Zero-contrast left atrial appendage closure, a feasible alternative for patients with a high risk of contrast-induced nephropathy: Systematic literature review and meta-analysis.

BACKGROUND: Left atrial appendage closure (LAAC) is an alternative to reduce thrombotic risk in patients with nonvalvular atrial fibrillation. This procedure conventionally requires the use of a contrast agent. A significant proportion of patients who undergo this procedure have chronic kidney disease, with a high risk of contrast-induced nephropathy. OBJECTIVE: We aimed to systematically review existing literature regarding the feasibility and safety of a zero-contrast LAAC technique. METHODS: We searched the MEDLINE/PubMed, Embase, and Cochrane Central Register of Controlled Trials databases for studies comparing a zero-contrast LAAC technique with conventional LAAC up to April 2024. From each study, we extracted baseline characteristics, feasibility, and safety outcomes. A random model meta-analysis was used to compare outcomes between groups. RESULTS: Five studies reporting data from 367 patients were included. A 100% successful implantation rate was reported in all the zero-contrast groups. The mean number of recaptures reached no significant difference between the groups (mean difference, -0.15; CI, -0.67 to 0.37; I2 = 0%; P = .58). The zero-contrast group had a significantly shorter fluoroscopy time (mean difference, -4.03; CI, -7.72 to -0.34; I2 = 67%; P = .03). Complications related to the procedure, peridevice leak, and device-associated thrombus rates were not significantly different between the groups. CONCLUSION: Zero-contrast LAAC is a feasible alternative. The success and complication rates are consistent with those of conventional LAAC. Aside from the inherent benefit of zero-contrast exposure, this technique allows a reduction in fluoroscopy time.

Molecular and cellular mechanisms leading to catatonia: an integrative approach from clinical and preclinical evidence.

This review aims to describe the clinical spectrum of catatonia, in order to carefully assess the involvement of astrocytes, neurons, oligodendrocytes, and microglia, and articulate the available preclinical and clinical evidence to achieve a translational understanding of the cellular and molecular mechanisms behind this disorder. Catatonia is highly common in psychiatric and acutely ill patients, with prevalence ranging from 7.6% to 38%. It is usually present in different psychiatric conditions such as mood and psychotic disorders; it is also a consequence of folate deficiency, autoimmunity, paraneoplastic disorders, and even autistic spectrum disorders. Few therapeutic options are available due to its complexity and poorly understood physiopathology. We briefly revisit the traditional treatments used in catatonia, such as antipsychotics, electroconvulsive therapy, and benzodiazepines, before assessing novel therapeutics which aim to modulate molecular pathways through different mechanisms, including NMDA antagonism and its allosteric modulation, and anti-inflammatory drugs to modulate microglia reaction and mitigate oxidative stress, such as lithium, vitamin B12, and NMDAr positive allosteric modulators.

Revisiting Excitotoxicity in Traumatic Brain Injury: From Bench to Bedside.

Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality. Consequences vary from mild cognitive impairment to death and, no matter the severity of subsequent sequelae, it represents a high burden for affected patients and for the health care system. Brain trauma can cause neuronal death through mechanical forces that disrupt cell architecture, and other secondary consequences through mechanisms such as inflammation, oxidative stress, programmed cell death, and, most importantly, excitotoxicity. This review aims to provide a comprehensive understanding of the many classical and novel pathways implicated in tissue damage following TBI. We summarize the preclinical evidence of potential therapeutic interventions and describe the available clinical evaluation of novel drug targets such as vitamin B12 and ifenprodil, among others.