Corrigendum to “Reducing Cardiac Steatosis: Interventions to Improve Diastolic Function: A Narrative Review”. [Current Problems in Cardiology volume 48 (2023) 1–2]

The authors regret the name of one of the authors of this paper (Razieh Ziaei MD) has been removed from the original paper. The authors would like to apologize for any inconvenience caused

Reducing Cardiac Steatosis: Interventions to Improve Diastolic Function: A Narrative Review

Heart failure is one of the main causes of morbidity and mortality around the globe. Heart failure with preserved ejection fraction is primarily caused by diastolic dysfunction. Adipose tissue deposition in the heart has been previously explained in the pathogenesis of diastolic dysfunction. In this article, we aim to discuss the potential interventions that can reduce the risk of diastolic dysfunction by reducing cardiac adipose tissue. A healthy diet with reduced dietary fat content can reduce visceral adiposity and improve diastolic function. Aerobic and resistance exercises also reduce visceral and epicardial fat and ameliorate diastolic dysfunction. Some medications, include metformin, glucagon-like peptide-1 analogues, dipeptidyl peptidase-4 inhibitors, thiazolidinediones, sodium-glucose co-transporter-2, inhibitors, statins, ACE-Is, and ARBs, have shown different degrees of effectiveness in improving cardiac steatosis and diastolic function. Bariatric surgery has also shown promising results in this field

IgA vasculitis nephritis (Schönlein-Henoch purpura with nephritis) following COVID-19 vaccination

IgA vasculitis nephritis (Schönlein-Henoch purpura nephritis) is an autoimmune circumstance characterized by palpable purpura involving the lower limbs, arthralgia, abdominal pain and kidney involvement. It is possible that a cytokine storm following coronavirus disease 2019 (COVID-19) could lead to an immunological dysregulation responsible for IgA vasculitis nephritis in these cases. Reactivation or first onset of IgA vasculitis nephritis is uncommon; however, there have been increasing reports of this disease, as a complication of COVID-19 vaccination. It is possible that COVID-19 mRNA vaccination may trigger several auto-inflammatory and autoimmune cascades. Previous research has shown that Toll-like receptors play a role in the development of IgA vasculitis nephritis. Following injection of a COVID-19 mRNA vaccine, the uptake of double-stranded RNA by-products will trigger Toll-like receptors, leading to a series of intracellular cascades starting an innate immunity-driven process of cell-mediated and humoral- mediated immunity