Background: We aimed to investigate the clinical and angiographic characteristics of patients with acute coronary syndrome (ACS) who survived this devastating earthquake and were admitted to our hospital in Antakya/Türkiye. Materials and Methods: We retrospectively examined the impact of the earthquake on the occurrences of acute coronary syndromes in Antakya/Türkiye. All 248 consecutive patients with ACS, also survivors of the earthquake in Antakya, were enrolled as the earthquake group. The earthquake group was created from patients hospitalized between February and June in 2023 after the earthquake. In total, 209 consecutive ACS patients who were hospitalized in our cardiology clinic in similar months of 2022 named as the control group. Results: Patients admitted before the earthquake were more hospitalized with multivessel disease compared to after the earthquake group (P <.001). Myocardial infarction with non-obstructive coronary artery disease (MINOCA) was the main reason for the significant increase rate of ACS after the earthquake. The earthquake patient group had lesser diabetes mellitus than the control group (P <.001). The risk of men suffering from ACS after an earthquake is approximately 2.1 times higher than women (P =.023). Those with a history of revascularization are approximately 1.8 times more likely to have ACS after an earthquake (P =.05). The risk of experiencing ACS after an earthquake is approximately 3.5 times higher for those with a family history than for those without (P <.001). Conclusion: Effects of the devastating earthquake on the heart are the increase in MINOCA patients triggered by great sudden environmental stress and the decrease in diabetes due to worsening nutritional conditions, respectively.

Background Dual antiplatelet therapy (DAPT) is the treatment of choice for patients with acute and chronic coronary syndromes as it reduces mortality and prevents recurrent thrombotic complications. The assessment of both ischaemic burden and bleeding risk is crucial in deciding which DAPT to choose and how long it should be continued. Objectives The aim of our study was to perform prospective clinical follow-up of patients receiving fixed-dose combination therapy (ASA 75 mg + clopidogrel 75 mg). Our study is a multicentric, cross-sectional, observational, cohort study. Methods A total of 1500 patients who were started on fixed-dose combination DAPT for acute or chronic coronary syndrome were included in the study. Primary endpoints were hospitalization for any reason, hospitalization for cardiovascular cause, acute myocardial infarction, stent thrombosis, target vessel revascularization and bleeding; the secondary endpoints were death for any reason or cardiovascular cause and stroke. The significance level adopted in the statistical analysis was 5%. Results Median age was 63 years; 78.5% of the patients were receiving DAPT treatment for acute coronary syndrome. The rates of hospitalization for cardiovascular reasons, acute myocardial infartion, stent thrombosis and target-vessel revascularization were 7.9%, 2.3%, 1.3% and 4.2%, respectively. While the rate of BARC type 1 bleeding was 3.3%, the rate of BARC type 5, 3, or 2 bleeding was 0.6%. The secondary endpoints which were death from any cause, cardiovascular death and stroke were 0.5%, 0.3% and 0.3%, respectively. Conclusion: Our study shows that fixed-dose combination therapy is effective and safe in appropriately selected patients with acute or chronic coronary syndromes.

Rhabdomyoma is the most prevalent cardiac tumor found in fetal and neonatal life. Although rhabdomyoma usually exists in multiple foci, it rarely manifests as a unitary solid cardiac rhabdomyoma in fetal life. Most cardiac rhabdomyomas present with tuberous sclerosis (TSC). Rhabdomyomas are usually asymptomatic; however, the size and speed of tumor growth can present life-threatening challenges. The clinical manifestations of tumors vary depending on their location. Giant cardiac rhabdomyomas have different fatal consequences. Due to their fast growth rate, cardiac rhabdomyomas can conspicuously show themselves in different sizes and, depending on their location, can cause arrhythmias, cardiac shock, fetal hydrops, and obstruction of ventricular outflow tracts, both prenatally and early postnatally. This case report highlights the importance of using the cerebral-placental ratio in fetal life to determine postnatal outcomes and to plan possible treatment options for pediatric patients with giant cardiac rhabdomyoma. Article published online: 23 January 2025 © 2025. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany

