Panminerva medica最新文献

Introduction: Recently, the FFR-Guidance for Complete Nonculprit Revascularization (FULL REVASC) trial in ST elevation myocardial infarction (STEMI) patients with multiple vessel disease (MVD) did not show differences in the composite endpoint of death from any cause, myocardial infarction, or unplanned revascularization than culprit-lesion-only percutaneous coronary intervention (PCI) at 4.8 years, although complete revascularization is a recommendation IA in current guidelines. We want to determine through an updated meta-analysis whether complete revascularization is associated with decreased mortality and hard clinical endpoints compared to culprit lesion only PCI.

Evidence acquisition: We searched MEDLINE, Embase, ISI Web of Science, and Cochrane Central Register of Controlled Trials) from January 1990 to April 2024 using the terms "percutaneous coronary intervention" combined with "non culprit lesions" or "culprit lesion" or "complete revascularization" or "incomplete revascularization." Additionally, a "snowball search" was conducted. Only randomized clinical trials (RCT) reporting mortality, re-infarction or new revascularization after at least 12 months and using predominantly drug eluting stents were included. The summary effect of different revascularization strategies on cardiovascular endpoints was estimated and measures of effect size were expressed as odds ratios (ORs).

Evidence synthesis: Eight RCT involving 9515 patients were included, with a follow-up range between 12 months and 4.8 years. Main findings show that culprit lesion revascularization was associated with an increased risk of MI (OR: 1.38; 95% CI: 1.05 to 1.81, I2 42%) and ischemia-guided revascularization (OR: 2.81; 95% CI: 1.86 to 4.26, I2 80%) compared to complete revascularization, without differences in overall mortality (OR: 1.15; 95% CI: 0.98 to 1.36, I2 2%).

Conclusions: In patients with STEMI and MVD without cardiogenic shock, our metanalysis showed that complete revascularization with PCI significantly reduced the risk of non-fatal myocardial reinfarction and ischemic-driven revascularization compared to culprit vessel-only revascularization, without differences in overall mortality.

Tricuspid regurgitation (TR), an underrecognized disease, overlooked by clinicians for many years due to its assumed benign nature. Recent epidemiological studies suggest significant TR may be seen in up to 6% of elderly patients. An increase in prevalence is expected due to the higher incidence of various clinical predictors of TR progression. Increasing severity of TR is associated with worse outcomes with a novel morphologic classification providing a more refined prediction of outcomes. Advances in cardiac imaging, particularly echocardiography, are integral to the diagnosis of disease severity which not only includes quantitation of TR, but also an assessment of the right atrium, right ventricle and pulmonary arterial circulation. Once identified and quantified, TR management requires a multi-disciplinary heart team management including structural imagers, heart failure specialists, electrophysiologist, cardiac surgeons and interventionalists. Data to support medical therapies are lacking although guidelines support the management of congestive signs and symptoms, as well as comorbidities such as left heart failure and rhythm management. The risks of surgical interventions are slowly improving, however, transcatheter therapies are now available to treat patients with high surgical risk. This manuscript will provide a state-of-art review of this fast-moving field, including current scientific evidences, but also upcoming perspectives with multiple ongoing clinical studies.

Since the publication of the recent North American and European guidelines on management of Clostridioides difficile infection (CDI), new evidence describing the epidemiology, testing and treatment of CDI has emerged. Despite all advances in infection control and antibiotic stewardship, the incidence and burden of CDI in the hospitals and the community remains at a stable high. Coupled with the incidence of primary CDI, there is a stable high incidence of recurrent CDI. Testing for primary and recurrent CDI remains a clinical challenge owing to high sensitivity of the PCR (leading to false positives) and somewhat limited sensitivity of EIA for toxin. The pathophysiology of recurrent CDI involves an ongoing disruption of the microbiota owing to the infection and the treatment of CDI employed. Broad spectrum antibiotics such as vancomycin leads to further disruption of microbiota compared to fidaxomicin which has a lower disruption of the microbiota and leads to fewer recurrences. Owing to these data fidaxomicin is considered as the first line antibiotic for recurrent CDI. Intravenous bezlotoxumab is a monoclonal antibody that reduces the risk of recurrence in high-risk patients but does not restore the microbiota. Experimental fecal microbiota transplantation (FMT) has been available for more than a decade. Owing to the success of FMT, two new non-invasive donor dependent Food and Drug Administration (FDA) approved therapies have been available since late 2022. This review summarizes all these conundrums regarding CDI and provides clinical pearls to use in day-to-day practice.

