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BACKGROUND: The COVID-19 (coronavirus disease 2019) pandemic is a global health emergency that is straining health care resources. Identifying patients likely to experience severe illness would allow more targeted use of resources. This study aimed to investigate the association between the thymus index (TI) on thorax computed tomography (CT) and prognosis in patients with COVID-19. METHODS: A multicenter, cross-sectional, retrospective study was conducted between March 17 and June 30, 2020, in patients with confirmed COVID-19. The patients' clinical history and laboratory data were collected after receiving a signed consent form. Four experienced radiologists who were blinded to each other and patient data performed image evaluation. The appearance of the thymus was assessed in each patient using 2 published systems, including the TI and thymic morphology. Exclusion criteria were lack of initial diagnostic thoracic CT, previous sternotomy, pregnancy, and inappropriate images for thymic evaluation. A total of 2588 patients with confirmed COVID-19 and 1231 of these with appropriate thoracic CT imaging were included. Multivariable analysis was performed to predict the risk of severe disease and mortality. RESULTS: The median age was 45 (interquartile range, 33-58) years; 52.2% were male. Two hundred forty-nine (20.2%) patients had severe disease, and 60 (4.9%) patients died. Thymus index was significantly associated with mortality and severe disease (odds ratios, 0.289 [95% confidence interval, 0.141-0.588; P = 0.001]; and 0.266 [95% confidence interval, 0.075-0.932; P = 0.038]), respectively. Perithymic lymphadenopathy on CT imaging had a significantly strong association with grades of TI in patients with severe disease and death ( V = 0.413 P = 0.017; and V = 0.261 P = 0.002, respectively). A morphologically assessable thymus increased the probability of survival by 17-fold and the absence of severe disease by 12-fold. CONCLUSION: Assessment of the thymus in patients with COVID-19 may provide useful prognostic data for both disease severity and mortality.

Acute heart failure (AHF) represents a broad spectrum of disease states, resulting from the interaction between an acute precipitant and a patient's underlying cardiac substrate and comorbidities. Valvular heart disease (VHD) is frequently associated with AHF. AHF may result from several precipitants that add an acute haemodynamic stress superimposed on a chronic valvular lesion or may occur as a consequence of a new significant valvular lesion. Regardless of the mechanism, clinical presentation may vary from acute decompensated heart failure to cardiogenic shock. Assessing the severity of VHD as well as the correlation between VHD severity and symptoms may be difficult in patients with AHF because of the rapid variation in loading conditions, concomitant destabilization of the associated comorbidities and the presence of combined valvular lesions. Evidence-based interventions targeting VHD in settings of AHF have yet to be identified, as patients with severe VHD are often excluded from randomized trials in AHF, so results from these trials do not generalize to those with VHD. Furthermore, there are not rigorously conducted randomized controlled trials in the setting of VHD and AHF, most of the data coming from observational studies. Thus, distinct to chronic settings, current guidelines are very elusive when patients with severe VHD present with AHF, and a clear-cut strategy could not be yet defined. Given the paucity of evidence in this subset of AHF patients, the aim of this scientific statement is to describe the epidemiology, pathophysiology, and overall treatment approach for patients with VHD who present with AHF.

Introduction: Cardiovascular diseases (CVDs) are the leading cause of death worldwide according to World Health Organization (WHO) data. Atherosclerosis is considered as a chronic inflammatory disease that develops in response to damage to the vascular intima-media layer in most cases. In recent years, epigenetic events have emerged as important players in the development and progression of CVDs. Since noncoding RNA (ncRNAs) are important regulators in the organization of the pathophysiological processes of the cardiovascular system, they have the potential to be used as therapeutic targets, diagnostic and prognostic biomarkers. In this study long noncoding RNA (lncRNA) and mRNA gene expression were compared between coronary atherosclerotic plaques (CAP) and the internal mammary artery (IMA) which has the same genetic makeup and is exposed to the same environmental stress conditions with CAP in the same individual. Methods: lncRNA and mRNA gene expressions were determined using the microarray in the samples. Microarray results were validated by RT-qPCR. Differentially expressed genes (DEGs; lncRNAs and mRNAs) were determined by GeneSpring (Ver 3.0) [p values < 0.05 and fold change (FC) > 2]. DAVID bioinformatics program was used for Gene Ontology (GO) annotation and enrichment analyses of statistically significant genes between CAP and IMA tissue. Results and Conclusions: In our study, 345 DEGs were found to be statistically significant (p < 0.05; FC > 2) between CAP and IMA. Of these, 65 were lncRNA and 280 were mRNA. Thirty-three lncRNAs were upregulated, while 32 lncRNAs were downregulated. Some of the important mRNAs are SPP1, CYP4B1, CHRDL1, MYOC, and ALKAL2, while some of the lncRNAs are LOC105377123, LINC01857, DIO3OS, LOC101928134, and KCNA3 between CAP and IMA tissue. We also identified genes that correlated with statistically significant lncRNAs. The results of this study are expected to be an important source of data in the development of new genetically based drugs to prevent atherosclerotic plaque. In addition, the data obtained may contribute to the explanation of the epigenetic mechanisms that play a role in the pathological basis of the process that protects the IMA from atherosclerosis.

