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Damage of the cardiovascular system in lysosomal storage disease - mucopolysaccharidosis

Pyvovar SM, Rudyk IS, Lozykc TV

Pol Merkur Lekarski, 2021 Dec 16;49(294):448-452.
PMID: 34919092

The analysis of literature data reflecting the issues of the pathology of the cardiovascular system in mucopolysaccharidosis are presented. It was found out that heart and vessels damage is one of the cardinal signs of this pathology, often leading to death. Cardiac pathology is recorded in all types of mucopolysaccharidosis, but it is most significant for patients with three clinical variants of Hurler syndrome, Hunter, and Maroteaux-Lamy syndromes. Typical signs of damage to the cardiovascular system in mucopolysaccharidosis are thickening of the valves with the development of their dysfunction (while the severity of damage to the left-sided valves is more pronounced), myocardial hypertrophy, conduction disturbance, coronary artery disease, arterial hypertension. Many researchers emphasize the difficulties of clinical and functional examination of the cardiovascular system in patients with mucopolysaccharidosis, which is due to the presence of physical and intellectual limitations in patients, ands a gradual increase in symptoms. For the treatment of cardiovascular pathology at mucopolysaccharidosis, medical and surgical methods are used, including enzyme replacement therapy and stem cell transplantation.
Influence of various risk factors on the level of ST2 biomarker in patients with heart failure and diabetes mellitus type 2

Rudyk IS, Medentseva OO, Gasanov IC, Babichev DP

Pol Merkur Lekarski, 2021 Apr 18;49(290):95-98.
PMID: 33895752

Heart failure (HF) despite the progress in treatment remains the main health problem worldwide. Biomarker ST2 is currently being studied in patients with HF due to its high potential predictive value and promising prospects for use as a component of biomarker-controlled therapy. The factors that can impact on the ST2 biomarker level in diabetic patients with heart failure with preserved ejection fraction (HFpEF) are still not well known.
AIM: The aim of the study was to determine the influence of various risk factors on ST2 levels in patients with HFpEF and diabetes mellitus type 2 (T2DM).
MATERIALS AND METHODS: A total of one hundred and thirty-four patients (74 females and 60 males, 51 diabetic patients and 83 patients without T2DM with HFpEF were examined. Duration of HF and T2DM, common risk factors, such as smoking, overweight, clinical examination, parameters of carbohydrate and lipid metabolism, glomerular filtration rate (GFR) and M235T polymorphism of ATG have been used. Multivariate backward stepwise cox regression analysis was performed in Statistica 10,0. p<0,05 was considered statistically significant.
RESULTS: ST2 level in patients with HFpEF associated with T2DM exceeded this value in patients with HFpEF without T2DM and was 23.26 ng/ml (18.5: 29.3) vs. 20.39 ng/ml (18.3: 24.6), respectively (p<0,05). To assess the cumulative effect of the studied factors on the ST2 level, we performed the Cox's stepwise multivariate regression analysis. Smoking, HOMA-IR (Homeostatic Model Assessment for Insulin Resistance), glucose, HbA1 and insulin levels were found to be the most significant factors influencing ST2 levels in patients with HF and T2DM, indicating a significant effect of DM type 2 on ST2 concentration.
CONCLUSIONS: Smoking, HOMA-IR, glucose, HbA1, and insulin levels can significantly affect ST2 levels in patients with T2DM and HFpEF.
The effect of beta-blockers on a course of chronic heart failure in patients with a low triiodothyronine syndrome

