Panminerva medica最新文献

Rheumatoid arthritis (RA) is an autoimmune inflammatory condition that primarily affects the joints and periarticular soft tissue. The development of joint swelling is traditionally regarded as the starting point of the disease. Emerging evidence indicates that RA patients often experience a preclinical stage characterized by immunological and inflammatory changes before developing the disease. The review discusses ongoing efforts to predict the transition from this preclinical phase to clinical RA and describes studies aimed at preventing the onset of RA in individuals at risk. Over the past two decades, there have been significant advancements in RA management and outcomes. An increasing number of patients can now achieve disease remission, and in some cases, this remission persists without ongoing treatment, which is effectively a cure. As new therapies and evolving scientific evidence emerge, recommendations for RA management are continuously evolving. Despite these improvements in the management of RA, many patients still do not respond to multiple conventional or more advanced therapies, including biologic and targeted synthetic disease modifying anti-rheumatic drugs, or experience disease flares when treatments are tapered or discontinued. This situation underscores the need for reliable biomarkers to guide therapy more effectively, improve personalized treatment approaches and monitoring strategies (i.e. precision medicine). In conclusion, this review provides a comprehensive overview of RA, covering new research on the 'pre-clinical' phase of the disease, as well as its epidemiology, pathogenesis, clinical manifestations, diagnosis, imaging, and management strategies. It highlights key clinical aspects of RA and addresses ongoing challenges in disease management, particularly in the areas of prevention and treatment.

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.

Background: Takotsubo syndrome (TTS) is an acute reversible heart dysfunction affecting mostly post-menopausal women, frequently precipitated by a significant stressful event, presenting as an acute coronary syndrome (ACS) in the absence of obstructive coronary artery disease. The pathogenesis is not fully understood, but a close relationship between individual's mind, brain, neuroendocrine system and the heart may be involved in a mind-heart axis. The purpose of this study was to compare the prevalence of psychopathological findings in TTS patients as compared to healthy subjects, patients affected by psychiatric diseases and patients affected by ACS.

Methods: This observational study enrolled 40 female subjects divided into 4 subgroups: TTS patients, healthy subjects, psychiatric patients and ACS patients, matched for age. Psychosocial factors and psychopathological dimensions have been evaluated. Patients who signed informed consent were interviewed by the administration of a complex psychometric battery, including Mini International Neuropsychiatric Interview, Hamilton Rating Scale for Depression, State Trait Anxiety Inventory, Form Y.

Results: Comparing the groups, the TTS group showed a statistically significant difference vs. ACS group concerning psychological violence subscale (P=0.049) of the Childhood Trauma Questionnaire, while significant statistical difference emerged in TTS group vs. healthy subjects control group, regarding cyclothymia subscale (P=0.008). Statistically significant differences were documented in TTS group vs. psychiatric cohort in cyclothymia subscale (P=0.012). Moreover, comparison between TTS and ACS group, revealed a statistically significant difference in the sub-scale of self-confidence and management of negative emotions (P=0.0028). One of the most significant features was the evidence of statistically significant differences in TTS vs. ACS group, concerning total and average value of anxiety (P=0.014 and P=0.031 respectively) and in the comparison of TTS group vs. healthy subjects (P=0.005 for the total anxiety value and P=0.021 for the average value). Finally, both depression and mania were statistically significant raised in the TTS group compared to the healthy subjects' group (P=0.00 and P=0.013, respectively).

Conclusions: Psychosocial and psychopathological dimensions of TTS patients have been explored and analyzed in a cohort of TTS patients vs. ACS, healthy subjects and psychiatric patients, showing statistically significant differences among the various groups. Psychopathological symptoms were more frequent in TTS patients, suggesting an evident involvement of mind-heart axis in this disease. Future studies are needed to investigate the cause-effect relationship between psychopathological features and the occurrence of TTS.

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 p38 mitogen-activated protein kinase pathway plays an important role in the pathogenesis of osteoarthritis (OA) involving in hypertrophy, calcification, and apoptosis of chondrocytes (CHs). In this study, we focused on a p38 inhibitor named Pamapimod (PAM) in the effect of CH hypertrophy degeneration.

Methods: CHs were isolated from the cartilage collected from OA patients. Insulin-Transferrin-Selenium (ITS) medium was used as a hypertrophic inducer to establish CH hypertrophy model. Asiatic acid (AA) was used to activate p38 phosphorylation. We transfected CHs with myocyte enhancer factor 2C (MEF2C)-plasmid to upregulate MEF2C expression. Chondrogenic gene expression such as type II collagen and SOX-9, and hypertrophic genes such as type X collagen, MMP-13, and Runx-2 were analyzed by western blot, real-time polymerase chain reaction or immunofluorescence.

Results: ITS and AA all contributed to the CHs hypertrophy with an upregulation of p-p38 and MEF2C protein expression. PAM treatments significantly inhibited p-p38 and MEF2C expression, down-regulated type X collagen, MMP-13, and Runx-2 expression and upregulated type II collagen and SOX-9 levels. PAM indirectly affected MEF2C expression and resulted in CHs hypertrophy suppression.

Conclusions: PAM protects CHs hypertrophy by the inhibition of the p38/MEF2C pathway.