Blood pressure response during exercise testing provides valuable prognostic information. This study examined the association between blood pressure recovery ratio (BPRR) and SYNTAX score (SS) in patients with stable coronary artery disease (CAD). . A total of 98 patients (mean age 57.3 ± 7.3 years) with ≥50% lesion in ≥1 coronary artery who underwent coronary angiography after an exercise test were included. Patients were classified into low SS (≤22) and intermediate-high SS (>22) groups. BPRR was calculated as the ratio of third-minute to peak exercise systolic blood pressure (SBP). BPRR was significantly higher in the intermediate-high SS group (0.96 ± 0.05) than in the low SS group (0.87 ± 0.06) (p < 0.001). It showed a positive correlation with SS, E/e' ratio, and left atrial volume, and a negative correlation with LVEF. In multivariate analysis, BPRR (OR: 1.446, p < 0.001) and LVEF (OR: 0.802, p = 0.005) were independent predictors of intermediate-high SS. Each 0.01 unit increase in BPRR increased risk by 44.6%. ROC analysis identified a BPRR cut-off of 0.928 (AUC = 0.892). BPRR, a simple and accessible parameter from exercise testing, is independently associated with CAD severity. It may enhance the non-invasive prediction of intermediate to high SS.

A 14-month-old toddler with a heart murmur was admitted to the Department of Pediatric Cardiology. Physical examination revealed a blood pressure of 105/60 mmHg, a pulse of 100/min, and a 2/6° mid systolic ejection murmur in the left upper sternal area. The patient’s electrocardiogram was normal. A transthoracic echocardiographic examination relieved a massive (5×4.8×5 cm) homogeneous, hyper echogenic mass extending from the basal to the mid-segment and covering the full anterior half of the ventricle cavity ([Fig. 1a]). The mass was suspected of either benign rhabdomyoma or fibroma. Then, the patient was referred to the Department of Radiology for a cardiac MRI examination to make a differential diagnosis. On MRI, the cine images showed a single well-defined tumor in the myocardium involving the interventricular septum on the left ventricular wall that was isointense to the myocardium. The tumor was isointense in T1- and T2-weighted turbo spin-echo axial images without signal loss with fat suppression. In T2-weighted images, there were also heterogeneous hypo intense areas in the center of the tumor ([Fig. 1]b, [1]c). There was no first-pass enhancement (1D). However, in the late contrast-enhanced scans obtained 10 minutes after gadolinium administration, the mass had intense peripheral enhancement with no enhancement in the center ([Fig. 1e]). With these characteristic findings, the mass was diagnosed as a ventricular fibroma. The Cardiac MRI also showed that the tumor extended the left ventricular outflow tract, causing a mild dynamic outflow gradient ([Fig. 1f]). Cardiovascular surgery was consulted. It was decided that the surgical operation should not be performed due to the existence of massive intramural myocardial involvement; however, if the cardiac outflow obstruction occurs and the obstruction induces severe hemodynamic deterioration or arrhythmia in the infant’s heart, surgical intervention would be a necessity to treat cardiac fibroma. Cardiac MRI is an effective method to characterize tissue and improves the diagnostic accuracy. It is important to distinguish cardiac fibroma and isolated giant rhabdomyoma. On cardiac MRI, both tumors are well-marginated from the surrounding myocardium that appears benign. Furthermore, a benign tumor with limited vascularity, rather than a malignant tumor with abundant vascularity, is reflected by a hypointense signal on first-pass perfusion imaging as compared to the surrounding myocardium. Furthermore, cardiac fibroma is the only tumour that exibits iso signal intensity on T1-weighted imaging and low-signal intensity on T2-weighted imaging. This indicates low water content, which is different from malignant tumours and many other benign tumours (Teis A et al., Circulation 2011; 124: 1481–1482). An abundance of fibrotic tissue in cardiac fibroma is shown by the hyperintensity of the entire mass on LGE. Therefore, tissue characterization using MRI can provide additional information to diagnose cardiac fibroma non-invasively without the need for tissue biopsy and can expedite preventative surgery to avoid sudden death (Kimura A et al., Eur Heart J Case Rep 2020 4: 1–5). In conclusion, we want to contribute our experience with a case of probable myocardial fibroma diagnosed with magnetic resonance imaging (MRI) that underlines the diagnostic importance of the late enhancement pattern to differentiate myocardial fibroma from rhabdomyoma. Article published online: 07 February 2025 © 2025. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany

