CLN2 Batten disease is a rare lysosomal storage disorder arising from mutations in the gene encoding tripeptidyl peptidase 1 (TPP1), resulting in progressive lysosomal dysfunction, vision loss, seizures, motor and cognitive decline, and early death. Our work in the CLN2R207x mouse model shows CNS-targeted treatment rescues brain pathology, though early mortality persists. This prompted further investigation into peripheral disease pathology. To investigate systemic effects of CLN2 Batten Disease, we conducted metabolomic, lipidomic, and proteomic profiling. Multi-omics analyses revealed widespread dysregulation of pathways associated with cardiovascular dysfunction. Directed follow-up assessments using electrocardiogram, echocardiogram, and immunohistochemistry confirmed cardiac abnormalities. Echocardiograph analysis suggests signs of cardiomyopathy in CLN2 mice, supported by prolonged cardiac polarization as indicated by QTc and cardiomyopathy index. Histological analysis also points to potential disruptions in lipid-based cardiometabolism compared to wildtype controls. Given the emerging evidence of cardiac involvement, we have initiated ongoing studies using CLN2R207X mouse cardiomyocytes to assess cellular metabolism and mitochondrial function. These efforts aim to better define cardiac bioenergetics and lysosomal contributions to peripheral pathology in CLN2 disease. Together, our findings underscore the need for therapeutic strategies that address both central nervous system and peripheral pathology in CLN2 Batten disease, with particular focus on the heart as a potential contributor to morbidity and mortality.