Aim. To determine whether pregnancy is associated with a worsened clinical course and long-term prognosis in patients with hypertrophic cardiomyopathy (HCM), and to evaluate differences in maternal, obstetric, and cardiovascular outcomes between obstructive and non-obstructive disease forms.

Material and methods. This single-center, ambispective cohort study was conducted at a perinatal center. The study included 102 patients with clinically confirmed HCM, who underwent 114 pregnancies between 2011 and 2025. Clinical status, electrocardiographic (ECG) and echocardiographic examinations were assessed in the first and third trimesters of pregnancy, in the early postpartum period, and during follow-up. The risk of sudden cardiac death (SCD) was calculated using the ESC HCM Risk-SCD score. The median follow-up was 5,8 years.

Results. Obstructive and non-obstructive HCM was diagnosed in 33,3% and 66,7%, respectively. As pregnancy progressed, the incidence of clinical manifestations increased from 35% to 57%. During pregnancy, transient echocardiographic changes were observed, including an increased left atrial size (p=0,001 and p=0,002 for the obstructive and non-obstructive HCM, respectively). With the non-obstructive HCM, a more pronounced increase in interventricular septal thickness was noted (p<0,001). After delivery, most echocardiographic parameters returned to baseline values. In the second and third trimesters, a tendency towards an increase in the frequency of ventricular tachyarrhythmias was noted, followed by a decrease in the long-term period. SCD risk increased from the first trimester to the postpartum period and then decreased. With the obstructive HCM, premature births (36,8% vs 15,8%, p=0,036) and Cesarean delivery (71,1% vs 39,5%, p=0,012) were more often recorded. During the follow-up period, one sudden cardiac death (SCD) was recorded, and two patients underwent heart transplantation.

Conclusion. Pregnancy in patients with HCM is associated with transient clinical and echocardiographic changes, most pronounced in the second and third trimesters, with regression after delivery. Despite a higher incidence of obstetric complications in the obstructive HCM, pregnancy  is  not  associated with  a  worse  long-term  prognosis  when  monitored  at  a  specialized  center.

Aim. To study dromotropic dysfunction based on electrocardiography (ECG) data and compare ECG parameters with dilated cardiomyopathy (DCM) genotypes and cardiac magnetic resonance imaging (MRI) data, as well as to evaluate the prognostic role of MRI/ECG abnormalities in patients with familial DCM.

Material and methods. The study included 65 genotyped patients with dilated cardiomyopathy (48/73,8% men, age 38 [25; 52] years, left ventricular ejection fraction 35 [21; 45]%) with pathogenic and likely pathogenic (P/LP) variants in the genes encoding proteins titin (TTNtv — 36,9%), lamin A/C (LMNA — 33,8%), desmoplakin, desmin, and filamin-C (DSP, DES, FLNC — 29,2%). The follow-up period was 5 years (Me 62 [46; 92] months). The primary endpoint of life-threatening ventricular tachyarrhythmias (VT) and a composite endpoint of all cardiovascular death were analyzed.

Results. MRI signs of myocardial fibrosis were detected in 49,2% of cases. Ring-like fibrosis involving the inferior-septal segments was detected in 16 (24,6%) patients, sub/transmural pattern with inferior wall scar was observed in half of the cases. In 75% (12 of 16) cases of ring-like inferior scar (in 100% of individuals with sub/transmural fibrosis), ECG showed left posterior fascicular block (LPFB) (χ2=28,1; p=0,0001; C’=0,89). Isolated and combined variants of LPFB were detected in 18,5% of carriers of LP/P variants in the LMNA, DSP, DES, and FLNC genes. Multivariate Cox regression analysis identified following four independent predictors of VT: LMNA genotype (hazard ratio (HR) 6,83; 95% confidence interval (CI): 2,35-19,9; p=0,0001), ring-like inferior-septal fibrosis (HR 3,33; 95% CI: 1,47-7,56; p=0,004), LPFB (HR 3,07; 95% CI: 1,48-6,38; p=0,003) and non-sustained fast VT (HR 1,018; 95% CI: 1,006-1,031; p=0,003). According to multivariate Cox regression, the following factors were identified as predictors of lethal events: ring-like fibrosis involving the inferior wall (HR 4,74; 95% CI: 2,32-10,1; p=0,0001), LPFB (HR 3,12; 95% CI: 1,47-6,61; p=0,003), LV systolic dysfunction (LVEF: HR 0,937; 95% CI: 0,895-0,981; p=0,005), and RV contractile dysfunction (TAPSE: HR 0,888; 95% CI: 0,818-0,963; p=0,004).

