Long COVID has been associated with significant cardiovascular complications, including fibrosis, functional impairment, and chronic inflammatory and immune responses. However, the underlying mechanisms driving these cardiac pathologies following COVID-19 infection remain understudied. Previously, we characterized a mouse model of long COVID and observed enhanced expression of kinin B1 receptor (B1R) in the infected animals. Here, we investigated the role of B1R in mediating long COVID induced cardiac pathologies. K18-hACE2 transgenic mice were infected intranasally with SARS-CoV-2 and evaluated at 28 days post-infection (dpi) to model long COVID and the effects of pharmacological blockade of B1R were evaluated. Persistent upregulation of B1R expression was accompanied by apoptosis, disrupted cardiomyocyte architecture, fibrosis, impaired gap junction integrity, and sustained inflammation and immune cell infiltration. B1R blockade restored gap junction integrity, reduced fibrosis and apoptosis, and mitigated inflammation and immune activation. Together, these data indicate that B1R plays a critical role in long COVID induced cardiac remodeling and damage, highlighting its potential as a target for treating long-lasting cardiovascular complications following SARS-CoV-2 infection.