The human heart is capable of functioning for decades despite minimal cell turnover or regeneration, suggesting that molecular alterations help sustain heart function with age. However, identification of compensatory remodeling events in the aging heart remains elusive. Here we present the proteomes of rhesus monkeys and rats, from which we show that age-associated remodeling of the cardiomyocyte cytoskeleton is highly-conserved and beneficial rather than deleterious. Targeted transcriptomic analysis in Drosophila confirms conservation and implicates vinculin as a unique regulator of cardiac aging. Increased cardiac vinculin expression reinforced the cortical cytoskeleton and enhanced myofilament organization, leading to improved contractility, hemodynamic stress tolerance, and lifespan. These findings suggest that the heart has molecular mechanisms to sustain function and longevity which may be assisted by therapeutic intervention.