Conclusion. Rarely diagnosed in the general population, LPFB is found in 18,5% of patients with genetic DCM. LPFB is associated with inferior septal fibrosis and poor clinical outcomes, suggesting that LPFB should be considered a new prognostic factor for high risk of fatal VT and death.

Aim. To evaluate the contribution of polygenic risk scores to a short-term mortality prediction model in patients with dilated cardiomyopathy (DCM).

Material and methods. The study included 137 patients with DCM. The mean age was 56,8±13,5 years; 115 (83,9%) were men. The median follow-up period was 17 [13; 22] months. During the follow-up period, 26 patients (19,0%) died. To identify predictors of short-term all-cause mortality, a classification tree model was constructed based on the chi-squared automatic interaction detection (CHAID) algorithm, supplemented by polygenic risk scores (PRS) for DCM and heart failure (HF). The model prognostic value was assessed using ROC analysis with area under the curve (AUC) calculation.

Results. In the constructed model, the most significant predictors of short-term all-cause mortality were parenteral furosemide administration during the index hospitalization, high genetic risk according to the PGS005079 HF scale (cutoff value of 0,42), a ferritin level <101 ng/mL, and signs of systemic circulatory overload. The proportion of correctly classified cases was 81,0%, and the misclassification rate was 18,9%. According to ROC analysis, the model AUC was 0,786 (p<0,0001), sensitivity — 81,0%, and specificity — 61,4%.

Conclusion. Short-term all-cause mortality prognosis in patients with dilated cardiomyopathy (DCM) is associated with the need for parenteral loop diuretics during the index hospitalization, decreased ferritin levels, a high genetic predisposition to heart failure (as assessed by the PGS005079 PGS), and signs of more severe heart failure decompensation involving the systemic circulation.

Aim. To describe the characteristics of peak myocardial strain, time-to-peak strain, and peak systolic strain rate (PSSR) at the basal, mid, and apical left ventricular (LV) levels in the longitudinal, circumferential, and radial directions in patients with amyloid cardiomyopathy (ACM) using feature-tracking cardiac magnetic resonance (FT-CMR) imaging.

Material and methods. This single-center observational study included 25 patients with verified ACM. Cardiac MRI was performed on 1,5 and 3,0 T scanners, acquiring shortand long-axis cine steady-state free precession (SSFP) images. Postprocessing analysis of LV strain was performed on cine SSFP images using feature tracking (CVI42, Circle Cardiovascular Imaging Inc.). Peak strain, TTP, and PSSR were assessed in the radial, circumferential, and longitudinal directions at the basal, mid, and apical LV levels. Quantitative values are presented as M±SD.

Results. Peak longitudinal strain progressively increased in absolute value from basal to apical segments as follows: -1,02±9,55% (basal) ® -8,47±5,69% (mid) ® -12,18±3,01% (apical), consistent with a pattern of comparatively preserved apical longitudinal strain. The peak circumferential strain also increased from basal to apical segments as follows: -14,47±2,89% ® -15,73±3,50% ®-18,42±4,69%. The peak radial strain was highly variable as follows: 60,00±33,11% (basal), 25,69±13,37% (mid), and 50,86±37,97% (apical). The mean TTP was highest at the apical level for all following directions: radial 357,11±114,83 ms; circumferential 391,97±62,42 ms; longitudinal 394,52±63,25 ms. Longitudinal PSSR was -0,86±2,18; -0,96±0,95 and -0,85±0,40 1/s (basal, mid, apical), while circumferential PSSR — -0,91±0,28; -0,94±0,18 and –1,18±0,88 1/s, and radial PSSR — 7,48±10,30; 2,19±1,72 and 6,74±7,86 1/s.

