Left ventricular free-wall rupture (LVFWR) is a rare but often fatal complication of acute myocardial infarction (AMI). While typically requiring emergency surgical intervention, spontaneous healing is exceptionally uncommon. This case is noteworthy for the spontaneous resolution of a left ventricular rupture in a hemodynamically stable patient, successfully managed with multimodality imaging and selective surgical revascularization. A 66-year-old white European male with a history of hypertension and smoking presented with non-ST elevation myocardial infarction (NSTEMI) and was managed conservatively. Transthoracic echocardiography showed preserved left ventricular ejection fraction (55

Long COVID (LC) is a multisystem condition defined by persistent symptoms lasting at least three months after acute SARS-CoV-2 infection, affecting 10–30% of individuals. Cardiovascular manifestations – including chest pain, dyspnea, palpitations, and exercise intolerance – are frequent, and multimodality imaging has become central to the assessment of these patients, providing detailed structural, functional, and tissue-level information. This review summarizes the role of echocardiography (ECHO), cardiac magnetic resonance (CMR), coronary computed tomography angiography (CCTA), nuclear imaging, and electrocardiographic (ECG) monitoring in evaluating cardiovascular involvement in LC. Imaging findings range from subtle myocardial or right ventricular dysfunction, tissue changes such as myocardial edema or fibrosis, microvascular impairment, and pericardial involvement, to cases with minimal or no detectable structural abnormalities. Multimodality imaging guides diagnosis, phenotyping, risk stratification, and individualized follow-up, forming part of structured symptom-oriented clinical pathways. Psychosocial factors also influence how patients experience symptoms and diagnostic testing. Many individuals with persistent symptoms develop anxiety related to possible cardiac disease or the results of imaging examinations. Clear explanation of the purpose, safety, and expected findings of each imaging test can reduce patient anxiety, improve cooperation during examinations, and help contextualize borderline imaging abnormalities. Despite growing evidence, the prognostic significance of many imaging abnormalities remains uncertain. Longitudinal, outcome-based studies are needed to standardize imaging protocols, clarify clinical implications, and refine management. A multimodality imaging-guided, multidisciplinary, and psychosocially informed approach is essential for optimizing cardiovascular evaluation and care in patients with LC.

Ischaemic heart disease shows important differences between men and women, requiring an understanding of sex and gender dissimilarities to improve outcomes. This Scientific Statement provides an updated review of the current knowledge from risk factors to prognosis. It discusses the unequal impact of certain traditional risk factors between men and women, along with additional factors, such as hormonal changes and treatments (including those for transgender people and cancer), pregnancy-related complications, and autoimmune diseases, which contribute to the sex-specific risk profiles. Moreover, it outlines functional and structural sex differences in the pathophysiology (e.g. coronary atheroma plaques and burden, coronary dissection, vasospasm, and microvascular disease) with women being more prone to microvascular disease and endothelial dysfunction, while paradoxically experiencing less severe myocardial ischaemia at similar levels of coronary stenosis. The document further addresses the evaluation of diagnostic tools, which often have a male-centric bias, resulting in underdiagnosis in women who also tend to receive less guideline-recommended treatment. Additionally, women can have different responses and side effects to various preventive and therapeutic treatments, potentially contributing to the worse prognosis documented in acute coronary syndromes with obstructive coronary artery disease, particularly at a young age. Considering all these sex and gender differences and the low enrolment of women in randomized controlled trials, questions arise regarding the optimal treatment for women. Addressing sex differences requires conducting sex-specific research to close the knowledge gap. Overall, the Scientific Statement highlights all relevant sex- and gender-specific dissimilarities to advance clinical practice and identify directions for future research to improve guideline recommendations for equitable care.

Despite major advances in guideline-directed medical therapy (GDMT), many patients with heart failure with reduced ejection fraction (HFrEF) remain symptomatic, with persistent limitations in functional capacity and health status, underscoring the need for adjunctive therapeutic strategies. Direct cardiac microcurrent (C-MIC) therapy is a non-excitatory bioelectrical intervention device to modulate myocardial remodeling rather than rhythm or acute contractility. C-MIC therapy influence myocardial biology, including pathways related to fibrosis, inflammation, and cellular homeostasis by delivering continuous, subthreshold direct current. Preclinical studies across cardiomyocytes, animal models, and cardiac fibroblasts suggest that microcurrent exposure may attenuate profibrotic signaling, regulate extracellular matrix turnover, and improve calcium handling, providing a mechanistic rationale for reverse remodeling. Early clinical experience, including first-in-human studies and a randomized trial in carefully selected patients with non-ischemic HFrEF, demonstrates feasibility and a consistent signal of improvement in left ventricular function, functional capacity, and patient-reported outcomes. However, the current evidence base remains limited by small sample size, open-label designs, and the absence of sham-controlled evaluation. All available clinical data are derived from surgically implanted systems, and the effectiveness of less invasive configurations remains uncertain. Accordingly, C-MIC should be considered an investigational therapy. Future development will require rigorous mechanistic validation, optimization of device programming and delivery parameters, and confirmation of efficacy in adequately powered, sham-controlled trials to define its role in contemporary HF management.