Duchenne muscular dystrophy (DMD) is an X-linked progressive muscular disease, not a bone disease. Clinical manifestations of DMD are progressive cardiomyopathy, and muscle weakness (Mah JK et al., Neuromuscul Disord 2014; 24(6): 482–491). The molecular cause of DMD is a mutation in the dystrophin gene, which leads to disruption in the sarcolemma of both cardiomyocytes and skeletal myofibers, ultimately affecting muscle cell integrity [Bushby K et al., Lancet Neurol 2010; 9(1): 77–93]. The primary characterization of DMD is the rapid deterioration of the skeletal muscles. There have been many reported cases of co-occurrence of DMD and cardiac involvement. Cardiac involvement most commonly manifests as lateral wall fibrosis due to ongoing inflammation [Mavrogeni S et al., Int J Cardiol 2009; 132(3): e123–e124]. Acute myocarditis may mimic the early cardiac symptoms of cardiomyopathy, further complicating diagnosis in DMD patients [Veronese G et al., Anatol J Cardiol 2018]. Cardiomyopathy in DMD is a direct result of progressive myocardial fibrosis, not typically triggered by viral myocarditis [Karcic A, Conrad AR, N Engl J Med 2000; 343: 299–300]. However, acute myocarditis is rarely presented in DMD patients. The diagnosis of acute myocarditis can be made based on the findings of cardiac MRI and noninvasive tests. Chronic elevation of cardiac Troponin T has been observed in DMD patients, but Troponin I, a cardiac-specific biomarker, is typically not elevated in this population unless there is concurrent myocarditis (Barthel BL et al., Muscle Nerve 2021; 64(1): 43–49). Specifically, troponin T may be chronically elevated in DMD patients due to skeletal muscle involvement, while troponin I remains a specific marker for cardiac injury and is typically only elevated in cases of acute myocarditis or myocardial infarction. Elevated Troponin I in DMD patients may therefore indicate an underlying viral infection, which can contribute to myocarditis or other forms of cardiac stress. A 13-year-old boy with Duchenne muscular dystrophy (DMD) due to a deletion of exons 45 to 50 in the DMD gene was diagnosed in the Department of Medical Genetics at the age of eight years. The patient was admitted to the ED due to heavy chest pain. His physical examination in the ED revealed he was afebrile; his heart rate was 97 bpm, his blood pressure was 120/65 mm Hg, and he had 97% oxygen saturation on room air. His cardiac examination was normal, with no abnormal sound or murmur. His pulmonary examination revealed normal auscultation, his jugular venous pressure was normal, and no extremity edema was detected. A complete blood count revealed WBC: 13,400/mm³, Hemoglobin: 12.2 g/dL Hematocrit: 36.2%, Platelets: 354,000/mm³, CRP: 0.53 mg/dL (normal<5 mg/L), Troponin I: 7454.4 ng/mL (normal<0.04 ng/mL), CK-MB: 60 U/L, CK: 1088 U/L The patient was transferred to the Department of Pediatric Cardiology for further examination. ECG was normal. There was no pathology on the echocardiographic examination. Left ventricular ejection and shortening fraction were measured at 60% and 30, respectively. Even though the patient's general condition was normal, the patient was still monitored for rhythm abnormalities. Enterovirus RNA was identified by PCR. Other viral panels were unremarkable and thus omitted. Given his elevated Troponin I levels, the patient was admitted to the pediatric ward for close monitoring. On the first day of hospitalization, Troponin I levels increased gradually to 36,950 ng/mL) ( the normal range should be between 0 and 0.04 ng/mL). Intravenous immunoglobulin (IVIG) treatment was administered at 400 mg/kg/dose over a 12-hour infusion. Following the infusion, Troponin I levels rose to 64,486 ng/mL. ([Tab. 1]). Cardiac magnetic resonance (MRI) was done on the patient to clarify the etiology. Cardiac MRI revealed anterior, anterolateral, and inferolateral wall myocardial edema with elevated T2 values and late gadolinium enhancement (LGE) in the basal to mid inferolateral walls consistent with acute myocarditis ([Fig. 1] [2]). Also, parvovirus B19 IgM was detected as positive. He was diagnosed with acute myocarditis due to clinical and laboratory findings. The same IVIG dose was continued for two more days, and non-steroid anti-inflammatory treatment (ibuprofen 2×400 mg) was started. No echocardiographic deterioration or arrhythmia occurred. A continuous decline in Troponin I was noted. By day 7, the patient was symptom-free. By day 10, he was discharged with Troponin I levels of 500 ng/mL and improved condition. Article published online: 31 July 2025 © 2025. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany