Background/Objectives: Acute coronary syndrome (ACS) remains a leading cause of sudden cardiac death worldwide; however, limited data exist regarding the relationship between coronary arterial and coronary venous dynamics in this context. The present study aimed to evaluate whether coronary sinus flow (CSF) dynamics obtained via transthoracic echocardiography (TTE) are associated with the long-term risk of ACS and cardiovascular events. Methods: This retrospective observational cohort study included 100 patients who underwent elective coronary angiography and had their CSF parameters assessed via TTE. All participants were followed up for a duration of up to 48 months. The primary endpoint was cardiovascular mortality, while secondary endpoints comprised the occurrence of ACS, refractory angina pectoris, and cerebrovascular events. Study endpoints were evaluated by dichotomizing the population into two groups using the median CSF value as the cutoff (low: CSF ≤ median; high: CSF > median). Results: The primary endpoint did not differ significantly between the two groups; however, refractory angina was significantly more common in the high CSF group [4 (8.2%) vs. 12 (24.5%), p = 0.029]. Similarly, the high CSF group exhibited a significantly higher rate of the composite endpoint than the low CSF group [13 (26.5%) vs. 25 (51.0%), p = 0.013]. In multivariate Cox analysis, CSF was an independent predictor of the composite endpoint (HR: 1.50; 95% CI: 1.11–2.02, p = 0.009). Conclusions: Baseline CSF measured by TTE was independently associated with the composite endpoint, whereas its association with isolated ACS was limited. CSF assessment may provide incremental prognostic information alongside conventional arterial and microvascular evaluation.

Acute coronary syndrome (ACS) remains a leading cause of death and morbidity worldwide. The pathophysiology of ACS has been largely interpreted through abnormalities of the coronary arteries and the microvascular bed. However, the coronary circulation is fundamentally a closed-loop system, in which the venous component represents the final link in myocardial blood return. In contrast to the extensive literature on arterial and microvascular disease, there are relatively few studies on the coronary venous system (CVS) in the context of ACS. The CVS is important in relation to ACS from two complementary perspectives. First, structural or functional abnormalities of the CVS can contribute to myocardial ischemia; second, coronary venous flow can reflect the hemodynamic outcomes of acute ischemia and reperfusion. The ‘vascular waterfall’ phenomenon is considered one of the primary mechanisms governing coronary venous return, linking myocardial compression and venous pressure to the flow from the coronary sinus (CS) into the right atrium. Experimental and clinical evidence has shown that CS thrombosis is associated with myocardial infarction and may also complicate ACS. Furthermore, studies evaluating CS blood flow generally show a decrease in the acute phase of ischemia and an increase after reperfusion. However, the existing evidence is limited and largely based on small observational studies. Therefore, this review aimed to examine the pathophysiological mechanisms and hemodynamic behavior of the CVS in ACS, starting from embryological development.

OBJECTIVE:Genetic susceptibility is increasingly recognized in cardiac arrhythmias. human leukocyte antigen-DQ2 and human leukocyte antigen-DQ8 alleles are established markers of immune-genetic dysregulation and chronic inflammation. This study investigated the association between human leukocyte antigen-DQ2/DQ8 positivity and incident atrial fibrillation in patients with heart failure with reduced ejection fraction. METHODS:This study was based on a prospectively followed cohort; the present retrospective analysis evaluated 50 heart failure with reduced ejection fraction patients (left ventricular ejection fraction <40%) and 50 age- and sex-matched controls. Participants were screened for human leukocyte antigen-DQ2/DQ8 alleles. All subjects were in sinus rhythm at baseline and followed for 24 months for the primary endpoint of incident atrial fibrillation. RESULTS:Incident atrial fibrillation occurred in 16% (n=8) of the heart failure with reduced ejection fraction group and 2% (n=1) of the control group. Among heart failure with reduced ejection fraction patients, human leukocyte antigen-positive status (positivity for DQ2 and/or DQ8) was found in 20 patients. Interestingly, all eight incident atrial fibrillation cases in the heart failure with reduced ejection fraction group occurred within the human leukocyte antigen-positive subgroup (40 vs. 0% in human leukocyte antigen-negative heart failure with reduced ejection fraction, p=0.031). human leukocyte antigen-positive heart failure with reduced ejection fraction patients exhibited a significantly higher atrial fibrillation risk compared to human leukocyte antigen-positive controls (p=0.0069), suggesting that structural heart disease and genetic predisposition synergistically increase arrhythmic risk. CONCLUSION:Human leukocyte antigen-DQ2/DQ8 positivity is significantly associated with incident atrial fibrillation in heart failure with reduced ejection fraction patients. These findings suggest human leukocyte antigen-related immune-genetic susceptibility contributes to atrial electrical vulnerability, positioning human leukocyte antigen typing as a potential novel biomarker for arrhythmic risk stratification in heart failure.