Beta blockers (BBs) are very important medications with numerous indications. They have been considered highly useful in the treatment of arterial hypertension with comorbidities such as heart failure, coronary artery disease, and arrhythmias. The focus of this review is to analyze whether a BB already prescribed to a patient is the right choice, given that BBs differ significantly – for example in their vasodilatory versus vasoconstrictive properties. Searches were performed on 11/11/2024 with the following results. In PubMed, using the search terms "graft acceptance" and "beta adrenergic blocker" (or "graft acceptance" and "beta blocker") no articles were found. In SCOPUS for the combined search terms "graft acceptance" and "beta adrenergic blocker" (or "graft acceptance" and "beta blocker") also yielded no items . In the web based search engine Google Scholar two items were retrieved, but neither was directly related to the topic. The review highlights several important factors influencing graft acceptance, including infection and host- versus- graft reaction, and tissue perfusion. Differences among BBs also affect peripheral vascular resistance and flow; therefore, they may influence tissue perfusion including graft perfusion. This could have consequences for graft acceptance. It is worth investigating whether vasodilatory BBs and/or highly β1-AR selective BBs provide bet-ter protection in graft preservation for patients already receiving BB therapy. The pragmatic outcome of such an investigation may enable clinicians to eventually switch to specific BBs when preparing for elective operations involving tissue graft implantation.

INTRODUCTION:Relationship between changes in cardiac function, functional capacity, and patient-reported health status in heart failure (HF) remains incompletely defined, which may help inform endpoint selection and clarify how distinct clinical domains reflect treatment response. METHODS:This post hoc analysis of the randomized cardiac microcurrent (C-MIC) II trial, which evaluated the efficacy and safety of C-MIC therapy in patients with chronic HF with reduced ejection fraction on optimal guideline-directed medical therapy, included 65 ambulatory patients with non-ischaemic dilated cardiomyopathy, New York Heart Association (NYHA) Class III-IV symptoms, and baseline left ventricular ejection fraction (LVEF) 25-35%. Correlations between changes in Kansas City Cardiomyopathy Questionnaire Overall Summary Score (KCCQ-OSS), 6-minute walk distance (6MWD), core lab-assessed LVEF (primary measure) and site-assessed LVEF, and peak oxygen uptake (peak VO2) were evaluated at 4 weeks, 2 months, 3 months, 4 months, and 6 months using Pearson coefficients with 95% confidence intervals (CI). RESULTS:The mean age was 60.0 ± 9.7 years and baseline LVEF was 29.8 ± 3.3%. Baseline 6MWD was 291.4 ± 61.6 m and KCCQ-OSS was 42.6 ± 22.7. From baseline to 6 months, changes in KCCQ-OSS (n = 63) and 6MWD (n = 61) showed modest correlations with core lab-assessed LVEF (r = 0.39; 95% CI: 0.16-0.58; P = .0015 and r = 0.39; 95% CI: 0.15-0.58; P = .0022, respectively). Changes in KCCQ-OSS and 6MWD correlated strongly (n = 62; r = 0.63; 95% CI: 0.46-0.76; P < .0001). Changes in KCCQ-OSS and 6MWD did not correlate significantly with changes in peak VO2 (P = .06 and P = .30, respectively). Changes in LVEF and peak VO2 (n = 55) demonstrated modest correlation (r = 0.41; 95% CI: 0.16-0.61; P = .002). Baseline correlations with peak VO2 were weak to modest but increased at 6 months for LVEF (n = 59; r = 0.56; 95% CI: 0.35-0.71; P < .0001). CONCLUSION:In advanced HF, improvements in health status and submaximal functional capacity associate modestly with LVEF, while LVEF correlates more closely with peak VO2. Cardiac function, functional capacity, and health status represent related but distinct domains, supporting multidimensional assessment in HF trials.

