Mucahit Yetim

Objective: Ischemia with no obstructive coronary arteries (INOCA) is increasingly recognized as a clinically relevant entity associated with adverse cardiovascular outcomes. Carotid intima-media thickness (CIMT) is a surrogate marker of early atherosclerosis and may provide insight into the systemic vascular involvement in INOCA. This study aimed to compare CIMT between patients with INOCA and healthy controls.Material and Method: A total of 145 patients with INOCA (mean age: 53.2 ± 9.1 years, 40% male) and 150 healthy controls (mean age: 56.7 ± 7.4 years, 44% male) were enrolled in this single-center case-control study between May 2018 and January 2024. The diagnosis of INOCA was based on the presence of typical angina, objective evidence of ischemia on treadmill exercise testing or myocardial perfusion scintigraphy, and without angiographic evidence of obstructive epicardial coronary artery stenosis (>50%) or vasospasm during invasive coronary angiography. CIMT was measured from the left common carotid artery using high-resolution B-mode ultrasonography. Comparisons between groups were performed, and receiver operating characteristic (ROC) curve analysis was conducted to assess the diagnostic performance of CIMT.Results: Baseline demographic, echocardiographic, and laboratory parameters were similar between INOCA patients and controls (all p > 0.05). Mean CIMT was significantly higher in the INOCA group compared with controls (0.58 ± 0.13 mm vs. 0.52 ± 0.11 mm, p < 0.001). ROC analysis demonstrated that CIMT >0.54 mm predicted the presence of INOCA with a sensitivity of 59% and a specificity of 52% (AUC: 0.605, 95% CI: 0.540–0.669, p = 0.002).Conclusion: Patients with INOCA exhibited significantly increased carotid intima-media thickness compared with healthy controls, suggesting that INOCA is associated with early systemic atherosclerosis. CIMT measurement may represent a simple and noninvasive method for identifying high-risk patients in this population.

High-sensitivity cardiac biomarkers have transformed modern cardiology by enabling earlier diagnosis and refined risk stratification in acute coronary syndromes and heart failure. However, increasing analytical sensitivity has also amplified the clinical impact of immunoassay interferences, particularly those caused by heterophile antibodies. These endogenous antibodies can interact with assay antibodies and generate false-positive or false-negative results, most notably in sandwich immunoassays used for cardiac troponins and natriuretic peptides. Persistent, clinically implausible biomarker elevations related to heterophile antibody interference have led to unnecessary invasive procedures, inappropriate pharmacologic treatment, repeated hospital admissions, and prolonged diagnostic uncertainty. Conversely, false-negative results may delay diagnosis, result in inappropriate discharge, and contribute to adverse clinical outcomes in high-risk patients. This review summarizes the immunological basis and analytical mechanisms of heterophile antibody interference, highlights cardiac biomarkers most commonly affected, and outlines key clinical red flags that should prompt suspicion. Practical laboratory strategies include polyethylene glycol precipitation as an initial approach to detect antibody-mediated interference, followed by dilution studies, heterophile blocking reagents, and cautiously interpreted alternative platform testing within assay-specific reference frameworks, together with close clinician-laboratory collaboration. Greater awareness of analytical interference is critical as cardiology becomes increasingly biomarker-driven. Integrating clinical judgment with structured laboratory verification can substantially reduce diagnostic error, improve patient safety, and prevent avoidable healthcare utilization in contemporary cardiovascular practice.

Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide, and excess adiposity is a major contributor to cardiovascular (CV) risk. However, obesity is a heterogeneous condition, and body mass index (BMI) alone fails to capture important differences in fat distribution and lean mass that substantially influence CV outcomes. Growing clinical and epidemiological evidence indicates that body composition, rather than body weight per se, provides a more accurate and biologically meaningful framework for CV risk assessment. This narrative review summarizes clinical evidence linking key components of body composition, including total and regional adiposity, skeletal muscle mass, and ectopic fat depots, to CV risk and prognosis. Central and visceral adiposity are consistently shown to be more strongly associated with cardiometabolic dysfunction, atherosclerosis, and CV events than generalized obesity. In parallel, reduced lean mass and sarcopenia emerge as independent predictors of adverse CV outcomes, particularly in older adults and patients with established CVD. Ectopic fat depots, such as epicardial and hepatic fat, further contribute to CV pathology through local and systemic mechanisms. Collectively, these findings highlight the limitations of BMI-centered approaches and support the integration of body composition measures into CV risk stratification. Emphasizing body recomposition, with reduction of harmful fat depots and preservation of skeletal muscle, may enable more precise, individualized strategies for CV prevention and management.

Amaç: Hipertansiyon hastalarında elektrokardiyografik parametreler ile sol ventrikül hipertrofisi (SVH) arasındaki ilişkinin araştırılması ve özellikle ventriküler aktivasyon zamanının (VAT) tanısal değerinin değerlendirilmesi amaçlandı.Gereç ve Yöntem: Esansiyel hipertansiyonu olan 320 hasta (ortalama yaş 61,9±7,8 yıl, %57,5 erkek) çalışmaya dahil edildi. Tüm hastalara transtorasik ekokardiyografi ve 12 derivasyonlu yüksek çözünürlüklü EKG çekildi. Hastalar ekokardiyografide SVH varlığına göre iki gruba ayrıldı. Demografik, laboratuvar, ekokardiyografik ve elektrokardiyografik parametreler karşılaştırıldı. Çok değişkenli lojistik regresyon ve ROC analizleri ile bağımsız öngördürücü parametreler belirlendi.Bulgular: Hastaların 114’ünde (%35,6) SVH saptandı. SVH (+) grupta sol atriyum çapı, interventriküler septal kalınlık, arka duvar kalınlığı, sol ventrikül kütlesi ve kitle indeksi anlamlı olarak daha yüksekti (tümü p

