Yakup Yiğit

Vasospastic angina can cause myocardial infarction and malignant ventricular arrhythmias, but a persistent coronary occlusion in a patient with established vasospasm creates an acute diagnostic and procedural dilemma. A man with recurrent troponin‐positive presentations and prior non‐obstructive coronary angiography developed 99% mid‐left anterior descending artery narrowing in 2024 that markedly regressed after intracoronary nitrate; ergonovine provocation was subsequently positive. In April 2026, at age 42, he presented with anterior ST‐segment elevation myocardial infarction after irregular use of vasodilator therapy. Angiography showed total occlusion of the left anterior descending artery at the previously nitrate‐responsive segment. Intracoronary nitrate did not restore flow, and ventricular fibrillation occurred during the procedure. Bailout drug‐eluting stent implantation restored flow. A proximal right coronary artery occlusion was also identified during the same procedure and treated with stenting. In June 2026, angiographically confirmed stent thrombosis required repeat percutaneous coronary intervention; an implantable cardioverter‐defibrillator was subsequently implanted after multidisciplinary review. This case highlights the need to consider superimposed thrombotic or structural mechanisms when coronary occlusion in a patient with established vasospastic angina does not resolve after intracoronary nitrate. Bailout revascularization may be necessary when flow cannot be restored in a hemodynamically unstable patient, but it does not eliminate the underlying vasomotor disorder.

We read with interest the study by Li et al

Background/Objectives: Metabolic syndrome (MS) has been demonstrated to be associated with subclinical myocardial dysfunction, which develops in the early stages. It has been hypothesised that traditional echocardiographic parameters may be insufficient in detecting these changes. The frontal QRS-T angle is an electrocardiographic parameter that is easily obtained and that reflects ventricular electrical heterogeneity. This study aimed to examine the relationship between the frontal QRS–T angle and left ventricular myocardial deformation, as assessed by four-dimensional strain echocardiography (4DSE), in patients with MS. Methods: The present cross-sectional study comprised 70 patients diagnosed with MS and 61 healthy individuals matched for age and gender. All participants underwent standard transthoracic and 4DSE examination and 12-lead electrocardiography. The values of global longitudinal strain (GLS), global circumferential strain (GCS), global radial strain (GRS) and global area strain (GAS) were analysed. The frontal QRS-T angle was calculated as the absolute difference between the QRS and T axes. The interrelationships between the variables were assessed using correlation and multivariate linear regression analyses. Results: Despite comparable left ventricular ejection fraction (LVEF) between the groups, 4DSE-derived myocardial deformation parameters, including GLS, GCS, GAS, and GRS, were significantly impaired in the MS group. The frontal QRS-T angle was found to be significantly higher in patients diagnosed with MS in comparison to the control group (p < 0.001). A significant correlation was identified between the frontal QRS-T angle and GLS (r = 0.498, p < 0.001). In multivariable linear regression analysis, the frontal QRS–T angle was independently associated with GLS (standardized β = 0.501, p < 0.001). In exploratory receiver operating characteristic (ROC) analysis, the frontal QRS–T angle showed moderate discriminatory ability for GLS-defined impaired myocardial deformation area under the curve (AUC) = 0.720). Conclusions: An increased frontal QRS–T angle in individuals with metabolic syndrome was independently associated with subclinical LV dysfunction despite preserved ejection fraction (EF). These findings suggest that the frontal QRS–T angle may serve as a simple and readily available electrocardiographic marker associated with impaired myocardial deformation, warranting further validation in larger prospective studies.

Background/Objectives: Inflammation plays a central role in the pathophysiology and prognosis of non-ST-segment elevation myocardial infarction (NSTEMI). This study aimed to investigate the clinical and prognostic significance of the Cumulative Inflammatory Index (IIC) in patients with NSTEMI. Methods: This single-center, retrospective study included 2274 individuals, comprising 1172 patients with NSTEMI and 1102 angiographic controls without acute coronary syndrome or obstructive coronary artery disease. IIC was calculated using mean corpuscular volume, red cell distribution width, neutrophil count, and lymphocyte count. The primary outcome was 360-day all-cause mortality in the NSTEMI cohort. Logistic regression, receiver operating characteristic curve analysis, and DeLong testing were performed. Results: Patients with NSTEMI had significantly higher IIC values than controls [9.08 (4.05–15.03) vs. 1.90 (1.45–2.89), p < 0.001]. Among NSTEMI patients, non-survivors had significantly higher IIC levels than survivors [14.25 (8.56–26.59) vs. 8.57 (3.73–14.06), p < 0.001]. In multivariable logistic regression analysis, IIC remained independently associated with 360-day all-cause mortality after adjustment for age, diabetes mellitus, estimated glomerular filtration rate, hemoglobin, albumin, and C-reactive protein (OR: 1.045, 95% CI: 1.029–1.060; p < 0.001). IIC showed a modestly higher area under the curve among the evaluated indices (AUC: 0.704). Conclusions: IIC was significantly elevated in patients with NSTEMI and was independently associated with 360-day all-cause mortality. IIC may serve as a simple adjunctive marker for risk stratification in patients with NSTEMI.

