Background: With a growing frequency, nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease worldwide. NAFLD has a strong correlation with other metabolic disorders, such as obesity, particularly abdominal obesity, even though the underlying causes or risk factors are not entirely understood. This study aims to investigate correlations between abdominal anthropometric measurements and the presence and intensity of liver steatosis as assessed by unenhanced computed tomography (CT). Methods: One hundred and nineteen patients (male/female, 66/53; mean age 54.54 +/− 12.90 years) underwent abdominal non–contrast-enhanced CT. CT images were examined to determine the attenuation of liver parenchyma, subcutaneous fat depth, and waist circumference (WC). Results: Among all patients, WC (r = −0.78, p < 0.0001), infraumbilical subcutaneous fat thicknesses (r = −0.51, p < 0.0001), right paraumbilical subcutaneous fat thicknesses (r = −0.62, p < 0.0001), and left paraumbilical subcutaneous fat thicknesses (r = −0.53, p < 0.0001) had a high inverse correlation with the liver attenuation values. The presence of T2D (OR: 2.40, p = 0.04), WC (OR: 11.45, p < 0.001), right paraumbilical (OR: 10.09, p < 0.001), left paraumbilical (OR: 2.81, p = 0.01), and infraumbilical (OR: 3.06, p = 0.007) were strongly independent predictors of NAFLD risk. Moreover, regarding the laboratory parameters, only the higher value of GGT (OR: 2.84, p = 0.009) is a predictor of NAFLD risk. Conclusions: Our data show that higher baseline values of all abdominal anthropometric measurements are correlated with liver attenuation and act as predictors of NAFLD risk.

The new coronavirus (COVID-19) outbreak was declared a pandemic by the World Health Organization on March 11, 2020. Since then, important changes have been observed in the medical world, both in terms of patient management and patient presentations to the hospital. A dramatic decrease in the number of cardiovascular emergencies presenting to the emergency rooms has been reported in every country affected by the COVID-19 pandemic. This resulted mainly from the fear of patients to present at the hospital due to the risk of infection with the new coronavirus. Moreover, a significant increase in the time spent for investigations and specialized treatment has been reported for patients suffering from acute cardiovascular diseases. This adds to the longer times reported from symptom onset to presentation, and also to the longer period spent for triage in the emergency room. The aim of this paper is to highlight the dramatic reduction in the number of cardiovascular emergencies during the COVID-19 period and its possible explanations.

Myocarditis is one of the relatively common complications of respiratory infection with SARSCoV-2. As several patients confirmed with the new SARS-CoV-2 are known with cardiovascular disease (CVD) and data from the literature show negative prognosis and a higher risk of complications, this subgroup of subjects represents a particular situation. Therefore, an adequate understanding of the mechanisms involved in myocardial injury and interaction between COVID-19 and CVD is essential for optimal further management. Studies have proved that in COVID-19 patient myocarditis is determined via three pathological mechanisms of cardiomyocyte injury: direct viral cell entry and binding to ACE2, vasculitis-mediated injury, and systemic inflammatory response leading to pro-inflammatory cytokine discharge. Studies show that the incidence of myocarditis in patients with SARS-CoV-2 is relatively low, 4.8%, but myocardial damage occurs in more than 25% of critical cases in the form of acute fulminant myocarditis with severe hemodynamic degradation, or develops when the severity of SARS-CoV-2 infection intensifies. The mortality rate in myocarditis from COVID-19 infection ranges between 50–70%, with poorer prognosis and a higher risk of complications in CVD patients. As in all of these cases increased troponin and natriuretic peptide levels proved to be a negative prognostic factor, for risk stratification and prompt treatment, cardiac biomarkers should be evaluated in all patients with COVID-19.

