Sodium-glucose cotransporter 2 inhibitors (SGLT2is) reduce cardiovascular events, especially in diabetic patients. However, the cardioprotective effects of early SGLT2i administration following acute myocardial infarction (AMI) remain unclear. This study aims to investigate the impact of SGLT2is on clinical outcomes in patients post-AMI. A comprehensive search was conducted in PubMed, CENTRAL, WOS, Scopus, and EMBASE up to April 2024. Risk ratio (RR) was used for dichotomous outcomes and mean difference (MD) for continuous outcomes, with 95% confidence intervals (CI). Seven studies with 11,407 patients were included. SGLT2is did not significantly reduce the incidence of major adverse cardiovascular events (MACE) (RR = 0.94, 95% CI [0.68, 1.29], p = 0.69), all-cause mortality (RR = 1.01, 95% CI [0.84, 1.21], p = 0.93), or stroke (RR = 0.61, 95% CI [0.29,1.28], p = 0.19). However, SGLT2is significantly reduced the risk of heart failure (RR = 0.76, 95% CI [0.63, 0.91], p < 0.01) and improved left ventricular ejection fraction (MD = 1.86, 95% CI [1.58, 2.14], p < 0.01). In post-AMI patients, SGLT2is do not significantly affect MACE or mortality but are associated with reduced heart failure risk and improved ejection fraction. PROSPERO identifier number: CRD42024506806.

Background and Objectives: The epidemiological data regarding mortality rates of adults with sarcoidosis and non-ischemic cardiovascular disease (CVD) are limited. A retrospective observational analysis was conducted to identify trends and disparities related to sarcoidosis and non-ischemic cardiovascular disease mortality among the adult US population from 1999 to 2022. Methods: We used the Centers for Disease Control and Prevention (CDC) WONDER database to extract death certificate data for the adult US population (≥25 years). The age-adjusted mortality rates (AAMRs) per 100,000 persons were calculated, and annual percent changes (APCs) were determined using Joinpoint. Results: Between 1999 and 2022, 23,642 deaths were identified related to non-ischemic CVD + sarcoidosis. The overall AAMR increased from 0.2 (95% CI, 0.2 to 0.3) in 1999 to 0.5 (95% CI, 0.5 to 0.6) in 2022. Females had a higher AAMR than males (0.6 vs. 0.5). Non-Hispanic (NH) blacks had the highest AAMR, followed by NH whites and Hispanic or Latinos. The southern region had the highest AAMR (0.7: 95% CI, 0.6–0.7), followed by the Midwest (0.6, 95% CI, 0.54–0.669), the Northeast (0.5, 95% CI, 0.5 to 0.6), and the West (0.4; 95% CI, 0.3–0.4). Urban and rural areas had comparable mortality rates (0.5 vs. 0.6). People aged 65+ had the highest AAMRs. Conclusions: The overall mortality rates for non-ischemic CVD and sarcoidosis have increased in the US from 1999 to 2022. Females and NH blacks had higher AAMRs, while a minimal variation was observed based on geographical regions. Early diagnosis and prompt management are the keys to reducing the mortality burden of non-ischemic CVD plus sarcoidosis.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) affects multiple body systems, including the nervous system. Cerebrovascular accidents can also occur. Patients with comorbid illnesses have severe manifestations and poor outcomes. Despite the proper mechanism of SARS-CoV-2 infection-associated stroke having not yet been settled, various possible mechanisms have been hypothesized. One possibility is that the virus causes endothelial dysfunction and immune-mediated injury. Another possibility is that the trans-neuronal spread of the virus affects brain tissue. In addition, hypercoagulability caused by SARS-CoV-2 infection could lead to a stroke. A virus-induced dysfunction of the renin-angiotensin system could also lead to a stroke. The immune response and vasculitis resulting from SARS-CoV-2 infection are also possible causes via a cytokine storm, immune dysfunction, and various inflammatory responses. SARS-CoV-2 infection may affect calcitonin gene-related peptides and cerebral blood flow and may lead to stroke. Finally, SARS-CoV-2 may cause hemorrhagic strokes via mechanisms stimulated by its interaction with angiotensin-converting enzyme 2 (ACE2), leading to arterial wall damage and blood pressure changes. In this article, we will present seven cases of stroke-associated SARS-CoV-2 infection.

It’s been 10 years now from the debut of clustered regularly interspaced short palindromic repeats-associated protein 9 (CRISPR/Cas9) era in which gene engineering has never been so accessible, precise and efficient. This technology, like a refined surgical procedure, has offered the ability of removing different types of disease causing mutations and restoring key proteins activity with ease of outperforming the previous resembling methods: zinc finger nucleases (ZFNs) and transcription activator-like effector nucleases (TALENs). Additionally, CRISPR-Cas9 systems can systematically introduce genetic sequences to the specific sites in the human genome allowing to stimulate desired functions such as anti-tumoral and anti-infectious faculties. The present brief review provides an updated resume of CRISPR-Cas9’s top achievements from its first appearance to the current date focusing on the breakthrough research including in vitro, in vivo and human studies. This enables the evaluation of the previous phase ‘the proof-of-concept phase’ and marks the beginning of the next phase which will probably bring a spate of clinical trials.

Introduction. Heart failure is a diverse life-threatening condition with complex biology and demanding therapeutic goals. Even when anemic patients are excluded, up to 59% of heart failure patients have low ferritin levels, making them especially vulnerable to iron deficiency. We aim to explore the benefits and safety of intravenous iron therapy among patients with heart failure and iron deficiency. Material and methods. We have searched the literature on PubMed (MEDLINE), Scopus, Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science (WoS), and EMBASE until 31st August, 2023. We used RevMan V. 5.4 to pool dichotomous data using a risk ratio (RR) with a 95% confidence interval (CI). This review has been registered and published in PROSPERO (CRD42023471419) Results. Fourteen randomized controlled trials with 6,626 patients were included. The intravenous iron group was favored over the control group in reducing hospital admissions for heart failure (first event) (RR= 0.83, 95% CI 0.71 to 0.97; p = 0.02) and (total events) (RR= 0.81, 95% CI 0.74 to 0.89; p < 0.0001). Also, the iron group had a 21% lower risk in terms of cardiovascular death and hospital admission for heart failure (number of events, rate per 100 patients in a year) (RR= 0.79, 95% CI 0.74 to 0.85; p < 0.00001). Concerning the adverse events, both ferric carboxymaltose and ferric derisomaltose showed a beneficial effect in reducing the cardiac disorder (RR= 0.81, 95% CI 0.76 to 0.87; p <0.0001), and (RR= 0.82, 95% CI 0.71 to 0.95; p = 0.009), respectively. Conclusions. Intravenous iron infusion in patients with heart failure has a favorable safety profile. It reduces total hospitalizations for heart failure and cardiovascular mortality, with no effect on all-cause mortality, cardiovascular mortality alone, or first-time hospitalization for heart failure.