Hypertrophic cardiomyopathy is one of the most common hereditary cardiomyopathies in daily practice. The different phenotypic manifestations and hemodynamic features often make diagnosis and therapy a clinical challenge. Diagnosis and imaging follow-up of cardiomyopathies are becoming increasingly multimodal. Despite the new imaging capabilities, echocardiography continues to play a key role in the primary differential diagnostic process, in the follow-up of patients, regardless of the therapeutic approach taken, and in the screening of relatives. Therefore, good knowledge of echocardiographic methods for assessment in these patients, of practical features and possible errors during the examination, is an essential prerequisite for high quality care. Precise systematic measurements and descriptions of the fi nding in each patient are the basis of good follow-up, adequate management planning and reassessment of therapy, and of seamless team care for the patient by various specialists. Confl icting or inconsistent imaging fi ndings, discrepancies in imaging fi ndings and clinical presentation, and the need for specialized therapy are valid reasons for referring the patient for a staged evaluation to an expert center for HCM.

Factor VII defi ciency is a rare inherited coagulation disorder characterized by decreased activity of factor VII, leading to variable bleeding tendencies that may not correlate with measured FVII levels. While many patients remain asymptomatic, others can experience severe spontaneous hemorrhages. The condition poses signifi cant challenges during surgical or invasive procedures due to the potential for uncontrollable bleeding. Data regarding percutaneous coronary intervention (PCI) in such patients are extremely limited, mostly confi ned to isolated case reports. PCI requires anticoagulation during the procedure and dual antiplatelet therapy afterward, both of which elevate bleeding risk. Conversely, administering FVII concentrate may increase the chance of thromboembolic events. Therefore, individualized planning and a multidisciplinary approach are crucial to balance these opposing risks. We present the case of a 75-year-old Bulgarian woman with congenital FVII defi ciency and severe three-vessel coronary artery disease who underwent successful transradial PCI without FVII replacement. Drug-eluting stents were implanted in the left anterior descending and circumfl ex arteries, enabling short-term dual antiplatelet therapy. No bleeding complications occurred peri-procedurally, and only one minor episode of epistaxis was observed during follow-up. This case illustrates that, with meticulous preparation and procedural care, PCI can be a safe and effective revascularization strategy in patients with congenital FVII defi ciency.

Psychogenic pseudosyncope is a state of apparent loss of consciousness, which is indistinguishable from true loss of consciousness by eyewitnesses. However, there are no hemodynamic and electroencephalographic stigmata of true syncope with real loss of consciousness. Sometimes a detailed history can raise doubts about the condition – a relatively long period of unconsciousness, unusual triggers, atypical prodromes and frequent attacks are suspicious signs, but they are far from specifi c in the population of patients presenting for differential diagnosis of syncopal episodes to the cardiologist. The gold standard for making the diagnosis is the provocation with a tilt-table test, in which psychogenic pseudosyncope is registered and simultaneously the absence of hemodynamic (and in the optimal case, electroencephalographic) signs of loss of consciousness is objectifi ed. It should be noted that the presence of psychogenic pseudosyncope does not automatically exclude the presence of true refl ex syncope in the particular patient. Treatment based primarily on a clear explanation of the condition and supportive communication with the patient can lead to a sharp reduction in the frequency of attacks. Pharmacological treatment of associated psychiatric disorders, as well as psychological support, is extremely effective. Cognitive-behavioural therapy is the most preferred approach in this patient population. In this review, we will present the diagnostic process in one patient and discuss the development of the understanding of this condition, the main clinical features and diagnostic approaches, the classifi cation and underlying pathology, as well as therapeutic methods.

Acenocoumarol, a vitamin K antagonist (VKA), has played a pivotal role in anticoagulant therapy for over 60 years. Derived from the coumarin family, acenocoumarol inhibits vitamin K epoxide reductase, disrupting the synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and effectively preventing thromboembolic events. Compared to warfarin, acenocoumarol offers a rapid onset and shorter half-life, providing clinicians greater therapeutic fl exibility. Despite advances and widespread adoption of direct oral anticoagulants (DOACs), acenocoumarol continues to hold clinical signifi cance, particularly in Europe, Latin America, and Asia, owing to extensive clinical experience, reversibility, and cost-effectiveness. However, its use necessitates regular monitoring of international normalized ratio (INR), with individualized dosage adjustments required due to genetic variability (CYP2C9, VKORC1 polymorphisms), drug-drug interactions, dietary infl uences, and special considerations in the elderly and patients with chronic kidney disease (CKD). Recent clinical trials have expanded our understanding of its effi cacy, safety, and optimal use. Precision dosing strategies, including genotype guidance and advanced INR monitoring based on body-surface area-adjusted estimated glomerular fi ltration rate (BSA-adjusted eGFR) dosing, promise enhanced safety and personalized treatment. Although DOACs are now widely adopted due to their predictable pharmacokinetics and lack of routine monitoring requirements, acenocoumarol remains indispensable in well-defi ned clinical scenarios such as in patients with mechanical heart valves, rheumatic mitral stenosis–associated atrial fi brillation, antiphospholipid syndrome, and other conditions in which individualized dose adjustment offers a therapeutic advantage.

Marantic endocarditis, also known as nonbacterial thrombotic endocarditis (NBTE), is a rare condition typically encountered in patients with malignancy and hypercoagulable states. It is characterized by the formation of sterile fi brin–platelet vegetations on cardiac valves, which frequently lead to systemic embolic events. We report the case of an 84-year-old woman admitted with progressive exertional dyspnea and intermittent dry cough. Echocardiography revealed mobile vegetations on the mitral and aortic valves, associated with signifi cant valvular regurgitation and pulmonary hypertension. The patient remained afebrile, with persistently negative blood cultures and low infl ammatory markers. Whole-body computed tomography subsequently demonstrated pancreatic tail carcinoma with hepatic and pulmonary metastases. A diagnosis of marantic endocarditis secondary to malignancy was established. Anticoagulation and supportive therapy were initiated. Several days after discharge, the patient developed an ischemic stroke. She died a few weeks later.

