The coronavirus disease 2019 (COVID-19) has shown unexpected viral infection traits. Initially thought to affect respiratory health primarily, it also involves the gastrointestinal system. However, many complications during the pandemic were caused by the virus, including neurological, cardiovascular, dermatological, and metabolic issues. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has also been linked to cardiac complications, such as myocardial infarction, in individuals without cardiovascular risk factors. SARS-CoV-2 vaccines exacerbated the situation with possible adverse events (AEs). Vaccine side effects, like thromboembolic events, can be life-threatening or simply bothersome. Postural orthostatic tachycardia syndrome (POTS) is a nonlethal cardiac complication seen with COVID-19 and its vaccines. In this review, we summarized the POTS-COVID-19 relationship comprehensively.

Cardiac complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been well-identified since the beginning of the current coronavirus disease 2019 (COVID-19) pandemic. Such conditions can occur of various etiologies, such as respiratory failure and hypoxemia, direct cardiac tissue damage due to viral replication, indirect myocarditis as systemic inflammation, and the interaction of different medications. Recently, with the start of the COVID-19 vaccination programs, COVID-19 vaccine-associated cardiac adverse events (AEs) have emerged and are increasingly being reported. Although these AEs are usually mild and self-limited, they can sometimes cause severe, catastrophic outcomes. This review compares the pathophysiology, diagnosis, and treatment of the de novo SARS-CoV-2 infection-related and COVID-19 vaccine-related myocarditis and pericarditis.

Background: Activation of the renin‐angiotensin‐aldosterone system contributes to hepatic inflammation in metabolic dysfunction‐associated steatotic liver disease (MASLD). Telmisartan, an angiotensin II receptor blocker with partial PPAR‐γ agonistic activity, has been hypothesized to confer metabolic benefits; however, current clinical evidence has not consistently demonstrated such effects. Aim: This systematic review and meta‐analysis evaluated the efficacy of telmisartan on metabolic, biochemical, and histological outcomes in MASLD. Methods: Electronic databases (PubMed, Embase, Web of Science, Scopus) were searched through 2026 for randomized controlled trials (RCTs) investigating telmisartan in adults with MASLD. Risk of bias was assessed using the RoB2 tool. Random‐effects meta‐analyses calculated pooled mean differences (MDs) with 95% confidence intervals (CIs). Results: Six RCTs comprising 258 participants (126 telmisartan, 132 controls) met the inclusion criteria. Telmisartan treatment was associated with a modest reduction in fasting blood sugar compared with controls (MD = −2.78 mg/dL; 95% CI −5.17 to −0.39; p = 0.023); however, this finding was accompanied by substantial heterogeneity (I ² = 91.8%) and should therefore be interpreted cautiously. No significant changes were observed for body mass index, waist circumference, HOMA‐IR, lipid profiles, ALT, or AST. Conversely, gamma‐glutamyl transferase (GGT) levels showed a modest but significant increase with telmisartan (MD = 5.40 U/L; 95% CI 0.51 to 10.29; p = 0.031). Histological analyses revealed a non‐significant trend toward fibrosis stage improvement (MD = −0.28; 95% CI −0.57 to 0.01; p = 0.060), with no significant improvements seen in the overall NAFLD activity score, steatosis, ballooning, or lobular inflammation. Most included trials carried a low overall risk of bias. Conclusion: Current evidence does not demonstrate consistent metabolic, biochemical, or histological benefits of telmisartan in MASLD. Although a modest reduction in fasting blood glucose was observed, substantial between‐study heterogeneity and the modest effect size limit confidence in this finding.