Chronic active myocarditis was found in 65% of DCM patients with HFrEF undergoing LVAD implantation, often linked to viral infection and associated with younger age and rapid symptom onset.
Chronic active myocarditis is highly prevalent (65%) in patients with severe DCM and HFrEF requiring LVAD, suggesting persistent inflammation plays a key role in advanced heart failure phenotypes.
Absolute Event Rate: 0% vs 0%
Abstract Chronic active myocarditis (MY) is histologically characterized by both active myocardial inflammatory cell infiltrate and replacement fibrosis. Recent studies have identified the persistance of myocardial inflammation as an important prognostic factor in patients with heart failure and reduced left ventricular (LV) ejection fraction (HFrEF). However, there is limited information regarding the impact of underlying MY on the various clinical presentations and phenotypes of HFrEF. Additionally, detailed histological characterization of the myocardium and its correlation with the etiology of dilated cardiomyopathy (DCM) remain insufficiently explored. Our study focused on the spectrum of histopathological findings and its correlation with the clinical features in patients with DCM and HFrEF undergoing a left ventricular assist device implantation (LVAD). Methods: We retrospectively analyzed the histopathological (HI) features of the myocardial specimens obtained from the apical segment of the LV extracted at the time of LVAD implantation. The diagnosis of MY was based upon the HI Dallas criteria and immunohistochemistry, including a large panel of specific antibodies and additional PCR analysis for viral infection. Results: A total of 249 p (82% men, 47±14 years, 66% non ischemic DCM), who underwent a LVAD implantation were enrolled. HI showed MY in 65% of the patients with DCM, and 95 % of them corresponded to chronic active lymphocitic MY (LIC). Virus infiltration was detected in 52% of the myocardial specimens with LIC and in 100% of the specimens with sarcoiditic infiltrate. Table 1 shows the type of MY according to the inflammatory infiltrate and its correlation with the etiology of the DCM. Patients with LIC were younger (43 vs 49 years, p0.005) and showed a more rapid onset of symptoms. Our findings show that chronic active MY can present either as acute heart failure or as a acute decompensation of chronic HFrEF. Conclusion: Our study demonstrates that chronic active MY is highly prevalent and underlies a broad spectrum of clinical presentations and etiologies responsible for DCM with HFrEF; these findings suggest a complex interaction between pre-existing genetic background, enviromental factors, viral infection and inflammation. The presence of chronic active MY might unveil an increased susceptibility to develop overt HFrEF and poorer functional recovery . This supports the model whereby inflammation interacts with other environmental and genetic factors to determine cardiac phenotype.
Cano et al. (Sat,) reported a other. Chronic active myocarditis was found in 65% of DCM patients with HFrEF undergoing LVAD implantation, often linked to viral infection and associated with younger age and rapid symptom onset.