Gulcın Turkmen Sariyildiz

Bio: Gulcın Turkmen Sariyildiz is an academic researcher from Atılım University. The author has contributed to research in topics: Cardiac imaging & Palpitations. The author has co-authored 2 publications.

Laboratory and Imaging Evaluation of Cardiac Involvement in Patients with Post-Acute COVID-19

Abstract: Background: In the post-acute COVID-19 syndrome, many patients suffer from palpitations, effort-associated fatigue, and even sudden death. The mechanism of heart involvement in this syndrome is uncertain. The main purpose of the study was to identify possible cardiac involvement causes in patients with post-acute COVID-19 by using biomarkers such as NT-proBNP and nitric oxide (NO) and cardiac imaging modalities. Methods: In this cross-sectional study, a total of 105 participants were included according to the existence of symptoms, and 40 of these participants were asymptomatic patients. The ages of the participants ranged from 20 to 50 years. All patients were healthy before COVID-19. The symptoms were defined as palpitations and/or fatigue association with exercise in post-acute COVID-19 term. The comparison of the two groups was made by using biochemical parameters (NT-proBNP, Troponin I, NO) and imaging techniques (echocardiography, cardiovascular magnetic resonance (CMR) and cardiac positron emission tomography (PET)). Results: The symptomatic patients had higher NT-proBNP levels compared with asymptomatic patients (132.30 +/- 35.15;76.86 +/- 16.79, respectively;p < 0.001). Interestingly, the symptomatic patients had lower NO levels than asymptomatic patients (9.20 +/- 3.08;16.15 +/- 6.02, respectively;p < 0.001). Echocardiography and CMR were normal. However, we found regional increased 18F-FDG uptake on cardiac PET to be compatible with myocardial fatigue. Conclusion: We found elevated NT-proNBP levels, low serum NO levels, and increased 18F-FDG uptake on cardiac PET in post-acute COVID syndrome. Cardiac PET could replace or be added to CMR for detecting subtle subacute/chronic myocarditis. The follow-up of patients with post-acute COVID-19 could target the possibility of risk of heart failure.

The coexistence of obstructive sleep apnea in patients with slow coronary flow: a cross-sectional study

Abstract: Amac: Obstruktif uyku apnesi (OUA) ve koroner yavas akim (KYA) ilginc olarak artmis sempatik aktivite ve endotelyal disfonksiyon gibi benzer patolojik mekanizmalara sahiptir. Fakat OUA ve KYA arasindaki birliktelik cok iyi bilinmemektedir. Eger tani konmazsa, OUA artmis kardiyovaskuler mortalite ve morbidite nedenlerinden biridir. Biz bu calismada koroner anjiyografi sonrasi KYA tanisi almis hastalarda OUA varligini arastirdik. Gerec ve Yontem: Bu prospektif kesitsel calisma Subat 2018-Aralik 2019 yillari arasi anjiyografiye alinan 4515 hastayi kapsamaktadir. Koroner anjiyografi sonrasi 4515 hastanin 336 sina YKA tanisi konmustur. Bu 336 hastanin 276 si Berlin anket bulgularina gore yuksek riskli olarak bulunmustur. Calisma grubu 276 hastadan olusmaktaydi. Bu hastalardan 75 ine polisomnografi testi yapilmistir. Kontrol grubu (40 hasta) normal koroner arterli ve OUA olmayan hastalardi. Bulgular: 4515 hastanin 336 si KYA tanisi almisti (%7.4). Berlin anket calismasi sonrasi 336 hastanin 276 si yuksek risk grubu idi (%82.1). Calisma grubu 188 erkek, 88 kadindan olusmaktaydi (toplam 276 hasta). Ortalama yas 48.48 ±7.61 yil idi. Vucut kitle indeksi 33.02±2.18 kg/m2 idi. Polisomnografi yapilan 75 hasta solunum bozukluk indeksine gore hafif ve orta/agir derece olarak iki gruba ayrilmistir. Biz solunum bozukluk indeksi ve duzeltilmis TIMI sayimi arasinda pozitif iliski saptadik. Hafif grupta CTFC-Lad degeri 32.73, orta/agir grupta CTFC-Lad degeri 35.04 (p=0.022). Hafif grupta CTFC-Cx degeri 31.67, orta/agir grupta CTFC-Cx degeri 35.26 (p=0.001). Hafif grupta CTFC-Rca degeri 32.57, orta/agir CTFC-Rca degeri 36.33 (p<0.001). Sonuc: Bu calisma OUA ve KYA arasinda birliktelik oldugunu ortaya koymustur. Ilave olarak biz solunum bozukluk indeksi ile ortalama duzeltilmis TIMI sayimi arasinda anlamli iliskiyi gosterdik. OUA ve KYA birlikteliginin saptanmasi KYA in patofizyolojisini anlamada yardimci olur.

