Myocarditis is still a major global health issue that frequently manifests due to oxidative stress, immune-mediated myocardial damage, and unpredictable clinical progression. Experiments with autoimmune myocarditis (EAM) models have shown different ways that T-cell subsets, proinflammatory cytokines, macrophage polarization, and mitochondrial dysfunction are all connected and play a part in both acute inflammation and chronic remodeling of the heart. As a possible multimodal intervention that could affect several of these disease-causing pathways, hyperbaric oxygen therapy (HBOT) has become popular. This therapy delivers 100% oxygen to different tissues at higher atmospheric pressures. Early research shows that HBOT improves the delivery of oxygen to the inflamed myocardium, suppress the activation of NF-κB and NLRP3 inflammasomes, lowers oxidative stress, protects mitochondrial function, and boosts immune-regulatory T-cell responses. Despite these potentially promising findings, there are still a number of important translational obstacles to overcome, such as inconsistent protocols, a lack of long-term outcome data, insufficient mechanistic profiling, and doubts about the best protocol length and patient selection. To assess safety and effectiveness in human myocarditis, future studies should aim to integrate multi-omics analyses, HBOT regimens that are already standardized, sophisticated imaging, and carefully planned early-phase clinical trials. Overall, the currently available evidence supports HBOT as a biologically plausible and potentially valuable adjunct therapy for autoimmune myocarditis, expressing the need for further mechanistic and clinical investigation.

Myocarditis remains a significant global health burden often accompanied by im-mune-mediated myocardial injury, oxidative stress, and unpredictable clinical progres-sion. Experimental autoimmune myocarditis (EAM) models have provided different in-sights into the interconnected roles of T-cell subsets, proinflammatory cytokines, mac-rophage polarization, and mitochondrial dysfunction in both acute inflammation and chronic cardiac remodeling. Hyperbaric oxygen therapy (HBOT), which delivers 100% oxygen at elevated atmospheric pressures, has emerged as a potential multimodal in-tervention capable of affecting several of these pathogenic pathways. Preclinical data demonstrate that HBOT enhances oxygen delivery to the inflamed myocardium, sup-presses the activation of NF-κB and NLRP3 inflammasomes, reduces oxidative stress, preserves mitochondrial function, and promotes immunoregulatory T-cell responses. Despite these promising results, significant translational challenges remain, including protocol variability, lack of long-term outcome data, incomplete mechanistic profiling, and uncertainties regarding optimal timing and patient selection. Future research should try to incorporate already standardized HBOT regimens, multi-omics analyses, advanced imaging, and well-designed early-phase clinical trials to evaluate safety and efficacy in human myocarditis. Overall, the currently available evidence supports HBOT as a bi-ologically plausible and potentially valuable adjunct therapy for autoimmune myocar-ditis, expressing the need for further mechanistic and clinical investigation.

Psoriasis is a chronic immune-mediated systemic disorder that extends beyond the skin and may adversely affect cardiovascular function. Herbal therapies have emerged as promising complementary approaches for mitigating psoriasis-associated cardiac complications. The present study aimed to evaluate the cardioprotective potential of Melissa officinalis (MO) extract in psoriasis. Twenty-four male Wistar albino rats were randomly assigned to four experimental groups: control, MO, psoriasis (PSORI), and PSORI+MO. After induction, animals received MO extract (200 mg/kg b.w.) orally for three weeks. Cardiac function was assessed using the Langendorff isolated heart preparation. Oxidative stress and inflammatory cytokines were determined in blood. Psoriatic rats exhibited impaired myocardial contractility and relaxation, accompanied by elevated SLVP and DLVP across all perfusion pressures. Administration of MO significantly improved cardiac performance and attenuated these hemodynamic disturbances. Oxidative stress markers and inflammatory cytokines were markedly reduced in the PSORI+MO group compared with PSORI. Cardiomyocyte diameter and cross-sectional area were increased in both PSORI and PSORI+MO groups relative to controls. Collagen content was substantially elevated in the PSORI group and remained increased, although to a lesser extent, in the PSORI+MO group compared with controls. These findings suggest that MO extract may represent a promising complementary strategy for reducing psoriasis-associated cardiovascular alterations.