Introduction: Systemic inflammation plays a key role in the pathophysiology of acute coronary syndrome (ACS), having a direct effect in promoting the progression and rupture of vulnerable coronary plaques. The aim of this study was to investigate the association between inflammatory biomarkers and the type of ACS (ST-elevation myocardial infarction – STEMI, non-ST-elevation myocardial infarction – NSTEMI, or unstable angina – UA) in patients with confirmed heart failure. Material and Methods: This study included a total of 266 patients admitted to the Clinical Department of Cardiology of the County Emergency Clinical Hospital of Târgu Mureș – Cardiac Intensive Care Unit (CICU) for ACS of various types (UA, NSTEMI or STEMI) between January 1, 2017 and December 31, 2020, in whom the diagnosis of heart failure was established based on clinical and paraclinical data. From the total number of patients, 36 were hospitalized for UA and 230 for MI, of which 165 were STEMI and 65 were NSTEMI. Results: Only hs-CRP and IL-6 were significantly higher in MI compared to UA. Mean hs-CRP was 4.9 ± 4.5 mg/mL in patients with UA vs. 20.4 ± 42.2 mg/mL in patients with MI (p = 0.001), and mean IL-6 was 7.2 ± 13.8 pg/mL in UA vs. 31.6 ± 129.2 pg/mL in MI (p <0.0001). ICAM seems to have had a greater discriminating power between STEMI and other types of ACS in those with heart failure, having a value more than double in those with STEMI (216.1 ± 149.6 ng/mL vs. 448.2 ± 754.4 ng/mL, p <0.0001). Conclusions: In patients with heart failure, the increase of inflammatory biomarkers such as hs-CRP is associated with the development of an acute myocardial infarction but not with its type. Adhesion molecules, especially ICAM, are elevated in patients with STEMI compared to other types of ACS, indicating a potential role of endothelial alteration in the development of an ACS when it adds to systemic inflammation linked to heart failure.

Study Type: Retrospective monocentric study. Purpose: To estimate the probability of severe aortic stenosis(SAS) by calculating the aortic valve calcium score (AVCS) using virtual noncontrast (VNC) reconstructions derived from non–ECG-gated dual-energy computed tomography (DECT) scans. Materials and Methods: This study retrospectively included 59 patients who underwent DECT scans for noncardiac indications and presented with visible aortic valve calcifications. AVCS was calculated on VNC images using semiautomatic software. All patients had an echocardiogram performed within 12 months before or after the DECT scan. We then analyzed the correlation between AVCS values and the degree of aortic stenosis. Results: Both male and female patients with SAS had a significantly higher mean AVCS (919.2 AU, SD=1262.4) compared with those with nonsevere aortic stenosis (NSAS) (127.9 AU, SD=278.6). AVCS demonstrated good diagnostic performance in distinguishing between severe and nonsevere AS in both female and male (AUC=0.91 and 0.95, respectively). Estimated thresholds values showed high sensitivity in both genders, with good specificity in men, and moderate in women. When analyzed irrespective of gender, AVCS demonstrated good ability to distinguish severe AS from mild and no stenosis (AUC=0.926), and moderate ability to distinguish moderate AS from mild and no stenosis (AUC=0.781). However, it lacked statistical significance in discriminating severe and moderate AS (AUC=0.714, P =0.1325). Conclusions: Aortic Valve Calcium Score obtained on VNC images from DECT examinations is a promising method for noninvasively differentiation between severe and nonsevere aortic stenosis, which could be potentially useful in patients who have undergone examinations for noncardiac indications.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) has been defined as clinical presentation of an acute coronary syndrome with laboratory evidence of myocardial necrosis, but with coronary stenosis of less than 50% on coronary angiography. On the other side, myocarditis is an inflammatory response triggered by viral, bacterial, fungal, lymphocytic, eosinophilic, or autoimmune myocardial injury, which may be associated with elevated myocardial necrosis serum biomarkers. We present the case of a young male patient with acute chest pain, ST-segment elevation, and high-sensitivity troponin levels of 22,162 ng/L.