Despite advances in drug therapies and invasive procedures in cardiology, heart failure (HF) remains one of the leading causes of mortality and morbidity worldwide. Given the high mortality and morbidity rates associated with HF, understanding its etiology—particularly its genetic basis—is crucial. Elucidating these mechanisms can expand therapeutic options, thereby improving patient life expectancy, enhancing quality of life, and reducing healthcare costs. This review discusses the human genome in the context of HF pathophysiology, its classifications, their genetic basis, and the specific role of Human Leukocyte Antigens (HLA) in HF. The HLA system is one of the most polymorphic regions of the human genome. Its main function is to regulate the human immune system. The most important characteristic of HLA mole-cules is that they allow for a wide variety of peptide presentations, contributing to inter-individual varia-bility in immune responses. This polymorphism is associated with numerous autoimmune and inflamma-tory diseases. In particular, HLA-DQ2 and HLA-DQ8 haplotypes are considered genetic risk factors for celiac disease and type 1 diabetes mellitus due to abnormal antigen presentation. Transgenic animal mod-els expressing human HLA-DQ alleles have demonstrated the development of autoimmune myocarditis progressing to dilated cardiomyopathy. HLA haplotypes should not currently be regarded as standalone diagnostic or prognostic markers for HF. Rather, they may represent one component of a broader immuno-genetic and inflammatory network, particularly in selected phenotypes such as myocarditis-related or idiopathic dilated cardiomyopathy.

Atrial fibrillation (AF) is a common arrhythmia with substantial morbidity and a need for accessible markers that reflect disease burden, while olfactory dysfunction and chronic inflammation may share overlapping vascular and neuroinflammatory pathways. We aimed to evaluate olfactory function in patients with AF and to explore the role of systemic inflammation using the systemic immune-inflammation index (SII). In this single-center case–control study, 85 consecutively enrolled adults (AF group, n = 43; control group, n = 42) underwent olfactory assessment with the Sniffin’ Sticks Extended Test, including odor threshold (OT), odor discrimination (OD), and odor identification (OI), from which the threshold–discrimination–identification (TDI) score was derived; SII was calculated from same-day complete blood counts. Compared with controls, patients with AF had higher SII (878 [368–5769] vs. 503 [243–1450], p = 0.007) and lower OT (4 [1–8] vs. 5 [2–10], p = 0.001), OD (7 [4–12] vs. 13 [8–16], p < 0.001), OI (7.7 ± 2.6 vs. 12.6 ± 1.7, p < 0.001), and TDI scores (19 [10–29] vs. 29.5 [25–39], p < 0.001). Within the AF group, olfactory performance was inversely associated with symptom severity assessed by the European Heart Rhythm Association (EHRA) classification, and TDI was negatively correlated with SII. These findings indicate that AF is associated with impaired olfactory function and elevated systemic inflammation, supporting olfaction and inflammatory indices as potential correlates of symptom burden that warrant confirmation in larger prospective cohorts with standardized rhythm monitoring.

Objectives: Genetic predisposition is one of the factors that contribute to the etiology of heart failure (HF). This study aimed to compare the prevalence of human leukocyte antigen (HLA)-DQ2 and HLA-DQ8 haplotypes in patients with HF with reduced ejection fraction (HFrEF) and healthy controls. Methods: This case control study was conducted in Western Türkiye, and included 100 participants: 50 patients diagnosed with HFrEF and 50 healthy matching controls. The frequency and distribution of HLA-DQ2 and HLA-DQ8 were compared between the groups. Results: No statistically significant differences in haplotype distribution were observed between patients and controls for any of the assessed parameters. HLA-DQ2 positivity was observed in 16.0% of the HFrEF group and 20.0% of controls, while HLA-DQ8 positivity was found in 24.0% and 26.0%, respectively. Subgroup analyses stratified by sex and HF etiology also did not reveal differences. Conclusions: The HLA-DQ2 and HLA-DQ8 haplotypes are not significantly associated with HFrEF in the population studied. Therefore, the utility of these haplotypes as standalone markers for early detection of HFrEF appears limited.