Objective: To evaluate the corrected index of cardio‐electrophysiological balance (ICEBc) and left ventricular mechanical dispersion (LVMD), in obese individuals and to examine their associations with obesity severity and electromechanical myocardial heterogeneity. Methods: This prospective case–control study included obese individuals (BMI ≥30 kg/m ² ) and normal‐weight healthy controls. All participants underwent standard 12‐lead electrocardiography and transthoracic echocardiography. The ICEB and corrected ICEB (ICEBc) were calculated from ECG recordings. LVMD was assessed using two‐dimensional speckle‐tracking echocardiography. Comparisons between groups and correlation analyses between ICEBc, LVMD, and body mass index (BMI) were performed using appropriate statistical methods, with p < 0.05 considered statistically significant. Results: Obese individuals had higher systolic and diastolic blood pressures. LVMD was significantly higher and global longitudinal strain was significantly lower in obese participants. QTc and ICEBc were significantly higher in obesity. Among obese subgroups, LVMD and ICEBc increased with obesity severity. LVMD showed a good positive correlation with ICEBc ( r = 0.675, p < 0.001). BMI correlated moderately with LVMD ( r = 0.543, p < 0.001) and weakly with ICEBc ( r = 0.257, p = 0.021). Conclusion: Obesity was associated with higher LVMD and ICEBc values, suggesting increased electrical and mechanical myocardial heterogeneity. LVMD and ICEBc may serve as complementary, non‐invasive surrogate markers of obesity‐related electromechanical remodeling. Larger longitudinal studies with rhythm monitoring are required to determine whether these parameters predict clinical arrhythmic events.

Kardiyak Pace Tipi ve Pacing Modları Gamze Yeter ARSLAN Kalıcı Kalp Pili Endikasyonları Yusuf HOŞOĞLU Ayşe HOŞOĞLU Pacemaker & ICD İmplantasyonu Yakup YİĞİT Leadless Pacemaker Yusuf Ziya ŞENER Geçici Transvenöz Pacing ve Komplikasyonları Didar Elif AKGUN Yavuz Selim AKGUN Primer Koruma Amaçlı İmplante Edilebilir Kardiyoverter Defibrilatör Tarık YILDIRIM Sekonder Profilaksi Amaçlı İmplante Edilebilir Kardiyoverter Defibrilatör Seda Elçim YILDIRIM İmplante Edilebilir Kardiyoverter-Defibrilatör Programlama Arzu YAZAR İmplante Edilebilir Kardiyoverter Defibrilatör (ICD) Mevcut Hastalarda Uygun Cihaz Şoklarının Yönetimi Neşri DANIŞMAN Şeyhmus KULAHCIOĞLU Uygunsuz İmplante Edilebilir Kardiyoverter Defibrilatör (ICD) Şokları ve Yönetimi Onur ALTINKAYA Subkutan ICD Ertan AYDIN Giyilebilir Kardiyak Defibrilatör Abdullah SARIHAN Lütfü BEKAR Genetik Testler Selahattin AKYOL Holter Ritim Monitörizasyonu Sinem ÖZBAY ÖZYILMAZ İmplante Edilebilir Loop Recorder Hatice TAŞKAN Tilt Table Testi Güney SARIOĞLU Pacemaker ve ICD Endikasyonu Belirlemede Kullanılan Testler-Kardiyak Görüntüleme (EKO ve MRG) Emirhan ÇAKIR Elektrofizyolojik Çalışma Muhammed Kemal KAHYALAR Kalp Yetersizliği Tedavisinde Kardiyak Resenkronizasyon Tedavisi Enfal ÇAKMAK AKSU Fatih AKKAYA Kardiyak Resenkronizasyon Tedavisi Endikasyonları ve Hasta Seçimi Tayfur ERDOĞDU Koroner Sinüs Anatomisi ve KRT Doğan İLİŞ KRT İmplantasyonu Kubilay ERSELCAN Cerrahi KRT İmplantasyonu Mahmut YARGI Kime KRT-D & Kime KRT-P Fahri CAKAN Kardiyak Resenkronizasyon Tedavisi Yanıt Tanımı ve İlişkili Faktörler Lütfü AŞKIN Elektrokardiyografi ve Ekokardiyografi ile Kardiyak Resenkronizasyon Tedavisi Optimizasyonu Şerif HAMİDEYİN Kardiyak Resenkronizasyon Tedavisi Programlama Fatih KÖKSAL Diyafragma Pacingi Yönetimi Emre ASİLTÜRK Atriyal Fibrilasyonda Atrioventriküler (AV) Nod Ablasyonu ve Kardiyak Resenkronizasyon Tedavisi Halil İbrahim DURMUŞ HİS-Demeti Pacing Ayça ARSLAN Sol Dal Pacing İnanç ARTAÇ HİS Optimize Kardiyak Resenkranizasyon Tedavisi Süleyman BARUTCU Sol Dal Optimize Kardiyak Resenkronizasyon Tedavisi Hakan Gökalp UZUN Jeneratör Replasmanı Yusuf Bozkurt ŞAHİN Lead Ekstraksiyonu Nihan BAHADIR Kardiyak İmplante Edilebilir Elektronik Cihazların (KİEC) İmplantasyonu Sonrası Takip Şeyhmus Erkan DEMİRCAN Baver EKİNCİ Atrial Yüksek Hız Epizot Yönetimi Muhammet GENEŞ Kardiyak İmplante Edilebilir Cihazlarda Telekardiyografik Değerlendirme Zelal TAHAOĞLU Pil Cebi Hematomu Sidar Şiyar AYDIN Pnömotoraks, Hemotoraks ve Brakiyal Pleksus Yaralanması Ali Nail KAYA Kardiyak İmplante Edilebilir Elektronik Cihazların Komplikasyonu Kardiyak Rüptür/Perikardiyal Efüzyon Burcu KODAL Lead Kusurları Mert Pehlivan ALTIN Lead Dislokasyonu Sendromları Vedat CİCEK Samet YAVUZ Lead İlişkili Triküspit Yetmezliği Timor OMAR Pacemaker Aracılı Taşikardi Lütfullah CANDAN Pacemaker Sendromu Murat KARACAM Gülümser Sevgin HALİL Oversense Sendromları Selahattin AYDIN Kardiyak İmplante Edilebilir Cihaz Enfeksiyonu Mürsel ŞAHİN Kiec İlişkili Lead Trombüsü ve Pulmoner Embolizm Emre YILMAZ Karotid Baroreseptör Stimülasyonu Fehmi ESER Ramazan DUZ Kardiyak Kontraktilite Modülasyonu Sümeyye Fatma ÖZER Pulmoner Arter Basıncı Monitorizasyonu Muammer KARAKAYALI Kardiyak İmplante Edilebilir Elektronik Cihaz İmplantasyon Sürecinde Antikoagülan Tedavi ve Antibiyotik Proflaksisi Ömer ŞİT Preoperatif Kardiyak İmplante Edilebilen Cihaz Ayarlama Ferit BÖYÜK Radyoterapi Sürecinde Kalp Pili & ICD Takibi Yusuf Ziya ŞENER Kardiyak İmplante Edilebilir Elektronik Cihazı Olan Hastada Manyetik Rezonans Görüntüleme Semih KALKAN Kalp Pili & İmplante Edilebilir Kardiyak Defibrilatör (ICD) Olan Hastalarda Spor Aktivitesi ve Sürücülük Ahmet Lütfü SERTDEMİR Ahmet Taha ŞAHİN LVAD İmplantasyonu Yapılan Hastada ICD Endikasyonu ve Yönetimi Berhan KESKİN Kardiyak Cerrahi Sonrası Pacing Muhammed Bahadır OMAR TAVİ Sonrası Pacemaker İmplantasyonu Mehmet KIŞ Çisem OKTAY Konjenital Kalp Hastalıklarında Kardiyak Pacing ve ICD Mücahit TAN Naci BABAT Sarkoidoz Kardiyak Pacing ve ICD Ercan CEĞİLLİ Pakize SUCU Kardiyak Amiloidozda Kardiyak Pacing ve ICD Onur ASLAN Hipertrofik Kardiyomiyopatide Kardiyak Pacing ve ICD Burcu OZYAZGAN Nadir Kardiyak Hastalıklarda Kardiyak Pacing ve ICD Songül USALP