Fragmented QRS (fQRS) is an electrocardiographic marker that reflects conduction abnormalities caused by myocardial scarring, fibrosis, or structural remodeling. Over the past two decades, fQRS has gained increasing attention for its diagnostic and prognostic implications in cardiovascular diseases (CVDs). In ischemic heart disease, fQRS is strongly associated with myocardial infarction, scar burden, and adverse cardiac outcomes, including ventricular arrhythmias and sudden cardiac death. Beyond coronary artery disease, fQRS has also been linked to poor prognosis in non-ischemic cardiomyopathies and heart failure, where it correlates with impaired ventricular function, arrhythmic events, and limited response to cardiac resynchronization therapy. Moreover, fQRS is observed in arrhythmogenic conditions such as Brugada syndrome and in structural disorders including congenital heart disease, myocarditis, and infiltrative cardiomyopathies, serving as a marker of myocardial fibrosis and a predictor of arrhythmogenic risk. The clinical utility of fQRS lies in its simplicity, availability, and low cost, as standard 12-lead electrocardiography is universally accessible. Its incremental prognostic value beyond conventional parameters such as left ventricular ejection fraction highlights its potential to refine risk stratification and guide therapeutic strategies, particularly in identifying candidates for implantable cardioverter-defibrillators. However, widespread clinical adoption is limited by inconsistent definitions, lack of standardization, and variability in interpretation. Future directions include large-scale validation studies, integration with multimodality risk assessment, and the application of artificial intelligence to improve automated detection and predictive accuracy. Overall, fQRS represents a promising, non-invasive tool that could enhance the management of patients across the spectrum of CVDs.

This study examined the association between a blunted nocturnal heart rate decline and ventricular arrhythmias, echocardiographic findings, and clinical characteristics in patients with isolated hypertension (defined as hypertension in the absence of other systemic comorbidities). A total of 229 adults who underwent transthoracic echocardiography and 24-hour Holter monitoring were retrospectively evaluated. Patients were classified as dippers (≥10% nocturnal heart rate reduction; n = 170) or non-dippers (P < .05 for all). They also exhibited more frequent ventricular and atrial ectopy. Patients in Lown classes 1-4 had higher systolic blood pressure, more pronounced left ventricular remodeling, and a greater arrhythmic burden. In multivariable analysis, concentric hypertrophy (Odds Ratio [OR]: 2.682; P = .034) and non-dipping nocturnal heart rate (OR: 9.254; P = .001) were independent predictors of arrhythmias. These findings suggest that non-dipping nocturnal heart rate (reflecting impaired parasympathetic activity and relative sympathetic predominance) is associated with adverse cardiac remodeling and increased arrhythmia risk in isolated hypertension.

Single coronary artery (SCA) is a rare congenital anomaly in which the entire myocardium is supplied by a single coronary ostium, and clinical significance depends largely on the anatomical course and presence of concomitant atherosclerotic disease. We report the case of a 58‐year‐old man presenting with exertional chest pain whose coronary computed tomography angiography revealed an SCA arising from the right coronary sinus with a critical 98% stenosis in the left main equivalent trunk supplying both the left anterior descending and circumflex territories. Although coronary artery bypass grafting was advised due to the high‐risk anatomy, the patient declined surgical revascularization. Elective percutaneous coronary intervention was performed using a 7 F JR guiding catheter, sequential predilatation, and implantation of appropriately sized drug‐eluting stents, resulting in full restoration of TIMI 3 flow without complications. This case underscores the value of modern coronary CT angiography in the detailed assessment of coronary anomalies and demonstrates that, in carefully selected patients who refuse or are unsuitable for surgery, percutaneous intervention can be a safe and effective alternative even in the setting of a left‐main‐equivalent lesion within a single‐origin coronary system.

Endocrine hypertension (HT) includes a group of secondary hypertensive disorders caused by hormonal excess, primarily primary aldosteronism (PA), pheochromocytoma and paraganglioma (PPGL), and Cushing syndrome (CS). Although relatively uncommon, these conditions confer a disproportionately high cardiovascular risk that extends beyond blood pressure elevation. Aldosterone, catecholamines, and cortisol each induce myocardial fibrosis, oxidative stress, and endothelial dysfunction, leading to left ventricular hypertrophy (LVH), arrhythmias, and heart failure. In PA, chronic aldosterone excess activates mineralocorticoid receptors in cardiac and vascular tissues, promoting collagen deposition, diastolic dysfunction, and atrial fibrillation (AF) that may regress after adrenalectomy or pharmacologic blockade. PPGL causes episodic catecholamine surges resulting in β-adrenergic overstimulation, calcium overload, and microvascular ischemia, producing reversible or sometimes persistent catecholamine-induced cardiotoxicity. CS induces concentric hypertrophy, metabolic derangements, and vascular injury through prolonged glucocorticoid exposure, with cardiovascular recovery often incomplete after biochemical remission. Despite distinct hormonal origins, these disorders share convergent mechanisms, including fibroblast activation, mitochondrial injury, and maladaptive remodeling, that define endocrine cardiomyopathy. Early detection and targeted hormonal treatment can reverse much of the cardiac and vascular damage, whereas delayed recognition leads to irreversible fibrosis and persistent diastolic dysfunction. Recognition of these hormone-specific mechanisms is crucial for clinicians to anticipate, manage, and prevent these deleterious cardiovascular effects. Advances in molecular genetics, cardiac imaging, and biomarker research are improving our understanding of genotype-phenotype relationships and long-term reversibility of injury. Endocrine HT should therefore be recognized as a systemic cardiovascular disorder in which hormonal excess functions as a primary pathogenic driver; timely diagnosis and multidisciplinary care remain key to reducing morbidity and mortality.