Long COVID and the cardiovascular system—elucidating causes and cellular mechanisms in order to develop targeted diagnostic and therapeutic strategies: a joint Scientific Statement of the ESC Working Groups on Cellular Biology of the Heart and Myocardial and Pericardial Diseases

Abstract: Abstract Long COVID has become a world-wide, non-communicable epidemic, caused by long-lasting multiorgan symptoms that endure for weeks or months after SARS-CoV-2 infection has already subsided. This scientific document aims to provide insight into the possible causes and therapeutic options available for the cardiovascular manifestations of long COVID. In addition to chronic fatigue, which is a common symptom of long COVID, patients may present with chest pain, ECG abnormalities, postural orthostatic tachycardia, or newly developed supraventricular or ventricular arrhythmias. Imaging of the heart and vessels has provided evidence of chronic, post-infectious perimyocarditis with consequent left or right ventricular failure, arterial wall inflammation, or microthrombosis in certain patient populations. Better understanding of the underlying cellular and molecular mechanisms of long COVID will aid in the development of effective treatment strategies for its cardiovascular manifestations. A number of mechanisms have been proposed, including those involving direct effects on the myocardium, microthrombotic damage to vessels or endothelium, or persistent inflammation. Unfortunately, existing circulating biomarkers, coagulation, and inflammatory markers, are not highly predictive for either the presence or outcome of long COVID when measured 3 months after SARS-CoV-2 infection. Further studies are needed to understand underlying mechanisms, identify specific biomarkers, and guide future preventive strategies or treatments to address long COVID and its cardiovascular sequelae.

Biomarkers in long COVID-19: A systematic review

Abstract: Purpose Long COVID, also known as post-acute sequelae of COVID-19, refers to the constellation of long-term symptoms experienced by people suffering persistent symptoms for one or more months after SARS-CoV-2 infection. Blood biomarkers can be altered in long COVID patients; however, biomarkers associated with long COVID symptoms and their roles in disease progression remain undetermined. This study aims to systematically evaluate blood biomarkers that may act as indicators or therapeutic targets for long COVID. Methods A systematic literature review in PubMed, Embase, and CINAHL was performed on 18 August 2022. The search keywords long COVID-19 symptoms and biomarkers were used to filter out the eligible studies, which were then carefully evaluated. Results Identified from 28 studies and representing six biological classifications, 113 biomarkers were significantly associated with long COVID: (1) Cytokine/Chemokine (38, 33.6%); (2) Biochemical markers (24, 21.2%); (3) Vascular markers (20, 17.7%); (4) Neurological markers (6, 5.3%); (5) Acute phase protein (5, 4.4%); and (6) Others (20, 17.7%). Compared with healthy control or recovered patients without long COVID symptoms, 79 biomarkers were increased, 29 were decreased, and 5 required further determination in the long COVID patients. Of these, up-regulated Interleukin 6, C-reactive protein, and tumor necrosis factor alpha might serve as the potential diagnostic biomarkers for long COVID. Moreover, long COVID patients with neurological symptoms exhibited higher levels of neurofilament light chain and glial fibrillary acidic protein whereas those with pulmonary symptoms exhibited a higher level of transforming growth factor beta. Conclusion Long COVID patients present elevated inflammatory biomarkers after initial infection. Our study found significant associations between specific biomarkers and long COVID symptoms. Further investigations are warranted to identify a core set of blood biomarkers that can be used to diagnose and manage long COVID patients in clinical practice.

