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One of the most challenging and prevalent side effects of LVAD implantation is that of right heart failure (RHF) that may develop afterwards. The purpose of this study is to review and highlight recent advances in the uses of AI in evaluating RHF after LVAD implantation. The available literature was scanned using certain key words (artificial intelligence, machine learning, left ventricular assist device, prediction of right heart failure after LVAD) was scanned within Pubmed, Web of Science, and Google Scholar databases. Conventional risk scoring systems were also summarized, with their pros and cons being included in the results section of this study in order to provide a useful contrast with AI-based models. There are certain interesting and innovative ML approaches towards RHF prediction among the studies reviewed as well as more straightforward approaches that identified certain important predictive clinical parameters. Despite their accomplishments, the resulting AUC scores were far from ideal for these methods to be considered fully sufficient. The reasons for this include the low number of studies, standardized data availability, and lack of prospective studies. Another topic briefly discussed in this study is that relating to the ethical and legal considerations of using AI-based systems in healthcare. In the end, we believe that it would be beneficial for clinicians to not ignore these developments despite the current research indicating more time is needed for AI-based prediction models to achieve a better performance.

Mitogen-activated protein kinase (MAPK) signaling is strongly implicated in cardiovascular remodeling in pulmonary hypertension (PH) and right ventricle (RV) failure. The effects of a newly designed p38 inhibitor, LASSBio-1824, were investigated in experimentally induced PH. Male Wistar rats were exposed to hypoxia and SU5416 (SuHx), and normoxic rats were used as controls. Oral treatment was performed for 14 days with either vehicle or LASSBio-1824 (50 mg/kg). Pulmonary vascular resistance and RV structure and function were assessed by echocardiography and catheterization. Histological, immunohistochemical and Western blot analysis of lung and RV were performed to investigate cardiovascular remodeling and inflammation. Treatment with LASSBio-1824 normalized vascular resistance by attenuating vessel muscularization and endothelial dysfunction. In the heart, treatment decreased RV systolic pressure, hypertrophy and collagen content, improving cardiac function. Protein content of TNF-α, iNOS, phosphorylated p38 and caspase-3 were reduced both in lung vessels and RV tissues after treatment and a reduced activation of transcription factor c-fos was found in cardiomyocytes of treated SuHx rats. Therefore, LASSBio-1824 represents a potential candidate for remodeling-targeted treatment of PH.