Conclusion. In patients with ACM, FT-CMR reveals a characteristic peak strain gradient with relative preservation of apical segments in the longitudinal direction, TTP prolongation in the apical segments in all directions, and directionally variable PSSR values. Comprehensive segmental FT-CMR assessment of strain, TTP, and PSSR can serve as an additional noninvasive tool for characterizing LV mechanics in amyloid lesions.

Aim. To evaluate the role of cardiac MRI parameters, including strain parameters, in predicting unfavorable left ventricular (LV) remodeling in the midterm after surgery in patients with ischemic cardiomyopathy.

Material and methods. The results of paramagnetic contrast-enhanced cardiac magnetic resonance imaging were analyzed in 29 patients with ischemic cardiomyopathy (mean age 59,4±9,4 years) before complex surgical treatment. The anatomical and functional cardiac characteristics, LV global strain indices, and myocardial structural features were assessed, including after contrast agent administration.

Results. Left ventricular (LV) global longitudinal strain (GLS), LV global radial strain (GRS), LV ejection fraction, and the number of LV segments with pathological delayed enhancement were significant predictors of LV endothelial dysfunction 9-24 months after surgery. According to ROC analysis, the sensitivity of preoperative LV GLS in predicting postoperative LV endothelial dysfunction was 90,9%, and the specificity was 85,7% for a GLS >-3,8. A correlation was found between the left atrial volume index (LAVI) and LV GLS (p<0,005, correlation coefficient ρ=0,55), between LAVI and LV GRS (p<0,005, correlation coefficient ρ= -0,51), between GLS and the number of LV segments with pathological delayed contrast enhancement (p<0,005, correlation coefficient ρ=0,43), and between GRS and the number of LV segments with pathological delayed contrast enhancement (p<0,005, correlation coefficient ρ= -0,38).

Conclusion. Changes in quantitative parameters of LV strain in patients with ischemic cardiomyopathy are the most sensitive marker of unfavorable LV remodeling in the postoperative period.

Brief description. A young female patient was admitted with suspected acute coronary syndrome. Troponins were positiveю Electrocardiography showed pathological Q waves and ST-segment elevation in the precordial leads. Coronary angiography was performed, and myocardial infarction was ruled out.

Acute myocarditis was initially suspected. However, a prolonged severe clinical course, multiorgan involvement, and poor response to treatment raised diagnostic doubts. Consequently, the patient was referred to a federal center, where the diagnosis of sarcoidosis was established.

Discussion. Diagnostic difficulties in this case were due to the similarity of clinical and laboratory manifestations of cardiac sarcoidosis to those of acute coronary syndrome and myocarditis. The combination of a prolonged disease course refractory to therapy together with multiorgan involvement were key factors that led to suspicion of a systemic process. These features justified the patient’s referral to a federal center for advanced imaging studies — magnetic resonance imaging, positron emission tomography combined with computed tomography — and morphological verification of the diagnosis.

Aim. To characterize the pregnancy and postpartum period in carriers of truncating TTN gene variants with a phenotype of dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM) with increased left ventricular (LV) trabeculation, and to evaluate the potential role of pregnancy as a trigger for decompensation of inherited cardiomyopathies.

Material and methods. Two cases of patients with DCM and HCM with increased LV trabeculation are presented. We analyzed medical history data, echocardiographic changes, Holter ECG monitoring and cardiac magnetic resonance imaging data, and pathological examination of the cardiac explant. In addition, nextgeneration sequencing using a targeted cardiac panel, including genes associated with cardiomyopathies, as well as phenotypically similar conditions, was performed.

