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Purpose of Review: Immune checkpoint inhibitors (ICIs) have improved the field of cancer, especially in patients with advanced malignancies. Nevertheless, cardiovascular immune-related adverse events (irAEs) with high mortality and morbidity have been observed, including myocarditis, pericarditis, and vasculitis. To date, only a few clinical risk factors have been described and are currently being investigated., Recent Findings: In this review, we address the four most prevailing risk factors for cardiovascular irAEs. ICI combination therapy is a predominant risk factor for developing ICI-mediated myocarditis. Additionally, ICI combined with other anti-cancer treatments (e.g., tyrosine kinase inhibitors, radiation, chemotherapy) seems to increase the risk of developing cardiovascular irAEs. Other risk factors include female sex, pre-existing cardiovascular disease, and specific tumors, on which we will further elaborate in this review. An a priori risk strategy to determine who is at risk to develop these cardiovascular irAEs is needed. Insights into the impact of risk factors are therefore warranted to help clinicians improve care and disease management in these patients., (© 2023. The Author(s).)

Purpose of Review: In this review, we highlight the most important cellular and molecular mechanisms that contribute to cardiac inflammation and fibrosis. We also discuss the interplay between inflammation and fibrosis in various precursors of heart failure (HF) and how such mechanisms can contribute to myocardial tissue remodelling and development of HF., Recent Findings: Recently, many research articles attempt to elucidate different aspects of the interplay between inflammation and fibrosis. Cardiac inflammation and fibrosis are major pathophysiological mechanisms operating in the failing heart, regardless of HF aetiology. Currently, novel therapeutic options are available or are being developed to treat HF and these are discussed in this review. A progressive disease needs an aggressive management; however, existing therapies against HF are insufficient. There is a dynamic interplay between inflammation and fibrosis in various precursors of HF such as myocardial infarction (MI), myocarditis and hypertension, and also in HF itself. There is an urgent need to identify novel therapeutic targets and develop advanced therapeutic strategies to combat the syndrome of HF. Understanding and describing the elements of the inflammatory and fibrotic pathways are essential, and specific drugs that target these pathways need to be evaluated.

Risk prediction in patients admitted with acute decompensated heart failure (ADHF) remains a challenge. Biomarkers may improve risk prediction, which in turn may help to better inform patients regarding short-term and long-term prognosis, therapy and care. Most data on biomarkers have been derived from patient cohorts with chronic heart failure. In ADHF, currently, risk tools largely rely on common clinical and biochemical parameters. However, ADHF is not a single disease. It presents in various manners and different etiologies may underlie ADHF, which are reflected by different biomarkers. In the last decade, many studies have reported the prognostic value of these biomarkers. These studies have attempted to describe a value for statistical modeling, e.g., reclassification indices, in an effort to report incremental value over a clinical model or the "gold standard". However, the overall incremental predictive value of biomarkers has been modest compared to already existing clinical models. Natriuretic peptides, e.g., (NTpro-)BNP, are the benchmark, but head-to-head comparisons show that there are novel biomarkers with comparable prognostic value. Multimarker strategies may provide superior risk stratification. Future studies should elucidate cost-effectiveness of single or combined biomarker testing. The purpose of this review was to provide an update on current biomarkers and to identify new promising biomarkers than can be used in prognostication of acute heart failure.