Association of Cardiovascular Diseases With Post-Traumatic Stress Disorder: An Updated Review.

The intricate relationship between post-traumatic stress disorder (PTSD) and cardiovascular disease (CVD) has garnered increasing attention due to its bidirectional impact and potential for significant health consequences. Epidemiological evidence suggests that PTSD may serve as a risk factor for incident CVD, while acute CVD events can trigger PTSD, subsequently increasing the risk of recurrent cardiovascular events. This dynamic interplay is characterized by the human stress response, disrupted behavioral and lifestyle factors, and potential physiological mechanisms. Notably, the immediate aftermath of a cardiovascular event presents a critical window for intervention, offering the possibility of preventing the development of PTSD and its associated physiological and behavioral sequelae. However, while candidate mechanisms linking PTSD and CVD have been identified, determining which mechanisms are most amenable to intervention remains a challenge. This article emphasizes the urgency of addressing key unanswered questions in this domain. Despite an evolving understanding of the association between PTSD and CVD, causal relationships remain to be firmly established. Comprehensive investigations into the intricate interplay of behavioral and biological mechanisms are essential for identifying precise targets for intervention. Innovations in research methodologies, including the exploration of PTSD symptom dynamics and their impact on cardiovascular function, hold the potential for identifying crucial intervention points. Drawing parallels from prior challenges in translating identified risk factors into effective interventions, the field must prioritize systematic investigations and early-phase intervention trials. By doing so, researchers and clinicians can potentially develop strategies to mitigate CVD risk in the context of PTSD and improve both cardiovascular and mental health outcomes.

The Synergistic Relationship Between Atrial Fibrillation and Diabetes Mellitus: Implications for Cardiovascular and Metabolic Health.

Type 2 diabetes mellitus (T2DM) and atrial fibrillation (AF) are widespread chronic conditions that profoundly impact public health. While the intricate mechanisms linking these two diseases remain incompletely understood, this review sets out to comprehensively analyze the current evidence about their pathophysiology, epidemiology, diagnosis, prognosis, and treatment. We reveal that T2DM can influence the electrical and structural properties of the atria through multiple pathways, including oxidative stress, inflammation, fibrosis, connexin remodeling, glycemic variability, and autonomic dysfunction. Moreover, it significantly influences AF's clinical course, elevating the risk of heart failure, stroke, and cardiovascular mortality. Our review also explores treatment options for individuals with T2DM and AF, encompassing antidiabetic and antiarrhythmic drugs and non-pharmacological interventions, such as cardioversion catheter ablation and direct current cardioversion. This review depicts an insight into the clinical interplay between T2DM and AF. It deepens our comprehension of the fundamental mechanisms, potential therapeutic interventions, and their implications for patient care. This comprehensive resource benefits researchers seeking to deepen their knowledge in this domain. Ultimately, our findings pave the way for more effective strategies in managing AF within the context of T2DM.

Management of Steroid-Resistant Nephrotic Syndrome in Children.

Nephrotic syndrome (NS) affects 115-169 children per 100,000, with rates varying by ethnicity and location. Immune dysregulation, systemic circulating substances, or hereditary structural abnormalities of the podocyte are considered to have a role in the etiology of idiopathic NS. Following daily therapy with corticosteroids, more than 85% of children and adolescents (often aged 1 to 12 years) with idiopathic nephrotic syndrome have full proteinuria remission. Patients with steroid-resistant nephrotic syndrome (SRNS) do not demonstrate remission after four weeks of daily prednisolone therapy. The incidence of steroid-resistant nephrotic syndrome in children varies between 35 and 92 percent. A third of SRNS patients have mutations in one of the important podocyte genes. An unidentified circulating factor is most likely to blame for the remaining instances of SRNS. The aim of this article is to explore and review the genetic factors and management of steroid-resistant nephrotic syndrome. An all language literature search was conducted on MEDLINE, COCHRANE, EMBASE, and Google Scholar till September 2021. The following search strings and Medical Subject Headings (MeSH) terms were used: "Steroid resistance", "nephrotic syndrome", "nephrosis" and "hypoalbuminemia". We comprehensively reviewed the literature on the epidemiology, genetics, current treatment protocols, and management of steroid-resistant nephrotic syndrome. We found that for individuals with non-genetic SRNS, calcineurin inhibitors (cyclosporine and tacrolimus) constitute the current mainstay of treatment, with around 70% of patients achieving full or partial remission and an acceptable long-term prognosis. Patients with SRNS who do not react to calcineurin inhibitors or other immunosuppressive medications may have deterioration in kidney function and may develop end-stage renal failure. Nonspecific renal protective medicines, such as angiotensin-converting enzyme inhibitors, angiotensin 2 receptor blockers, and anti-lipid medications, slow the course of the illness. Recurrent focal segmental glomerulosclerosis in the allograft affects around a third of individuals who get a kidney transplant, and it frequently responds to a combination of plasma exchange, rituximab, and increased immunosuppression. Despite the fact that these results show a considerable improvement in outcome, further multicenter controlled studies are required to determine the optimum drugs and regimens to be used.