Results. A patient with a heterozygous truncating variant of TTN (chr2:178581583, NM_001267550.2: c.66685C>T; p.Gln22229Ter) developed fulminant dilated cardiomyopathy in the early postpartum period. A patient with a HCM phenotype and increased LV trabeculation and a heterozygous truncating variant of TTN (chr2:178552954, NM_001267550.2: c.89943_89946del; p.Val29982CysfsTer12) also developed a significant decrease in ejection fraction in the postpartum period.

Conclusion. The presented cases demonstrate that pregnancy and the early postpartum period can act as a hemodynamic and neurohumoral trigger, contributing to the clinical manifestation or decompensation of inherited cardiomyopathies in carriers truncating TTN variants. However, given the isolated nature of these observations and the lack of a comprehensive family survey, the data obtained should be considered a hypothesis requiring confirmation in larger case series.

Introduction. Despite recent advances in the diagnosis and treatment of various cardiomyopathies (CMP), the diagnosis of restrictive cardiomyopathy (RCM) remains the most challenging due to the heterogeneity of etiologic factors and the lack of timely interpretation of echocardiographic criteria for myocardial restriction. The association of RCM with the most common cardiovascular diseases further complicates its diagnosis. At the same time, the prognosis for patients with RCM, especially those with a genetic basis, is significantly worse than for other forms of cardiomyopathy.

Brief description. This article presents a case of a 47-year-old female patient diagnosed with myocardial infarction complicated by heart failure (HF) refractory to cardiotropic therapy. Delayed assessment of cardiac anatomical parameters (atrial dilation with small ventricular sizes), the type of left ventricular diastolic dysfunction, and the characteristics of myocardial longitudinal strain abnormalities led to a late RCM diagnosis, imitating HF secondary to myocardial infarction. Identification of the genetic disease nature (a mutation in the genes encoding sarcomeric proteins) facilitated the selection of a curative treatment option — heart transplantation.

Discussion. This clinical example highlights the need for a thorough approach to diagnosing various cardiomyopathy types using primary and secondary echocardiographic criteria, and, if necessary, genetic testing, especially in cases of refractory heart failure despite ongoing cardiotropic therapy.

Restrictive cardiomyopathy (RCM) is a rare disease characterized by impaired diastolic function o due to increased myocardial stiffness. The prognosis for RCM is often unfavorable, especially in children. In most cases, the disease is genetic in nature. Clinical manifestations are varied. This case highlights the complexity of diagnosing and treating RCM after SARS-CoV-2-related myocarditis.

Introduction. The severity of hepatitis A (HA) is determined not only by the severity of necrobiotic liver damage but also by extrahepatic manifestations (acute kidney injury, myocarditis, etc.). Virus-associated myocardial damage in HA is a rare but dangerous complication, potentially leading to life-threatening complications.

Brief description. Myocarditis in a patient with HA began with progressive heart failure, a decrease in left ventricular ejection fraction to 43%, and the risk of pulmonary edema, which required transfer to the intensive care unit. The patient made a full recovery. After 3 months, echocardiography revealed no intracardiac abnormalities.

Discussion. The presented case demonstrated the possibility of myocarditis development at 4 weeks of HA within jaundice remission in a patient with no previous history of cardiovascular disease, which can be explained by immunoreactivity dysfunction. This case highlights the importance of early diagnosis of myocarditis in HA to prevent an adverse outcome, as well as the need to raise physician awareness of the potential for immune-mediated pathology at any stage of hepatitis A.

