30 research outputs found

    MR imaging of hepatocellular carcinoma: prospective intraindividual head-to-head comparison of the contrast agents gadoxetic acid and gadoteric acid

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    The routine use of dynamic-contrast-enhanced MRI (DCE-MRI) of the liver using hepatocyte-specific contrast agent (HSCA) as the standard of care for the study of focal liver lesions is not widely accepted and opponents invoke the risk of a loss in near 100% specificity of extracellular contrast agents (ECA) and the need for prospective head-to-head comparative studies evaluating the diagnostic performance of both contrast agents. The Purpose of this prospective intraindividual study was to conduct a quantitative and qualitative head-to-head comparison of DCE-MRI using HSCA and ECA in patients with liver cirrhosis and HCC. Twenty-three patients with liver cirrhosis and proven HCC underwent two 3 T-MR examinations, one with ECA (gadoteric acid) and the other with HSCA (gadoxetic acid). Signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR), wash-in, wash-out, image quality, artifacts, lesion conspicuity, and major imaging features of LI-RADS v2018 were evaluated. Wash-in and wash-out were significantly stronger with ECA compared to HSCA (P < 0.001 and 0.006, respectively). During the late arterial phase (LAP), CNR was significantly lower with ECA (P = 0.005), while SNR did not differ significantly (P = 0.39). In qualitative analysis, ECA produced a better overall image quality during the portal venous phase (PVP) and delayed phase (DP) compared to HSCA (P = 0.041 and 0.008), showed less artifacts in the LAP and PVP (P = 0.003 and 0.034) and a higher lesion conspicuity in the LAP and PVP (P = 0.004 and 0.037). There was no significant difference in overall image quality during the LAP (P = 1), in artifacts and lesion conspicuity during the DP (P = 0.078 and 0.073) or in the frequency of the three major LI-RADS v2018 imaging features. In conclusion, ECA provides superior contrast of HCC-especially hypervascular HCC lesions-in DCE-MR in terms of better perceptibility of early enhancement and a stronger washout

    Mini Review: Sudden Cardiac Death

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    Sudden cardiac death (SCD) is a sudden unexpected death due to a demise of the myocardium. SCD also includes an acute precipitating trigger that lies in the brain and a chronic electrical instability of the myocardium. Most SCDs in absolute terms occur in subjects with no known pre-existing heart disease. The incidence of SCD may be about 20% per year in patients with heart failure and those with markers of arrhythmias, compared with about 1-2% in the general population, i.e., subjects with no “known” pre-existing heart disease. Some early symptoms of SCD include fatigue, fainting, blackouts and dizziness due to blood stopping to flow to the brain and other organs of the body. SCD is responsible for a sizable portion of the over 19 million deaths globally each year from CVDs. Acute anxiety, hypertension, hyperlipidemia, family history, arrhythmias, diabetes mellitus, prediabetes, metabolic syndrome and obesity are risk factors to precipitate SCD. In addition, other behavioral risk factors including type A personality, physical inactivity, smoking, male gender, women after menopause, unhealthy diet and modern lifestyle, such as regularly eating fast foods or foods rich in saturated fats, and late-night sleep; excess sugar, alcohol and salt intake can also predispose to SCD. Deficiency in some cations and vitamins, especially magnesium, potassium, flavonoids and trace elements, and thiamine, have been associated with SCD. One or a combination of these risk factors can lead to pathological conditions and cardiovascular diseases (CVDs) that predispose to SCD. The most common physio-pathological event is the rupture of the vulnerable atherosclerotic plaque with athero-thrombosis, observed in the majority of the patients with acute coronary syndromes (ACSs) and SCD. In an animal experiment, it has been reported that neutrophil-depleted animals had worsened cardiac function, increased fibrosis, and progressively developed heart failure, indicating that high neutrophil counts are considered a predictor of adverse clinical outcomes and mortality in patients with ACS. These cells may have a detrimental effect in the acute inflammatory phase after infarction. ACSs in patients with type 2 diabetes double the risk of SCD, and the risk is greater with higher blood glucose. ACS patients with STEMI and NSTEMI have increased risk of SCD, with several gender differences in presentation to emergency care. Recent advances in cardiac imaging techniques as CMR (Cardiac Magnetic Resonance Imaging) can help in the preclinical detection of patients at risk of serious cardiac arrhythmias and SCD. Late gadolinium has been used to identify areas of myocardial fibrosis which is arrhythmogenic in cardiomyopathy, right ventricular dysplasia and some cases of mitral valve prolapsed syndrome as well. Speckle tracking echocardiography is recently used as an important tool in the diagnosis of non STEMI in critical care departments, which can add greatly to the triage of diagnosis of ACS. Finally, tissue Doppler imaging and deformation imaging is crucial for the early detection of patients at risk for SCD in certain patients with hypertrophic cardiomyopathy in the preclinical phase. In order to prevent SCD, it is imperative to impose an aggressive management of cardiovascular risk factors, including performing exercise regularly, educating patients about the dangers of CVDs, promoting a healthy diet, restricting consumption of sugar and salt, advocating moderation in alcohol consumption and smoking cessation to promote a heart healthy behavior to all, young children in particular

    Pre-heart failure at 2D- and 3D-speckle tracking echocardiography: A comprehensive review

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    Chronic heart failure (CHF) has different stages and includes pre-HF (PHF), a state of high risk of developing myocardial dysfunction and advanced CHF. Some major behavioral risk factors of PHF might predispose to biological risk factors such as obesity, diabetes mellitus, dyslipidemia, hypertension, myocardial infarction, and cardiomyopathy. These risk factors damage the myocytes leading to fibrosis, apoptosis, cardiac hypertrophy, along with alterations in cardiomyocyte’ size and shape. A condition of physiological subcellular remodeling resulting into a pathological state might be developed, conducting to PHF. Both PHF and heart failure (HF) are associated with the activation of phospholipases and protease, mitochondrial dysfunction, oxidative stress and development of intra-cellular free Ca2+ [Ca2+]i overloading to an elevation in diastolic [Ca2+]i. Simultaneously, cardiac gene expression is activated leading to further molecular, structural and biochemical changes of the myocardium. The sub-cellular remodeling may be intimately involved in the transition of cardiac hypertrophy to heart failure. 2D- and 3D-speckle tracking echocardiography (STE) have been used to quantify regional alterations of longitudinal strain and area strain, through their polar projection, which permits a further assessment of both sites and degrees of myocardial damage. The examination of strain can identify sub-clinical cardiac dysfunction or cardiomyocyte remodeling. During remodeling of the myocardium cardiac strain is attenuated, therefore it is an indicator of disease assessment
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