Background: The finding of mutations that activate epidermal growth factor receptor (EGFR) in people with lung adenocarcinoma resulted in the creation of a new class of biological treatments called tyrosine kinase inhibitors (TKI). These medications have changed how patients with EGFR mutations are clinically managed, nearly doubling their survival rate compared to standard chemotherapy. Though 1st and 2nd generation EGFR TKIs are initially highly effective, typically within 9-14 months all tumors with the mutation progress due to secondary resistance mutations involving alternative molecular pathways. In most cases (up to 60%), this is due to the T790M mutation emerging in the EGFR gene.

Methods: The study included 85 patients with NSCLC with progression of the disease after treatment with TKI 1st and 2nd generation. The T790M mutation was determined by digital polymerase chain reaction (PCR) on the QIAcuity One 5plex digital PCR system and traditional real-time PCR. Real-time PCR analysis of the presence of the T790M mutation was performed using the Therascreen EGFR Plasma RGQ PCR Kit (Qiagen). Using a digital PCR system in QIAcuity One (Qiagen) nanoplanets, the T790M mutation was analysed by digital PCR. The age of the patients ranged from 37 to 85 years.

Results and conclusions: Of 85 patients with NSCLC with disease progression after TKI treatment, T790M mutations were detected during digital PCR in 30 of 85 patients, which is 35.2% of the sample, and with traditional real-time PCR, positive mutations came out only in 3 out of 85 patients.

Background: The aim of this study is to explore the effect of micro ribonucleic acid (miR)-21-5p on spinal cord injury (SCI) in rats and its mechanism of action.

Methods: The rat model of SCI was established, and the key miRNAs were screened using the microarray assay and miRNA-mRNA interaction network. After intrathecal injection of agomir-21 and antagomir-21, the effect of miR-21 expression on motor function recovery of rats was evaluated using the Basso-Beattie-Bresnahan (BBB) score. The expression level of miR-21 in spinal cord tissues was determined via quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and the effect of miR-21 expression on apoptosis in spinal cord tissues was determined via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and Western blotting. Moreover, the effects of agomir-21 and antagomir-21 on SCI-induced expressions of inflammatory factors interleukin-8 (IL-8), IL-1β, IL-6 and tumor necrosis factor-α (TNF-α) in spinal cord tissues were detected through qRT-PCR. Finally, Western blotting was performed to detect the effects of agomir-21 and antagomir-21 on the phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (AKT) signaling pathway and its downstream molecules in each group.

Results: The screening results of the microarray assay revealed that the mRNA and miRNA expression profiles in spinal cord tissues had significant differences in model group from those in sham group. The BBB score was significantly higher in agomir-21 group than that in model group. Compared with that in model group, the apoptosis of spinal cord tissues was obviously weakened in agomir-21 group, while it was obviously enhanced in antagomir-21 group. Agomir-21 group had evidently lower Bax/Bcl-2, and Caspase-3 and Caspase-9 protein expressions, while antagomir-21 group had evidently higher Bax/Bcl-2 and Caspase-3 protein expression than model group. Besides, the expressions of inflammatory factors IL-8, IL-1β, IL-6 and TNF-α were remarkably lower in agomir-21 group than those in model group, while they were remarkably higher in antagomir-21 group than those in model group. Finally, it was found that the protein expressions of phosphorylated PI3K (p-PI3K)/PI3K and p-AKT/AKT rose markedly, while the protein expressions of phosphatase and tensin homolog deleted on chromosome ten (PTEN) and endothelial nitric oxide synthase (eNOS) declined markedly in agomir-21 group compared with those in model group. However, the opposite results were observed in antagomir-21 group compared with those in model group.

Conclusions: MiR-21-5p may reduce the apoptosis and inflammation in spinal cord tissues of rats through the PI3K/AKT pathway.