INTRODUCTION:High blood pressure (BP) damages various structures. The damaged structures are named hypertension-mediated organ damages (HMODs). Some of HMODs are acute (i.e., intracranial haemorrhage), while the others are chronic (e.g., left ventricular hypertrophy (LVH)). The aim of the paper was to investigate how HMODs compare to each other, and to answer the question of whether HMODs are divided into acute and chronic forms in the major medical publications - guidelines. METHODS:A search for 'acute hypertension-mediated organ damage' and 'acute target organ damage' was performed in the whole papers in SCOPUS. Moreover, the available guidelines on hypertension are analysed. RESULTS:Our results show that the mentioned chronic HMODs differ a lot, both in number and qualitatively, i.e. which HMODs are specified. The difference regarding the number of HMODs listed reflects partially the different approach; some guidelines state organ damage in general, and the other guidelines provide extensive lists. DISCUSSION:A substantial number of arterial hypertension (HTN) guidelines do not list both acute and chronic HMODs; several guidelines refer to acute HMODs, and some others to chronic HMODs. In a number of HTN guidelines, acute (e.g., intracranial haemorrhage) and chronic HMODs (such as LVH) were mixed. In the vast majority of guidelines, the acute and chronic HMODs are not directly divided. CONCLUSION:Consensus is clearly missing about the definition and classification of HMODs. Multiple reasons suggest that HMODs should be divided into acute and chronic subgroups. We presented some of the arguments and examples to start with.

Refractory arterial hypertension (HTN) is a newly described severe phenotype of anti-hypertensive therapy failure. It is defined as uncontrolled blood pressure on (near-)maximal treatment using ≥ 5 antihypertensive drugs, two of which are long-acting thiazide-like diuretics (e.g. chlorthalidone) and mineralocorticoid receptor antagonists, with an additional requirement in one of the first reports: uncontrolled blood pressure after a minimum of three visits to the department. We observed important differences in the definitions of refractory HTN over time and even in the same period in the most important documents in medicine today - guidelines. The AIMs of the study were threefold: to underline the high risk and consequent importance of this phenotype of HTN, to analyze the evolution of the definition of refractory HTN and the consonance in the guidelines on the topic, to study potential insufficiencies of the current definitions, and possibly suggest some improvements. Patients with refractory HTN are at a higher risk of developing cardiovascular complications such as heart failure (HF), left ventricular hypertrophy (LVH), or stroke than those with controlled resistant HTN. Moreover, hypertension-mediated organ damage and comorbidities such as diabetes and obstructive sleep apnea are more prevalent in patients with refractory HTN. Some guidelines list treatment for refractory HTN, but the definition of refractory HTN is actually resistant to HTN. Generally, what is recognized as insufficient for the definition of resistant HTN is also likely true for refractory HTN.

Cardiovascular diseases, malignancy, and diabetes mellitus are the most common chronic non-communicable diseases affecting the population in Serbia. According to The Cancer Registry of the Republic of Serbia, breast cancer is the most common cancer affecting women in Serbia. Every year, 4600 women get diagnosed with BC, and 1600 women die from this disease. Every eighth woman in Serbia is diagnosed with BC. This review aims to summarize clinical and theoretical information about breast cancer, metabolic syndrome and cardiovascular risk connection. The literature search was conducted through PubMed, Google Scholar and cross-references in January 2024. We concluded that although there is a well-established connection between cardiovascular risk, metabolic syndrome, inflammation, dyslipidemia, obesity, diabetes mellitus and breast cancer, more multicenter prospective clinical studies are needed to establish the precise association and pathophysiological mechanisms.

Aims Individuals without standardized modifiable risk factors (SMuRF), which implicitly include those with diabetes, have been paradoxically reported to experience higher mortality following acute coronary syndromes (ACS). We aim to clarify the independent impact of diabetes on 30-day mortality after ACS and explore how grouping it with other SMuRF might obscure its true effect.Methods and results We analyzed 70 953 first-time ACS patients using inverse probability weighting to adjust for potential confounding. Mortality within 30 days post-ACS was the primary outcome. Diabetic patients without other SMuRF showed a significantly higher 30-day mortality compared with those without any SMuRF, with relative risks (RRs) of 1.29 for women (95% CI, 1.06-1.57) and 1.40 for men (95% CI, 1.16-1.69). When diabetes was combined with other SMuRF, its impact on mortality was diluted. Diabetic patients who were also smokers had RRs of 1.39 in women (95% CI, 0.92-2.09) and 0.89 in men (95% CI, 0.68-1.17), those with hypercholesterolaemia had RRs of 0.91 in women (95% CI, 0.66-1.25) and 0.75 in men (95% CI, 0.53-1.06) and those with hypertension showed RRs of 1.14 in women (95% CI, 0.99-1.32) and 1.12 in men (95% CI, 0.96-1.31).Conclusion Diabetes independently increases 30-day mortality risk in ACS. Aggregating it with other SMuRF masks this risk due to dilution bias, highlighting the need for individualized risk factor assessment strategies.