© 2023 Turkish Society of Cardiology. All rights reserved.Objective: Diabetes mellitus (DM) progresses with dynamic changes in renal blood flow and glomerular filtration. Renal frame count (RFC) is a cineangiographical parameter that is capable of presenting microvascular and macrovascular changes in the renal blood flow. We aimed to show the changes, which may be caused by DM in the perfusion, by using RFC. Methods: A total of 110 hypertensive subjects consisting of 55 DM patients and 55 non-DM patients, as a control group who underwent renal angiography, were retrospectively enrolled in the study. The RFC values of all subjects were calculated and compared to each other. Results: There were no significant differences between the two groups in terms of basal demographic characteristics and antihypertensive medications. The RFC value measured from the left renal artery was significantly lower in the DM group compared to the control group (11.33 ± 2.55, 13.49 ± 3.24, respectively; P

Acute heart failure is associated with high mortality and rehospitalization rates and required urgent evaluation and early initiation or intensification of therapy. The risk of death and heart failure rehospitalization is greatest in the early post-discharge period, particularly within the first 3-6 months, and declines over time, which is referred as a vulnerable period of acute heart failure hospitalization. Therefore, implementation of guidelines-directed optimal therapy is not only so crucial in the acute phase but also very important in the pre-discharge and early post-discharge period in reducing mortality and rehospitalization rates. The pre-discharge period represents a window of opportunity for treatment optimization which includes to eliminate congestion, to treat comorbidities or precipitating factors, and to initiate or uptitrate oral therapy before discharge. Early assessment in the post-discharge period based on clinical evaluation and laboratory exams, further optimization of disease-modifying therapy is associated with lower 30-day hospitalization for heart failure. In clinical practice, clinicians usually focus on acute phase intravenous medications and short-term device therapies and, in fact, neglect short- and long-term comprehensive approaches. This paper reviews management strategies that may help reduce mortality and heart failure rehospitalizations in pre-discharge and post-discharge periods and include adopting holistic approaches for heart failure, increasing optimization of evidence-based therapies, treating cardiac and noncardiac comorbidities, improving care transitions, monitoring, and disease management.

Objective: Predicting outcomes is an essential part of evaluation in patients with heart failure (HF). While there are multiple individual laboratory and imaging variables, as well as risk scores available for this purpose, they are seldom useful during the initial evaluation. In this analysis, we aimed to understand predictive usefulness of Thrombosis in Myocardial Infarction Risk Index (TIMI-RI), a simple index that is calculated at bedside using three commonly available variables, using data from a multicenter HF registry. Subjects and Methods: A total of 728 patients from 23 centers were included to this analysis. Data on hospitalizations and mortality were collected by direct interviews, phone calls and electronic databases. TIMI-RI was calculated as defined before. Patients were divided into three equal tertiles to perform analyses. Results: Rehospitalization for HF was significantly higher in patients within the 3rd tertile, and 33.5% of patients within the 3rd tertile were dead within one-year follow up as compared to 14.5% of patients within the 1st tertile and 15.6% patients within the 2nd tertile (p

Warfarin therapy has some difficulties in terms of close monitoring and dosage. This study aims to evaluate the effect of same-fixed versus different-variable physician-based monitoring of warfarin therapy on treatment quality and clinical end-points.A total of 625 consecutive patients requiring warfarin treatment were enrolled at seven centers. INR values of the patients measured at each visit and registered to hospital database were recorded. Time in therapeutic range (TTR) was calculated using linear interpolation method (Rosendaal's method). A TTR value of ≥65% was considered as effective warfarin treatment. If a patient was evaluated by the same-fixed physician at each INR visit, was categorized into the same-physician (SP) group. In contrast, if a patient was evaluated by different-variable physicians at each INR visit, was categorized into variable physician (VP) group. Enrolled patients were followed up for bleeding and embolic events.One hundred and fifty-six patients (24.9%) were followed by SP group, 469 (75.1%) patients were followed by VP group. Median TTR value of the VP group was lower than that of SP group (56.2% vs. 65.1%, respectively, p=0.009). During median 25.5 months (9-36) of follow-up, minor bleeding, major bleeding and cerebral embolic event rates were higher in VP group compared to SP group (p0.001, p=0.023, p0.001, respectively). In multivariate analysis, INR monitoring by VP group was found to be an independent predictor of increased risk of bleeding events (OR 2.55, 95% CI 1.64-3.96, p0.001) and embolism (OR 3.42, 95% CI 1.66-7.04, p=0.001).INR monitoring by same physician was associated with better TTR and lower rates of adverse events during follow-up. Hence, it is worth encouraging an SP-based outpatient follow-up system at least for where warfarin therapy is the only choice.

Heart failure (HF) has been classified as reduced ejection fraction (HFrEF), mildly reduced ejection fraction (HFmrEF) and preserved ejection fraction (HFpEF) by the recent HF guidelines. In addition, HF with improved ejection fraction has been defined as a subgroup of HFrEF. In HFrEF, diagnostic workup and evidence-based pharmacological and device-based therapies have been well established. However, HFpEF, which comprises almost half of the HF population, represents significant uncertainties regarding its pathophysiology, clinical phenotypes, diagnosis and treatment. Diagnostic criteria of HFpEF have been changed a few times over the years and still remained a matter of debate. New paradigms including a prominent role of co-morbidities. inflammation, endothelial dysfunction have been proposed in its pathophysiology. As a complex, multifactorial syndrome HFpEF consists of many overlapping clinical and hemodynamic phenotypes. In contrast to HFrEF, clinical outcomes of HFpEF have not improved over the last decades due to lack of proven effective therapies. Although HFrEF and HFpEF have different clinical spectrums and proposed pathophysiological mechanisms, there is no clear defining syndrome postulated for HFmrEF. Clinical characteristics and risk factors of HFmrEF overlap with HFrEF and HFpEF. HFmrEF is also referred as a transitional zone for dynamic temporal changes in EF. So. HFpEF and HFmrEF, both namely HF with non-reduced ejection fraction (HF-NEF), have some challenges in the management of HF. The purpose of this paper is to provide a comprehensive review including epidemiology, pathophysiology, clinical presentation and phenotypes of HF-NEF and to guide clinicians for the diagnosis and therapeutic approaches based on the available data in the literature.