Cardiac impairments in postacute COVID‐19 with sustained symptoms: A review of the literature and proof of concept

Abstract: Although acute COVID‐19 is known to cause cardiac damage in some cases, there is still much to learn about the duration and relative permanence of the damage that may occur. Long COVID is a condition that can occur when COVID‐19 symptoms remain in the postviral acute period. Varying accounts of long COVID have been described across the literature, however, cardiac impairments are sustained in many individuals and cardiovascular assessment is now considered to be an expected follow‐up examination. The purpose of this review and proof of concept is to summarize the current research related to the assessment of cardiac function, including echocardiography and blood biomarker data, during the follow‐up period in patients who recovered from COVID‐19. Following a literature review, it was found that right ventricular dysfunction along with global longitudinal strain and diastolic dysfunction are common findings. Finally, more severe acute myocardial injury during the index hospitalization appears to exacerbate cardiac function. The available literature implies that cardiac function must be monitored in patients recovered from COVID‐19 who remain symptomatic and that the impairments and severity vary from person‐to‐person. The proof‐of‐concept analysis of patients with cardiac disease and respiratory disease in comparison to those with sustained symptoms from COVID‐19 suggests elevated systolic time interval in those with sustained symptoms from COVID‐19, thus reducing heart performance indices. Future research must consider the details of cardiac complications during the acute infection period and relate this to the cardiac function in patients with long COVID during mid‐ and long‐term follow‐up.

The Evaluation of Oxidative Stress in the Young Adults with COVID-19 mRNA Vaccines Induced Acute Pericarditis- Myopericarditis

Abstract: Background During COVID-19 pandemic, several vaccines have been developed such as mRNA vaccines. However, acute pericarditis and myocarditis/myopericarditis cases have been described after mRNA vaccination. The mechanism for the development of cardiac involvement is unknown. Potential mechanism for oxidative stress associated with vaccine-induced heart involvement is unidentified. This study aimed to examine the role of oxidative stress and the heart involvement in young adults vaccinated with COVID-19 mRNA vaccines. Methods In this cross-sectional study, a total of 23 participants were included and 10 of these participants were asymptomatic patients (control group). Comparison of the cardiac involvement and control group was made by using troponin I, C-reactive protein (hsCRP), D-dimer levels, and oxidative stress tests including nitric oxide, and imaging techniques (ECG, echocardiography, cardiovascular magnetic resonance). Results The median age of acute pericarditis group (10 patients) was 22 years (Q1-Q3: 18.5–31), and the mean age was 24.4±7.5 years. The median age of myopericarditis group (3 patients) was 22 years (Q1–Q3 18.0–25.0), and the mean age was 21.6 ±3.5 years. All the myopericarditis cases were male. The patients with myopericarditis had higher troponin I level, hsCRP, and D-dimer levels (troponin I level; 1600.00 ng/mL; D-dimer; 1.20 μg/mL, hsCRP; 3.0 mg/L, respectively; p < 0.05). Serum nitric oxide levels and OSI (total oxidant status, H2O2/total antioxidant status) were lower in myopericarditis group than the control and acute pericarditis group (p < 0.05). This shows inflammatory and procoagulant state. Conclusion Vaccine-induced myopericarditis cases are associated with oxidative stress test abnormality (abnormal NO, OSI levels). However, there is no relationship between NO levels and other oxidative stress tests difference in vaccine-induced acute pericarditis. It is thought that vaccine-induced pericarditis and myopericarditis could have different pathogenesis. This could make it necessary to reassess the second dose of vaccination for vaccine-induced cardiac involvement cases.