Introduction: This study aimed to investigate the relationship between left ventricular ejection fraction (LVEF) measured on preoperative transthoracic echocardiography (TTE) and peak systolic velocity (PSH) and resistance index (DI) calculated on postoperative renal Doppler ultrasonography. Methods: The study retrospectively included 68 renal transplant patients. TTE measurements were taken for all patients, and LVEF was recorded. Renal Doppler ultrasonography recorded PSH and DI. Patients were divided into two groups based on LVEF below 55% (group 1, n=24) and above (group 2, n=44). Results: Of the patients participating in our study, 21 (30.8%) were female and 47 (69.2%) were male. The mean age of the patients in the study was 53.2±9.27 years. Urea was significantly lower in patients with LVEF values above 55% (85.9±31.5 vs. 103.3±35.2; p=0.02). On the other hand, PSV and RI were significantly lower in the group with LVEF values above 55% (188.2±33.1 vs. 238.7±40.2; p=0.02; 0.64±0.15 vs. 0.78±0.19; p=0.04, respectively). A negative correlation was also found between LVEF values and PSV and RI (r= -0.731, p=0.007; r= -0.602, p=0.01, respectively). Conclusion: In this study, renal transplant patients with echocardiographic LVEF greater than 55% had significantly lower RI and PSV determined by renal Doppler ultrasonography.

Aims: Erectile dysfunction (ED) and coronary artery disease (CAD) are disorders with similar pathophysiology and the prevalence of ED may be as high as 75% in cardiovascular patients. Ranolazine is a second line therapy in CAD patients with angina. It inhibits the late sodium current in cardiomyocytes. It also has positive effects on endothelial dysfunction which is a common disruption on both CAD and ED. We aim to evaluate the effect of ranolazine on ED in CAD patients with angina complaints. Methods: A total of 37 CAD patients were included for the study. Ranolazine was started to patients with angina symptoms. Sexual Health Inventory for men (SHIM) questionnaire was used to evaluate the status of ED. The questionnaire was applied to patients before the start and at the 6th month of ranolazine treatment. Results: The SHIM scores of each question did not change significantly after the follow up period (p>0.05). The total SHIM score at the beginning was 10.7 ± 5.4 and after 6 months the SHIM score was 10.7 ± 6.3 and the difference was statistically insignificant (p=0.757). The changes in the SHIM classes were not statistically significant (p=0.454). Conclusion: Ranolazine does not have positive or negative effects on ED at CAD patients with angina pectoris. Further studies with larger patient population must be done to confirm the results of the study.

Background: Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia worldwide and is associated with an increased risk of thromboembolism, ischemic stroke, impaired quality of life, and mortality.The latest research that shows the prevalence and incidence of AF patients in Türkiye was the Turkish Adults' Heart Disease and Risk Factors study, which included 3,450 patients and collected data until 2006/07.The Turkish Real Life Atrial Fibrillation in Clinical Practice (TRAFFIC) study is planned to present current prevalence data, reveal the reflection of new treatment and risk approaches in our country, and develop new prediction models in terms of outcomes. Methods:The TRAFFIC study is a national, prospective, multicenter, observational registry.The study aims to collect data from at least 1900 patients diagnosed with atrial fibrillation, with the participation of 40 centers from Türkiye.The following data will be collected from patients: baseline demographic characteristics, medical history, vital signs, symptoms of AF, ECG and echocardiographic findings, CHADS2-VASC2 and HAS-BLED (1-year risk of major bleeding) risk scores, interventional treatments, antithrombotic and antiarrhythmic medications, or other medications used by the patients.For patients who use warfarin, international normalized ratio levels will be monitored.Follow-up data will be collected at 6, 12, 18, and 24 months.Primary endpoints are defined as systemic embolism or major safety endpoints (major bleeding, clinically relevant nonmajor bleeding, and minor bleeding as defined by the International Society on Thrombosis and Hemostasis).The main secondary endpoints include major adverse cardiovascular events (systemic embolism, myocardial infarction, and cardiovascular death), all-cause mortality, and hospitalizations due to all causes or specific reasons. Results:The results of the 12-month follow-up of the study are planned to be shared by the end of 2023. Conclusion:The TRAFFIC study will reveal the prevalence and incidence, demographic characteristics, and risk profiles of AF patients in Türkiye.Additionally, it will provide insights into how current treatments are reflected in this population.Furthermore, risk prediction modeling and risk scoring can be conducted for patients with AF.

Considering advances in the treatment of patients with acute coronary syndrome (ACS), ischemic relapses still occur within two years in up to 20% of these patients, and need to develop alternative strategies to reduce the long-term risks of ACS patients is highlighted in this recently published article [1]. Nelles et al. stated that cholesterol crystals (CCs) represent a high-risk structure that frequently occurs in culprit lesions in ACS. The results of this study demonstrated that CCs are associated with increased inflammation as well as the classic fragility features of atherosclerotic plaque.

