eening Instrument evaluation. Further investigations using various endpoints in other populations prenatally exposed to radiation are warranted.
Small studies have noted benefit with the use of catheter-directed therapy (CDT) versus standard of care in treatment of pulmonary embolism, but none have focused on the variability of clinical practice with this modality.
International Classification of Diseases (ICD) codes were used to retrospectively identify consecutive adult patients admitted to an intensive care unit (ICU) with pulmonary embolism over a 2-year period. We evaluated inpatient mortality and major bleeding and assessed treatment variation.
Of 284 patients included, 46 underwent CDT (9 massive pulmonary embolism, 37 submassive pulmonary embolism). Significantly more patients who underwent standard treatment had a history of congestive heart failure and diabetes. Obesity, higher troponin levels, and right heart strain were significantly more likely in the CDT group. No significant difference in inpatient mortality or major bleeding events was observed between the treatment groups. Tissue plasminogen activator use varied widely in the CDT group, and inferior vena cava filter utilization was significantly more common in the CDT group (18; 41%) compared with the standard group (40; 17%) (P < 0.01).
In this study, no significant difference in inpatient mortality or major bleeding was found in patients in the intensive care unit with pulmonary embolism who underwent CDT compared with standard care. It may be beneficial to standardize this procedure given the potential benefit of CDT in patients with submassive pulmonary embolism.
In this study, no significant difference in inpatient mortality or major bleeding was found in patients in the intensive care unit with pulmonary embolism who underwent CDT compared with standard care. Selleckchem PF-06873600 It may be beneficial to standardize this procedure given the potential benefit of CDT in patients with submassive pulmonary embolism.
Cardiac troponin, a marker of myocardial injury, is frequently observed in patients with COVID-19 infection. Our objective was to analyze myocardial injury and its prognostic implications in patients with and without COVID-19 infection treated in the same period of time.
The present study included patients treated in a university hospital with cardiac troponin I measurements and with suspected COVID-19 infection, confirmed or ruled out by polymerase chain reaction analysis. The impact was analyzed of cardiac troponin I positivity on 30-day mortality.
In total, 433 patients were distributed among the following groups confirmed COVID-19 (n=186), 22% with myocardial injury (n=41); and ruled out COVID-19 (n=247), 21.5% with myocardial injury (n=52). The confirmed and ruled out COVID-19 groups had a similar age, sex, and cardiovascular history. Mortality was significantly higher in the confirmed COVID-19 group than in the ruled out group (19.9% vs 5.3%, P <.001). In Cox multivariate regression analysis, cardiac troponin I was a predictor of mortality in both groups (confirmed COVID-19 group HR, 3.54; 95%CI, 1.70-7.34; P=.001; ruled out COVID-19 group HR, 5.57; 95%CI, 1.70-18.20; P=.004). The predictive model analyzed by ROC curves was similar in the 2 groups (P=.701), with AUCs of 0.808 in the confirmed COVID-19 group (0.750-0.865) and 0.812 in the ruled out COVID-19 group (0.760-0.864).
Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances.
Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances.
The ankle-brachial index (ABI) is an indicator of peripheral artery disease (PAD). The aim of this study was to assess the association between PAD, measured with the ABI, and cognitive function in persons with overweight or obesity and metabolic syndrome.
Cross-sectional study conducted with baseline data from the PREDIMED-Plus study, which included 4898 participants (after exclusion of those without ABI measurements) aged between 55 and 75 years, and with overweight or obesity and metabolic syndrome. At the baseline assessment, we measured the ABI with a standardized protocol and assessed the presence of other cardiovascular risk factors (eg, diabetes, dyslipidemia, hypertension). Cognitive function was evaluated using several tests validated for the Spanish population (mini-mental state examination [MMSE], phonological and semantic verbal fluency test, WAIS-III working memory index [WMI], parts A and B of the trail making test (TMT), and clock drawing test). Generalized linear models were used to assess the association between the ABI and cognitive function.
Among the participants, 3.4% had PAD defined as ABI ≤ 0.9, and 3.3% had arterial calcification defined as ABI ≥ 1.4. PAD was associated with age, systolic blood pressure and obesity indicators, while arterial calcification was also associated with obesity and diabetes. No significant associations were observed between cognitive function and ABI or PAD.
In our sample, the presence of PAD increased with age, blood pressure, and obesity. No significant association was observed between ABI, PAD, or cognitive function.
In our sample, the presence of PAD increased with age, blood pressure, and obesity. No significant association was observed between ABI, PAD, or cognitive function.Alzheimer's disease (AD), an age-dependent neurodegenerative disorder, is the main cause of dementia. Common hallmarks of AD include the amyloid β-peptide (Aβ) aggregation, high levels of hyperphosphorylated tau protein (p-tau) and failure in redox homeostasis. To date, all proposed drugs affecting Aβ and/or p-tau have been failed in clinical trials. A decline in the expression of the transcription factor Nrf2 (nuclear factor-erythroid 2-p45 derived factor 2) and its driven genes (NQO1, HO-1, and GCLC), and alteration of the Nrf2-related pathways have been observed in AD brains. Nrf2 plays a critical role in maintaining cellular redox homeostasis and regulating inflammation response. Nrf2 activation also provides cytoprotection against increasing pathologies including neurodegenerative diseases. These lines of evidence imply that Nrf2 activation may be a novel AD treatment option. Interestingly, recent studies have also demonstrated that Nrf2 interferes with several key pathogenic processes in AD including Aβ and p-tau pathways.Selleckchem PF-06873600
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