BACKGROUND AND AIMS:Recent studies suggest that patients without standard modifiable cardiovascular risk factors (SMuRFs), hypertension, hypercholesterolemia, diabetes, or smoking, may experience higher short-term mortality after acute coronary syndrome (ACS) than those with risk factors. This study examined the relationship between SMuRF burden, ACS-free survival, and short-term outcomes, and explored potential mechanisms including index-event and dilution bias. METHODS:We analyzed data from 70,953 Caucasian patients with first-time ACS enrolled between 2005 and 2021 in the ISACS-TC Registry (NCT04008173). Patients with prior coronary heart disease were excluded. Traditional SMuRFs were identified from clinical history. The primary outcome was 30-day all-cause mortality; secondary measures included age at ACS onset and early death from hospital admission (≤1 day). Inverse probability weighting models adjusted for baseline imbalance. RESULTS:At least one SMuRF was present in 84 % of patients. Increasing SMuRF number was associated with progressively younger age at ACS (women: 67.1 vs 61.9 years; men: 62.8 vs 58.9 years; both P < 0.001). Conversely, 30-day mortality showed an inverse pattern, being highest in SMuRF-less patients and lowest among those with multiple SMuRFs (women: 16.3 % vs 7.7 %; men: 11.5 % vs 4.8 %). Diabetes alone conferred excess mortality (RR 1.29 [95 % CI 1.06-1.57] in women; 1.40 [1.16-1.69] in men), whereas isolated smoking, hypertension, or hypercholesterolemia were associated with lower risk. Early deaths at admission (≤1 day) were more frequent in SMuRF-less patients (36.8 % vs 31.7 %), suggesting arrhythmic mechanisms. CONCLUSIONS:SMuRFs remain strong determinants of earlier ACS onset and shorter ACS-free survival. The apparent paradox of higher mortality in SMuRF-less patients likely reflects index-event and dilution bias. Prevention strategies targeting smoking, hypercholesterolemia, and diabetes remain crucial to extend ACS-free life expectancy.

INTRODUCTION:Isolated systolic hypertension (ISH) is important because of its very high prevalence. Anemia is also a highly prevalent non-communicable disease. The paper aims to answer the study questions: 1) Is there a relation between anemia and dBP?; 2) Is there a link between ISH and anemia?; 3) Are ISH and anemia important due to their prevalence?; 4) Is the cardiovascular risk increased in ISH patients with anemia?5) Is this recognized in HTN guidelines? METHODS:Search 1 was done for 'isolated systolic hypertension' and 'anemia' in papers (excluding guidelines). Search 2 was performed for arterial hypertension (HTN) guidelines, to see if there is a part about 'isolated systolic hypertension' and about 'anemia', as well as about their relationship. We performed a SCOPUS, Springer Verlag, Elsevier, PubMed, and Google Scholar search. RESULTS:Diastolic blood pressure is often decreased in anemia, due to abundant pathophysiological mechanisms. Moreover, dBP is often low in both ISH and anemia. Third, anemia and ISH are important due to their high prevalence, especially in the elderly. DISCUSSION:The main result of the study is the identification of the important, clinically relevant, previously undefined problem: anemia in ISH. Cardiovascular risk is increased in ISH patients with anemia. The significance of anemia in ISH is not recognized in HTA guidelines, partially because they need to be concise. CONCLUSION:The overlooked problem of anemia in ISH needs recognition both in clinical practice, to avoid overzealous dBP reduct.

Introduction/Objective: Heart failure with preserved ejection fraction (HFpEF) accounts for more than half of chronic heart failure cases, and obesity is among its most common comorbidities, which has reached epidemic proportions and is associated with the progressive deterioration of HFpEF. Oxidative stress and systemic inflammation, largely driven by visceral adipose tissue, promote endothelial dysfunction, coronary microvascular injury, myocardial remodeling and stiffness through fibrosis, the key pathophysiological mechanisms in HFpEF. This review paper aims to summarize current evidence on the epidemiological association between obesity and HFpEF, as well as the pathophysiological mechanisms linking these conditions. It also presents clinical and experimental findings demonstrating that obesity, HFpEF, and inflammation constitute interconnected components of one and the same circulus vitiosus. Methods: This review draws upon relevant literature and clinical research retrieved from the PubMed, NCBI, and ResearchGate databases, focusing primarily on the underlying pathophysiological mechanisms and evidence derived from clinical trials. Particular emphasis was placed on modern weight-management pharmacotherapies (SGLT2 inhibitors, GLP-1 receptor agonists) and management of major comorbidities (DM, AHT, OSA, and NAFLD), with the aim of reducing the considerable burden of morbidity and mortality in this growing patient population. Results: Better understanding of the interacting mechanisms in obesity and HFpEF supports development of therapeutic strategies such as dual GLP-1/GIP agonists and anti-cytokine approaches aimed at reducing systemic inflammation and the risk of HFpEF worsening, with potential improvements in functional capacity and quality of life. Conclusion: Obesity is a major comorbidity in HFpEF, with inflammation playing a central role in pathogenesis. Targeted anti-inflammatory and metabolic therapies show potential to reduce morbidity and mortality and enable a more individualized treatment approach.