Objective: Endothelium-related events in patients with coronavirus disease 2019 are linked to a poor prognosis. Lipoprotein(a) plays a role in vascular endothelial cell dysfunction. This research aims to investigate whether baseline serum lipoprotein(a) levels could be a predictor for intensive care unit admission and related clinical parameters in coronavirus disease 2019 patients. Material and Methods: The research covers 126 patients who were hospitalized in intensive care unit or the non-intensive care unit in our hospital. This prospective cohort study was conducted from January 2021 to June 2021. The patients who were positive for severe acute respiratory syndrome coronavirus 2 according to real-time polymerase chain reaction test results were included in the study. Two groups were created according to the status of intensive care unit admission. Lipoprotein(a) was studied from blood samples taken at the time of hospital admission. Results: According to the results of the first clinical evaluation, 46 patients were admitted to the intensive care unit and 80 patients were admitted to non-intensive care unit in the hospital. Patients with intensive care unit admission had significantly higher serum lipoprotein(a) levels than patients without intensive care unit admission (40.9 ng/mL and 17.4 ng/mL, P < .001, respectively). The regression analysis revealed that serum lipoprotein(a) levels were independently related to intensive care unit admission (odds ratio 1.242, 95% CI 1.109-1.391, P < .001). In receiver operating characteristic curve analysis, lipoprotein(a) level ≥31.42 ng/mL had 82.6% sensitivity and 72.5% specificity in predicting intensive care unit admission. The risk of intensive care unit admission was seen to be 12.522-fold higher in cases with lipoprotein(a) level ≥31.42. Conclusion: Lipoprotein(a) could be used as a useful biomarker for the triage of coronavirus disease 2019 patients. Baseline serum lipoprotein(a) levels may serve as a useful prognostic biomarker in patients hospitalized for coronavirus disease 2019.

PURPOSE:In this prospective study we aimed to determine the rate of Fabry Disease (FD) in patients with left ventricular hypertrophy (LVH), and to evaluate the clinical presentations of patients with FD in a comprehensive manner. In addition, we aimed to raise awareness about this issue by allowing early diagnosis and treatment of FD.METHODS:Our study was planned as national, multicenter, observational. Totally 22 different centers participated in this study. A total of 886 patients diagnosed with LVH by echocardiography (ECHO) were included in the study. Demographic data, biochemical parameters, electrocardiography (ECG) findings, ECHO findings, treatments and clinical findings of the patients were recorded. Dry blood samples were sent from male patients with suspected FD. The α-Gal A enzyme level was checked and genetic testing was performed in patients with low enzyme levels. Female patients suspected of FD were genetically tested with the GLA Gene Mutation Analysis.RESULTS:FD was suspected in a total of 143 (16.13%) patients included in the study. The α-Gal-A enzyme level was found to be low in 43 (4.85%) patients whom enzyme testing was requested. GLA gene mutation analysis was positive in 14 (1.58%) patients. Male gender, E/e' mean ,and severe hypertrophy are important risk factor for FD.CONCLUSION:In daily cardiology practice, FD should be kept in mind not only in adult patients with unexplained LVH but also in the entire LVH population. Dry blood test (DBS) should be considered in high-risk patients, and mutation analysis should be considered in required patients.

Cardiovascular disease are common in patients with atrial fibrillation (AF) and imaging of the 15

Introduction: In chronic venous insufficiency (CVI), an increase in venous pressure causes the passage of intravascular blood cells and molecules into the surrounding tissues and induces histopathological changes in the lower extremities, leading to increased pigmentation in the legs, ulceration, and tissue loss to various degrees. This study aimed to investigate whether an increase in venous pressure in the coronary veins can lead to the aforemen-tioned histopathological changes. Material and methods: Twenty-four New Zealand rabbits were divided into the following three groups: experimental model of coronary venous hyper-tension (CVH) (n = 8), sham group (n = 8), and control group (n = 8). After 21 days postoperatively, tissue samples from each group were compared for perivascular inflammation, erythrocyte extravasation, macrophage infiltra-tion, and hemosiderin deposits by histopathological scoring under a light microscope. Matrix metalloproteinase-2 (MMP-2) activation was evaluated using immunohistochemical staining. Results: In the CVH group, hemosiderin accumulation was significantly high-er than in the sham and control groups (1.0 (1.0-3.0), 0.0 (0.0-1.0), 0.0 (0.0- 0.0); p < 0.001). Immunohistochemically, in the CVH group, MMP-2 levels were significantly higher than in the sham and control groups (2.0 (1.0-3.0), 0.0 (0.0-1.0), 0.0 (0.0-0.0); p < 0.001). Conclusions: This experimental study showed for the first time the histo-pathological and immunohistochemical changes in myocardial tissue, simi-lar to those observed in CVI, as a result of increased coronary venous pres-sure due to coronary vein ligation. Further studies are needed to understand the clinical implications of these results.