Subject: Rheumatoid arthritis patients are at risk of developing cardiovascular disease such as right heart failure and pulmonary hypertension (PH). Arterial stiffness can be used to assess pulmonary hemodynamics. Noninvasive approaches can also be used to assess pulmonary hemodynamics. Recently, there have been reports that pulmonary pulse transit time (PPTT) may also be a useful measure. This study aims to examine the effects of pulmonary hemodynamic alterations on PPTT in RA patients.Methods: Forty RA patients and 40 healthy controls were included in the study. Sociodemographic characteristics, laboratory data, and echocardiographic examinations were performed in both groups. Conventional echocardiographic examination included left and right ventricular systolic and diastolic diameters, right ventricular myocardial performance index (RVMPI), right ventricular diastolic function, estimated pulmonary artery systolic pressure (sPAP), tricuspid annular plane systolic excursion (TAPSE), pulmonary artery stiffness (PAS), and PPTT. Right ventricular diastolic and systolic volumes, right ventricular ejection fraction (RVEF), and right ventricular fractional area change (RVFAC) were determined by four‐dimensional echocardiography (4DE).Results: There was no difference between the sPAP values of the patients. RVMPI and PAS were increased in RA patients compared with controls. The PPTT was shortened in RA patients and correlated with RVEF, RVFAC, RVMPI, TAPSE/sPAP, disease duration, and C‐reactive protein (CRP). In univariate linear regression analysis, PPTT (p < .001) was thought to be an independent predictor of PAS. RVFAC, disease duration, and PAS were also independent predictors of PPTT.Conclusion: In RA patients, PPTT may be the first evidence of early abnormalities in pulmonary vascular hemodynamics. PPTT and PAS are the values that may predict each other in RA patients. Due to its more practical application, PPTT can be used instead of PAS to assess pulmonary hemodynamics.