BACKGROUND:In the C-MIC II trial, C-MIC therapy improved outcomes in patients with heart failure (HF) with reduced ejection fraction (HFrEF). We evaluated whether differences in background HF medication adjustments influenced the observed benefits. METHODS:Ambulatory patients with chronic non-ischemic HFrEF receiving guideline-directed medical therapy (GDMT) were enrolled. The primary outcome was change in GDMT and diuretic intensity over 6 months. Treatment effects on left ventricular ejection fraction (LVEF), Kansas City Cardiomyopathy Questionnaire Overall Summary Score (KCCQ-OSS), and 6-minute walk distance (6MWD) were assessed by baseline sodium-glucose cotransporter-2 inhibitor (SGLT2i) use for consistency. RESULTS:Among 65 patients, 25 (39%) had GDMT adjustments (C-MIC device: 44%; control 33%; p= 0.390). GDMT intensity increased in controls (Δ +0.36) but decreased (Δ -0.16; p= 0.100) in C-MIC group. Diuretic intensity decreased in C-MIC group (Δ -0.10) but increased in controls (Δ +0.12; p= 0.200). When stratified by baseline SGLT2i use, C-MIC therapy induced consistent improvements in LVEF (SGLT2i: +6% [95% CI 3-9; p<0.001] vs. without SGLT2i: +4% [95% CI 2-7; p=0.003]), KCCQ-OSS (SGLT2i: +42 points [95% CI 26-58; p<0.001] vs. without SGLT2i: +40 [95% CI 28-51; p<0.001]) and 6MWD (SGLT2i: +150 meters [95% CI 88-212; p<0.001] vs. without SGLT2i: +141 meters (95% CI 63-219; p<0.001]). CONCLUSION:Medication intensity decreased in C-MIC-treated patients but increased in controls, driven primarily by escalation of diuretics, likely reflecting worsening HF. Consistent improvements in LVEF, 6MWD and KCCQ-OSS across SGLT2i subgroups suggest that the observed benefits are independent of background pharmacologic intensification.

BACKGROUND:The C-MIC II trial demonstrated benefits of 6 months of cardiac microcurrent (C-MIC) therapy in patients with non-ischemic heart failure with reduced ejection fraction (HFrEF). The prospective C-MIC II Follow-Up Study evaluates safety and efficacy outcomes post-device deactivation. METHODS:Primary safety-related endpoints included all-cause, cardiovascular and device-related mortality and hospitalizations and adverse events (AEs). Secondary efficacy-related endpoints included changes in left ventricular ejection fraction (LVEF), Kansas City Cardiomyopathy Questionnaire Overall Summary Score (KCCQ-OSS), 6-minute walk distance (6MWD), New York Heart Association (NYHA) class and device reactivation rate. Here, we report 12-month results comparing the 6-month time-point (at the end of active therapy) with the 18-month time-point (12 months post-deactivation). RESULTS:Of 32 eligible patients, 31 (97%) were enrolled. At 12 months post-device deactivation, 3 patients (10%) were hospitalized and 1 died (3%); none were device-related. One device-related AE occurred and resolved completely. Improvements in LVEF (vs pre-implantation: +6%; 95% CI 5-8; p<0.0001) and KCCQ-OSS (vs pre-implantation: +43 points; 95% CI 36-49; p<0.0001) were sustained and unchanged from 6 months (LVEF: -0.1%; 95% CI -2-2; p=0.87; KCCQ-OSS:-2; 95% CI -8-4; p=0.49). The 6MWD remained improved (vs pre-implantation: +150 m; 95% CI 109-191; p<0.0001), with a modest decrease (-31 m; 95% CI -56- -7; p=0.013) from 6 months. Improvements in NYHA class (≥1-class improvement in 77% patients) were sustained. Three (10%) patients required device reactivation. CONCLUSION:Among patients previously treated with C-MIC device, improvements in LVEF, 6MWD, NYHA class and KCCQ-OSS were sustained, with a favorable safety profile 12 months post-deactivation.