Cannabidiol (CBD) is the primary non-psychoactive chemical from Cannabis Sativa, a plant used for centuries for both recreational and medicinal purposes. CBD lacks the psychotropic effects of Δ9-tetrahydrocannabinol (Δ9-THC) and has shown great therapeutic potential. CBD exerts a wide spectrum of effects at a molecular, cellular, and organ level, affecting inflammation, oxidative damage, cell survival, pain, vasodilation, and excitability, among others, modifying many physiological and pathophysiological processes. There is evidence that CBD may be effective in treating several human disorders, like anxiety, chronic pain, psychiatric pathologies, cardiovascular diseases, and even cancer. Multiple cellular and pre-clinical studies using animal models of disease and several human trials have shown that CBD has an overall safe profile. In this review article, we summarize the pharmacokinetics data, the putative mechanisms of action of CBD, and the physiological effects reported in pre-clinical studies to give a comprehensive list of the findings and major effects attributed to this compound.

Cannabidiol (CBD), a non-psychoactive compound derived from Cannabis Sativa, has garnered increasing attention for its diverse therapeutic potential. This comprehensive review delves into the complex pharmacokinetics of CBD, including factors such as bioavailability, distribution, safety profile, and dosage recommendations, which contribute to the compound’s pharmacological profile. CBD’s role as a pharmacological inhibitor is explored, encompassing interactions with the endocannabinoid system and ion channels. The compound’s anti-inflammatory effects, influencing the Interferon-beta and NF-κB, position it as a versatile candidate for immune system regulation and interventions in inflammatory processes. The historical context of Cannabis Sativa’s use for recreational and medicinal purposes adds depth to the discussion, emphasizing CBD’s emergence as a pivotal phytocannabinoid. As research continues, CBD’s integration into clinical practice holds promise for revolutionizing treatment approaches and enhancing patient outcomes. The evolution in CBD research encourages ongoing exploration, offering the prospect of unlocking new therapeutic utility.

BACKGROUND: Decompensated heart failure with reduced ejection fraction (HFrEF) is associated with systemic inflammation that predicts unfavorable outcomes. We aimed to determine whether anakinra, an IL-1 (interleukin-1) blocker, favors inflammation resolution (CRP [C-reactive protein]) and improves peak oxygen consumption (VO ₂ ) in patients with recently decompensated HFrEF. METHODS: We randomized 102 adult patients recently hospitalized for HFrEF and CRP ≥2 mg/L (2:1) to receive anakinra 100 mg subcutaneously daily (n=68) or placebo for 24 weeks (n=34). The primary end point was the peak VO ₂ change at 24 weeks. Data are presented as median (Q1, Q3) or number (%). RESULTS: Of the 102 patients, 84 had primary end point data available (57 treated with anakinra and 27 with placebo). Peak VO ₂ increased from 13.0 (10.9, 17.0) to 14.9 (12.0, 18.0) mL·kg⁻ ¹ ·min⁻ ¹ ( P <0.001) in the entire cohort, without significant differences between anakinra and placebo (+1.5 [−0.2, +3.4] and +1.2 [+0.5, +3.9] mL·kg⁻ ¹ ·min⁻ ¹ , respectively; P =0.40; median difference +0.30 mL·kg⁻ ¹ ·min⁻ ¹ [95% CI from −1.70 to +0.90]). A significant reduction in CRP levels was seen, with a −76% (−87%, −36%) in anakinra-treated patients and −48% (−77%, +14%) in the placebo group ( P =0.050 between groups). There were no unexpected treatment-related serious adverse events, and no differences in HFrEF events between groups. CRP<2 mg/L was achieved in 47% and 37% of the anakinra and placebo groups, respectively ( P =0.48). Patients achieving CRP<2 mg/L had a significantly greater increase in peak VO ₂ versus those with CRP≥2 mg/L (+2.6 [+0.7, +4.6] and +1.0 [−0.3, +1.9] mL·kg⁻ ¹ ·min⁻ ¹ ; P =0.007) and lower rates of HFrEF-related events (8% and 26%; P =0.045). CONCLUSIONS: Patients with recently decompensated HFrEF treated with maximally tolerated medical therapy had a significant improvement in CRP and peak VO ₂ . The addition of anakinra had a modest effect on CRP levels and no significant effect on peak VO ₂ or other clinically relevant secondary end points. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03797001.

Introducción: La endocarditis infecciosa (EI) es una complicación poco frecuente pero grave tras el reemplazo valvular aórticopor vía transcatéter (TAVR), con una evolución generalmente adversa. Objetivo: Describir la incidencia, características y evolución clínica intrahospitalaria de la EI post-TAVR. Material y métodos: Estudio unicéntrico, observacional y retrospectivo que incluyó pacientes mayores de 18 años con TAVRentre marzo de 2015 y mayo de 2025. La EI se clasificó como precoz (≤1 año post-TAVR) o tardía (>1 año), según criterios deDuke modificados. Se analizaron datos clínicos, microbiológicos e imagenológicos, tratamiento recibido, indicación quirúrgicay mortalidad intrahospitalaria. Resultados: Se incluyeron 521 pacientes con mediana de edad de 84 años (rango intercuartílico, RIC, 79-87); 65 % mujeres. Laincidencia de EI fue del 2,3 % (n=12): 42 % precoces y 58 % tardías. La mediana de edad del subgrupo con EI fue 83 años (RIC78-86), el 75 % hombres. Enterococcus faecalis fue el patógeno más frecuente. Ocho pacientes presentaron fiebre como síntomainicial, nueve vegetaciones ecocardiográficas, y cuatro fenómenos embólicos. Cuatro pacientes tuvieron indicación quirúrgica,pero solo uno fue operado. La mortalidad intrahospitalaria fue del 16 % (n=2), asociada a indicación quirúrgica no llevada acabo por fragilidad. Todos los pacientes recibieron antibiótico dirigido, y un tercio tratamiento supresivo en el seguimiento. Conclusiones: La EI post-TAVR presentó una prevalencia del 2,3 % en nuestra cohorte. Su evolución clínica, con alta morbimortalidad y limitada posibilidad quirúrgica, subraya la necesidad de estrategias diagnósticas y terapéuticas tempranas paramejorar el pronóstico.