ErbB2 inhibition was associated with an increased risk of atrial fibrillation, prolonged QTc interval, and increased P wave terminal force. CSK inhibition demonstrated potential links to conduction blocks, while PLCG2 inhibition led to changes in P wave terminal force, QTc interval, and an increased risk of left bundle branch block. BLK inhibition was associated with QTc interval shortening and atrioventricular block.

Our study found that the neutrophil-to-lymphocyte ratio elevation in the early phase after immune checkpoint inhibitors (ICIs) treatment in non-small-cell lung cancer is a predictive factor for ICI-related myocarditis. Regular and frequent cardiac monitoring may help to avoid the occurrence of severe and fatal cases.

Ibrutinib, a Bruton's tyrosine kinase inhibitor, has been associated with a significant increase in the risk of ventricular arrhythmias. In our present study, we aimed to investigate the cardiotoxicity of ibrutinib and explore the potential protective effects of metformin in ibrutinib-treated mice. Our findings revealed that long-term exposure to ibrutinib triggered ventricular myocardial apoptosis and fibrosis, leading to alterations in cardiac electrophysiological properties and an increased potential for ventricular arrhythmia. In this ibrutinib-induced model of cardiac toxicity, metformin demonstrated the ability to upregulate the AMPK and PI3K/AKT signaling pathway, thereby mitigating the ibrutinib-induced cardiotoxicity. As a result, we have demonstrated the protective effects of metformin in counteracting ibrutinib-induced cardiotoxicity and propose it as a potential pharmaceutical therapeutic strategy for related diseases.

HDAC6 have been found to be a key protein in the tumor–cardiovascular association. HDAC6 inhibitors may have important moderating effects in various types of cardiovascular diseases. HDAC6 inhibitors alone or in combination with other agents have shown promising prospects in the treatment of cardiovascular disease.

1. CTLA-4 inhibitors restore the T cell immune response against tumor cells. Tumors and cardiomyocytes, shared some muscle-specific antigens, which trigger a cross-reactivity with T cells. The inhibitors make cardiac cells susceptible to injury. 2. CTLA-4 inhibitors significantly increased the incidence of all-grade cardiovascular toxicity and severe cardiovascular toxicity in the patients. The risk of serious cardiovascular toxic events was independent of the type of adverse event.

A novel health system reliability method has been developed and applied to cardio and cancer death rate data. Accurate disease multiregional prediction is done.