Pyvovar SM, Rudyk IS, Kopytsya MP, Lozyk TV, Galchinskaya VI, Chenchik TO

Wiad Lek, 2020;73(7):1402-1409.
PMID: 32759428

OBJECTIVE: The aim: The aim is to study the effect of β-ABs in patients with LT3 S on the course of HF.
PATIENTS AND METHODS: Materials and methods: 354 patients with HF on a background of post-infarction cardiosclerosis were included in the 2-yeared follow-up study. LT3 S was diagnosed at 89 (25.1%) patients. The levels of thyroid-stimulating hormone, free T3f and T4f, and reversible T3 were determined. The echocardioscopy was performed.
RESULTS: Results: Patients with HF in combination with LT3 S have a heavier functional class by NYHA, greater dilatation of the left heart cavities, less myocardial contractility, a higher frequency of atrial fibrillation and re-hospitalization. The use of β-ABs in patients with HF without LT3 S leads to a likely decrease in hospitalization frequency, while in patients with LT3 S it has an opposite effect. The frequency of rehospitalization increases with an excess of β-ABs dose > 5 mg (equivalent to bisoprolol). At these patients a decrease in serum T3 level and negative dynamics of parameters of intracardiac hemodynamics are observed.
CONCLUSION: Conclusions: The use of β-ABs in patients with LT3 S leads to an increase in re-hospitalization at a dose over 5.0 mg (equivalent to bisoprolol). In these patients there is a decrease in serum T3, an increase in T4 level; and the ejection fraction decrease; and heart cavities size increase.
The association of polymorphisms of β-adrenergic receptors genes with the low triiodothyronine syndrome in patients with a heart failure

Pyvovar SM, Rudyk IS, Kopytsya MP, Lozyk TV, Galchinskaya VY, Bondar TM

Pol Merkur Lekarski, 2019 Nov 29;47(281):170-176.
PMID: 31812970

The course of heart failure (HF) and its progression is associated with comorbidities, genetic factors and a dynamics of a number of biomarkers. The low triiodothyronine syndrome (LT3S) is observed in some patients with HF. Extremely little data are available in the literature regarding the effect of β-adrenoreceptors (β-AR) genes polymorphisms on the development of LT3S and many contradictory results about their association with HF course. This encourages new research in this area.
AIM: The aim of study was to evaluate the relationship of β-adrenergic receptors gene polymorphisms with low triiodothyronine syndrome in patients with a heart failure.
MATERIALS AND METHODS: 354 patients with HF on a background of postinfarction cardiosclerosis were included to the study. At 89 (25.1%) patients LT3S was diagnosed. The course of HF was studied for 2 years. Mean levels of thyroid stimulating hormone (TSH), free T3f and T4f were evaluated. Genotyping of 4 single nucleotide polymorphisms (Gly389Arg of β1-AR gene, Ser49Gly of β1-AR gene, Gln27Glu of β2- AR gene and Ser275 of GNβ3 gene) was performed by polymerase chain reaction. Genetic and epidemiological analysis was performed using the SNPStats program.
RESULTS: The risk of LT3S in patients with HF increases with homozygous G/G variant of Gln27Glu polymorphism of the β2-AR gene (OR=2.21, p=0.037), described as a recessive model of inheritance. There was a tendency to increase the risk of LT3S development in the presence of the genotype C/T of the Ser275 polymorphism of the GNb3 gene (OR=1.75, p=0.054), described as an over-dominant model. The genotype C/G of the Gln27Glu polymorphism of the β2-AR gene was associated with a decreased risk of LT3S development (OR=0.54, p=0.037), described as over-dominant model. Patients with HF carriers the A allele (A/GA/A) of the Ser49Gly polymorphism of the β1-AR gene have a lower risk of repeated hospitalization due to HF decompensation (OR=0.50, p=0.032), described as a dominant model. There was a tendency to increase the risk of re-hospitalization in the G-allele (C/GG/ G) variant of the Gln27Glu polymorphism of the β2-AR gene (OR=1.68, p=0.057), described as a dominant heredity model. At patients with HF in combination with LT3S the risk of re-hospitalization increases at C/G variant of the Gln27Glu polymorphism of β2-AR gene (OR=1.25, p=0.025), described as an over-dominant model.
CONCLUSIONS: The results suggest that congenital genetic alterations in β-adrenergic pathways may be associated with the development of LT3S in patients with HF and the features of the HF course.