire and HeartQol questionnaires, QoL in the long-term of ST was significantly lower than the initial one before disease development. Mean reactive hyperemia index values after 1 year were 1.74±0.19.

Conclusion. Despite the complete restoration of LVEF in patients with TS, clinical manifestations of CHF persist. Using the STE technique during the long term, >90% of patients had abnormalities in the global tissue deformity of the left ventricle. These changes may explain the CHF clinical manifestations and QoL decrease in patients with TS during long-term disease.

Background. The extracellular matrix of vessels is degraded under the influence of matrix metalloproteinases (MMPs). MMP type 9 is of particular interest in arterial hypertension (AH) since its activity is regulated by a tissue inhibitor of matrix metalloproteinase type 1 (TIMP1). The balance of their ratio can shift in either direction depending on the disease stage and provoke vascular wall calcification.

Objective. This cross-sectional comparative study investigated the level of MMP9 and its type 1 tissue inhibitor and their relationship with the severity of thoracic aorta calcification in patients with resistant hypertension, depending on antihypertensive therapy effectiveness.

Material and methods. The study included 92 patients with resistant hypertension. All patients underwent 24-hour blood (BP) pressure monitoring (ABPM), and had their index of the thoracic aorta (ТАС) and the plasma levels of MMP9 and TIMP1 assessed.

Results. Patients were divided into groups based on whether they achieved the BP target level according to the results of ABPM: controlled (n=44) and uncontrolled (n=48) resistant AH. In the second group, most estimated parameters of ABPM were higher, and the variants of the daily BP profile for non-dipper and night-peaker systolic blood pressure (SBP) were more common than in the first group. In the second group, a more pronounced increase in TAC, TIMP1, and TIMP1/MMP9 levels was revealed. Evaluation of the relationship between the studied parameters revealed a positive relationship between TAC and age (r=0.683, p <0.00001), hypertension duration (r=0.610, p <0.00001) and a negative relationship with regular antihypertensive therapy duration (r=0.822, p <0.00001). ТАC was higher in individuals with higher values of SBP (r=0.513, р <0.00001), pulse BP (r=0.805, р <0.00001), rate of morning rise in BP (r=0.678, р <0.00001) and insufficient decrease in SBP at night (r=-0.822, р <0.00001). There was a positive correlation of moderate strength TAC with the level of low-density lipoproteins (r=0.490, p=0.0002), TIMP1 (r=0.344, p=0.005) and the TIMP1/MMP9 ratio (r=0.481, p <0.00001).

Conclusion. In patients with resistant hypertension, an increase in the TAC was revealed, which has a statistically significant direct correlation with the value of pulse BP, the morning rise in BP, and an insufficient decrease in SBP at night. An imbalance in the TIMP1/MMP9 ratio, rather than an isolated increase in MMP9, can indicate the intensity of the formation and degradation of the extracellular matrix components in patients with resistant AH, which triggers the vascular wall calcification process.

The review presents modern studies the effect of genetic polymorphisms on the efficienty and safety of therapy with new oral anticoagulants. Hepatic carboxylesterase encoded by the CES1 gene and P-glycoprotein encoded by the ABCB1 gene affect dabigatran pharmacokinetics. The role of glucuronidation enzymes (UGT2B15, UGT1A9, UGT2B7) involved in active dabigatran metabolism is poorly understood. An increase in the peak apixaban concentration was noted in patients with the rs4148738 polymorphism of the ABCB1 gene. Polymorphisms rs776746 and rs77674 of the CYP3A5 gene affect concentration of apixaban in Asian patients and thus increased the bleeding risk. The effect SULT1A1 sulfotransferase on the metabolism of apixaban has yet to be studied. The BCRP protein encoded by the ABCG2 gene is a poorly studied but promising direction for the pharmacokinetics of apixaban. ABCB1 and CYP3A4 of the cytochrome P450 system affect the rivaroxaban metabolism, however, the number of studies devoted to examining the effect of polymorphisms of these genes on the rivaroxaban pharmacokinetics limited. Thus, large studies are needed to clarify the clinical relevance of genotyping in target patients taking new oral anticoagulants.

Background. As is known, the treatment of the oncological process leads either to the occurrence of cardiovascular pathology, or to an increase in the risk of death from cardiovascular diseases. Currently, the concept of ˝cardiovascular toxicity˝ has been introduced, which is associated with the treatment of cancer (CTR-CVT). Systemic drug anthracycline-containing anticancer therapy can cause a number of cardiovascular complications, such as myocardial systolic dysfunction, coronary heart disease, cardiac arrhythmias, arterial hypertension. Particular attention is paid to anthracycline drugs, because they are still included in combinations of many adjuvant therapy regimens and first-line treatment of both the most common cancers and rarer ones.

Clinical Case Description. The article presents a clinical case of a patient who received adjuvant polychemotherapy for breast cancer in 2017 with AC ×4 →D ×4 regimen, in which chronic anthracycline-induced cardiomyopathy manifested years after completion of antitumor therapy. The development of anthracycline cardiomyopathy is possible even in patients with initially low cardiac risk.

Conclusion. The clinical case highlights the importance of monitoring patients after the end of anthracycline antitumor therapy, in particular, they are shown to periodically perform an echocardiographic study in order to detect delayed asymptomatic myocardial dysfunction.