This article presents a long-term (over 25 years) clinical follow-up of a patient with two following concurrent cardiovascular diseases: obstructive hypertrophic cardiomyopathy and coronary artery disease. The complex diagnostic process, treatment stages (surgical septal myectomy, pacemaker implantation, percutaneous coronary intervention, and coronary artery stenting), and patient progression are described. Particular attention is paid to the difficulties in differential diagnosis of angina in the presence of a combination of obstructive hypertrophic cardiomyopathy and coronary atherosclerosis, as well as the role of modern diagnostic methods, including microRNA testing. This case demonstrates the importance of lifelong follow-up of patients with hypertrophic cardiomyopathy due to the potential for disease progression and the development of new cardiovascular pathologies, as well as the specifics of their management.

Introduction. Atrial fibrillation is the most commonly diagnosed arrhythmia in patients with hypertrophic cardiomyopathy (HCM). According to current clinical guidelines, diagnostic testing for arrhythmias should be performed on all patients with HCM, regardless of their complaints, echocardiographic findings, or age. Given the high thromboembolism risk, anticoagulant therapy is prescribed to patients with HCM complicated by atrial fibrillation in all cases, regardless of the CHA₂DS₂-VAS_c score.

Brief description. This article presents a case of a young patient diagnosed with HCM without left ventricular outflow tract obstruction. During his examination, Holter electrocardiographic monitoring revealed episodes of paroxysmal atrial fibrillation. Given the patient’s young age, the short duration of the episodes of paroxysmal atrial fibrillation, and, unfortunately, the continued caution of many practicing physicians regarding the prescription of anticoagulant therapy, questions may have arisen regarding the need to initiate therapy at this stage.

Discussion. However, this case demonstrates the importance of diagnostic testing for arrhythmia in patients of any age diagnosed with HCM, as well as the need for timely initiation of anticoagulant therapy, regardless of risk stratification.

Introduction. The consumption of energy drinks (EDs) in combination with alcohol and nicotine products (vaping) is reaching epidemic proportions among young people. This dangerous combination has a pronounced cardiotoxic effect, triggering arrhythmias and heart failure (HF). The aim of this article was to present a clinical case of severe cardiomyopathy in a young patient secondary to the toxic effects of EDs, alcohol, and nicotine.

Brief description. A 22-year-old patient was hospitalized with progressive shortness of breath, weakness, and atrial fibrillation with a rapid ventricular rhythm (heart rate up to 150 bpm). There was a regular excessive consumption of energy drinks, alcohol, and vaping. Upon admission, biventricular heart failure with a left ventricular ejection fraction of 20%, cardiogenic shock, and multiple organ failure were detected. Coronary angiography revealed no coronary artery disease. Cardiac magnetic resonance imaging revealed diffuse hypokinesia without signs of fibrosis. Significant improvement was observed with intensive care, hemodialysis, and restoration of sinus rhythm by electrical cardioversion.

Discussion. This case shows the potential for reversibility of severe myocardial dysfunction in young individuals with timely diagnosis of tachycardiomyopathy and toxic damage.

Aim. To systematize published data evaluating the effectiveness of immunosuppressive therapy (IST) in the treatment of myocarditis and inflammatory cardiomyopathy.

Material and methods. A systematic search was conducted for studies evaluating the effectiveness of IST in the treatment of myocarditis and inflammatory cardiomyopathy between 1995 and 2025.

Results. Thirteen studies were included in the systematic review. Twelve studies found a positive effect of IST, including improved left ventricular (LV) ejection fraction (EF), reduced LV size and volume, and improved NYHA heart failure class. One study yielded mixed results (improvement was achieved in only 21 of 41 patients). When compared with the control group, significant improvements in LVEF were found in five studies. The first-line IST regimen is a combination of prednisolone and azathioprine (used in nine of the 13 studies). Mycophenolate mofetil may be used as second-line therapy. The most common duration of IST administration was 6 months (7 studies), 12 and 24 months (2 studies), and 19 and 36 months (1 study).

Conclusion. IST may be effective in carefully selected patients for chronic lymphocytic myocarditis and chronic inflammatory cardiomyopathy. As a first-line therapy, the most appropriate regimen is a combination of prednisolone and azathioprine. The duration of IST administration should be at least 6 months.