CardioSomatics

This expert consensus document discusses the high prevalence of cardiovascular diseases (CVDs) caused by atherosclerosis. It is now evident that the causes and pathogenesis of atherosclerotic cardiovascular diseases (ASCVD) cannot always be explained solely by lipid metabolism disorders associated with low-density lipoproteins (LDL). In recent years, an increasing number of studies have focused on hypertriglyceridemia (HTG), including its mechanisms and role in atherothrombogenesis. In this regard, it has become necessary to update key aspects that define the root causes of ASCVD in HTG and the role of triglyceride-rich lipoproteins (TRLs) and their remnants in this process. Epidemiologic and genetic studies have demonstrated a causal relationship between HTG and the development of ASCVD, independent of LDL-C levels. The role of TRLs in determining high residual cardiovascular risk under conditions of LDL-C control has been established, and evidence has been obtained supporting the preventive benefits of lowering elevated plasma triglyceride levels. This document presents the consensus positions of experts regarding the classification, etiology, and mechanisms of HTG, the importance of assessing TRLs/remnants, and a detailed discussion of their metabolism and pathophysiologic role in atherothrombosis. The experts also address the clinical assessment and patient management pathways for HTG, outlining both nonpharmacologic and pharmacologic strategies for its correction.

Background: α₂-Adrenoceptors (α₂-ARs) are a family of G protein–coupled receptors. They are located on presynaptic membranes of adrenergic fibers, postsynaptic membranes of cardiomyocytes and vascular smooth muscle cells, as well as in the peripheral and central nervous systems, intestinal and renal epithelium, and the sarcolemma of cardiomyocytes. The cardioprotective properties of myocardial α₂-ARs have been demonstrated. However, the specific contribution of α₂-ARs to myocardial responses after infarction remains insufficiently understood.

AIM: The work aimed to investigate the effect of α₂-AR stimulation on functional parameters of the isolated rat heart in a model of acute myocardial infarction.

METHODS: The experiment involved 48 outbred rats aged 100–120 days with a mean body weight of 200–250 g. Myocardial infarction was induced by ligation of the left anterior descending coronary artery. Ex vivo experiments were performed on isolated hearts. To evaluate the effects of α₂-AR stimulation, clonidine hydrochloride was administered at concentrations of 10^–9 M and 10^–6 M.

RESULTS: Activation of α₂-ARs (10^–9 M, 10^–6 M) produced opposite effects on the functional parameters of the isolated heart: it increased left ventricular developed pressure and coronary flow in sham-operated rats and those with acute myocardial infarction, whereas it decreased these parameters in healthy animals. Heart rate decreased in all groups during α₂-AR stimulation, whereas in healthy rats the α₂-AR agonist (10^–6 M) induced bidirectional changes. Stimulation of α₂-ARs (10^–9 M) reduced contraction duration and increased relaxation and total contraction cycle duration of the left ventricular myocardium in healthy and sham-operated rats, whereas bidirectional effects were observed in rats with acute myocardial infarction. Activation of α₂-ARs (10^–6 M) induced bidirectional changes in contraction, relaxation, and contraction cycle duration of the left ventricular myocardium in healthy rats. Clonidine hydrochloride (10^–6 M) did not affect contraction duration but increased relaxation and total contraction cycle duration in sham-operated rats and in those with acute myocardial infarction.

CONCLUSION: Activation of α₂-ARs in rats with acute myocardial infarction alters the parameters of left ventricular developed pressure and coronary flow, decreases heart rate, and exerts bidirectional effects on the time–velocity characteristics of the left ventricular myocardium.

Antiarrhythmic therapy is associated with a high risk of adverse effects, including extracardiac and cardiac (particularly proarrhythmic) complications, as well as events related to drug–drug interactions. Currently, safety monitoring during treatment with antiarrhythmic drugs (AADs) includes electrocardiographic surveillance and assessment of hepatic, renal, thyroid, and pulmonary function, along with screening for underlying cardiac pathology, including latent conduction system disorders (eg, congenital long QT syndrome). However, these measures do not always prevent adverse drug reactions. A search was conducted in PubMed and eLibrary for the period from January 2019 through December 2024 (in some cases, because of the limited number of sources, the range was extended). The total search depth spanned 1979–2024. This review summarizes contemporary approaches to safety monitoring for the most commonly prescribed AADs in clinical practice, including class IC agents (propafenone, lappaconitine hydrobromide, and diethylaminopropionylethoxycarbonylaminophenothiazine) and class III agents (amiodarone and sotalol). Prospects for implementing therapeutic drug monitoring and pharmacogenetic testing of AADs are also discussed.

Acute myocardial infarction (AMI) remains a major public health concern worldwide. The aim of this narrative review was to identify and summarize the results of epidemiological studies on AMI incidence in Russia and abroad. Russian and international publications were searched in the databases eLibrary, PubMed, and Google Scholar. The search covered the previous 5 years. The analysis showed that the incidence rate of AMI in the Russian population during the study period remained high, reaching 140.8 cases per 100,000 population by 2022. This rate was lower compared with some CIS countries (Belarus, 174.5 cases) and European countries (Sweden, 288.0 cases; United Kingdom, 288.0 cases; France, 180.2 cases; Hungary, 177.5 cases; Spain, 169.0 cases; Cyprus, 160.0 cases), as well as New Zealand (536.0 cases), the United States (439.9 cases), Japan (389.7 cases), Australia (352.0 cases), Iran (343.0 cases), China (231.6 cases), and Tanzania (172.0 cases). These findings indicate that the incidence of AMI remains high both in Russia and globally, with an upward trend among middle-aged individuals. This highlights the need for future multicenter epidemiological studies of AMI incidence in Russia, particularly among adults aged 45–59 years, to support the development of new diagnostic and therapeutic strategies.

BACKGROUND: The coexistence of cardiomyopathy and dextrocardia is of considerable clinical interest due to its rarity and the complexity of its pathogenesis, which may involve common embryogenetic abnormalities. A clinical case analysis was performed in a 45-year-old patient with dextrocardia who was admitted to the cardiology department. Data from physical examination, laboratory testing (complete blood count, biochemical analysis of blood and urine), and instrumental studies (echocardiography, electrocardiography, chest radiography, and cardiac magnetic resonance imaging) were used.

CASE DESCRIPTION: The article highlights current data on the etiology, genetic aspects, and clinical manifestations of the coexistence of cardiomyopathy and dextrocardia. Particular attention is given to mixed etiology, in which the interaction of genetic mutations (over 1,400 identified genes, including those encoding sarcomeric proteins) with exogenous factors (toxins, inflammation, and metabolic disorders) contributes to the complex pathogenesis and clinical course. An example of such a combined disorder is presented in a clinical case involving a rare anatomical anomaly—dextrocardia, in which the heart is located in the right hemithorax. This combination is quite rare in modern clinical practice; therefore, special attention should be given to a comprehensive diagnostic approach that considers genetic, environmental, and comorbid factors, as well as to the importance of an interdisciplinary strategy aimed at improving prognosis and quality of life.

CONCLUSION: The presented case underscores the importance of thorough diagnostics, including advanced imaging modalities (MRI), for identifying specific cardiomyopathy phenotypes such as left ventricular noncompaction (LVNC) in patients with rare anatomical anomalies. A comprehensive, individualized approach enables the successful implementation of standard therapeutic regimens and achievement of favorable outcomes. The need for further genetic testing is emphasized.