Left ventricular systolic dysfunction results from complex structural, cellular, and molecular disorders affecting the contractile apparatus of the myocardium and its energy homeostasis. This review discusses the key mechanisms of this process, with emphasis on myocardial contraction and its regulation by calcium dynamics and integrity of the sarcomeres. The main factors leading to the development of systolic dysfunction are presented: volume and tension overload, ischemia, infl ammation, amyloid and other deposits, neurohormonal activation and endocrine disorders, oxidative stress. In addition, cellular and molecular mechanisms are presented, such as defects in SERCA2a, and Na+/Ca 2+ exchanger, pathological Ca 2+ effl ux through RyR2, alterations in titin phosphorylation, myofi lament damage, proteasome dysfunction, impaired autophagy, epigenetic regulation, endoplasmic reticulum stress, and abnormalities in intercellular connectivity. The complex interaction between these processes leads to progressive myocardial remodeling, fi brosis, energy defi cit, and impaired myocardial contractility. Understanding these mechanisms is important for better understanding the pathogenesis of systolic dysfunction as well as for the development of new therapeutic strategies for its treatment.

Diastolic dysfunction is a condition in which ventricular fi lling is impaired, regardless of the presence of symptoms and irrespective of whether the ejection fraction is normal or reduced. Left ventricular diastolic dysfunction results from complex and interconnected biochemical and cellular mechanisms. Among them, impaired myocardial relaxation due to calcium dysregulation, altered titin phosphorylation affecting the passive elasticity of the myocardium, and extracellular matrix remodeling with the development of fi brosis mediated by signalling pathways such as TGF-β/SMAD and MAPK play a leading role. Additional contributing factors include oxidative stress and mitochondrial dysfunction, chronic infl ammation and activation of cytokine cascades, metabolic disturbances such as diabetes and obesity, as well as protein dysfunction related to endoplasmic reticulum stress and impaired proteolysis. All these processes in complex lead to impaired diastolic fi lling of the left ventricle, i.e., diastolic dysfunction. Due to its broad availability and proven clinical value, echocardiography is the primary method for diagnosing diastolic dysfunction. Invasive and other imaging modalities offer complementary information in complex or borderline cases, or when echocardiographic evaluation is diffi cult or impossible.

Editorial

Introduction: The EVOLUTION-HF is a prospective, multinational, real-world study designed to describe the demographic and clinical characteristics of patients initiating dapaglifl ozin for heart failure with reduced ejection fraction (HFrEF) in nine countries from the Central and Eastern Europe and Baltic Area. This manuscript presents the results of the Bulgarian cohort of the study. Methods: Enrolment period in Bulgaria was between February 2022 and October 2022, in 10 study sites. Demographic and clinical characteristics were collected at baseline (12 months before dapaglifl ozin initiation), and treatment for heart failure (HF), including guideline-directed treatment (GDMT) was collected prospectively until 12 months after dapaglifl ozin initiation. The HF treatment was administered as per routine clinical practice. Results: One hundred and fi fty patients were included in the full analysis set (mean age: 67 years, males 84%). At the time of initiation of dapaglifl ozin 10 mg/day, 69.3% of patients had treatment with renin-angiotensin-aldosterone system (RAAS) inhibitors and 35.3% all four GDMTs in HF. Almost 98% of patients remained on dapaglifl ozin at 6 months and 12 months. Seven (10.12%) dapaglifl ozin discontinuations were recorded throughout the study. The discontinuation rate of dapaglifl ozin was 4.65 per 100 patient-years and the median time-to-discontinuation was not reached. One patient stopped dapaglifl ozin between baseline and 6 month and between 6 month and 12 month-data collection, respectively. GDMT patterns were relatively stable over one year. Conclusion: A high rate of persistence of dapaglifl ozin was observed at 12-month follow-up after initiation for HFrEF. A substantial gap was noted related to GDMT strategy optimization, with only one third of patients receiving all four GDMT pillars. These results obtained in real-world practice in Bulgaria point to the unmet need for targeted efforts to improve GDMT adoption in patients with HFrEF.

Transcatheter aortic valve replacement (TAVR) is an effective therapeutic option for patients with severe symptomatic aortic stenosis who are at high surgical risk. Although generally safe, one of its rare but serious complications is clinical valve thrombosis, occurring in approximately 0.5% of cases. This condition can lead to prosthetic valve dysfunction, worsening heart failure, or thromboembolic events. Diagnosis usually begins with transthoracic echocardiography (TTE), while transoesophageal echocardiography (TOE) and multi-slice computed tomography (MSCT) are often required for more precise assessment. Since standardized treatment protocols are not yet established, management must be individualized according to clinical presentation and the degree of valve obstruction. Therapeutic approaches include oral anticoagulation, intravenous heparin, or, in severe cases with hemodynamic compromise, thrombolytic therapy. If conservative management fails, redo-TAVR or surgical valve explantation may be necessary. We present the case of a 78-year-old Bulgarian woman who developed progressive heart failure 12 days after TAVR. Imaging confi rmed bioprosthetic valve thrombosis. Intravenous heparin was ineffective, but thrombolytic therapy followed by oral anticoagulation led to complete thrombus resolution and restoration of valve function without bleeding complications. Clinical valve thrombosis after TAVR, though uncommon, is potentially fatal. MSCT remains the most accurate diagnostic tool, while TOE is valuable for its accessibility. Thrombolysis combined with vitamin K antagonist therapy can be an effective treatment option.