The effects of space irradiation on the cardiovascular systems remain a great mystery. After conducting studies on survivors of the atomic bomb, radiotherapy as a treatment for cancer and other diseases, and health data of astronauts who have participated in short and long duration space missions, the overall conclusion is that ionizing irradiation of any type results in cardiovascular damage. Problems manifest decades after irradiation exposure and the accumulating health complications have led to fatalities. However, little is known about space irradiation and how it affects our bodies. Predictive models that were developed to date were created based on events that have occurred on earth. National Aeronautics and Space Administration (NASA) plans for manned missions to the Moon and Mars in the near future. There is a great need for ground-based studies about the effects of cosmic irradiation on the human body. We examined molecular pathways in the heart tissue of adult 7-9 months old mice, an equivalent of middle-age for astronauts (35-55), after receiving a single low dose full body of either 56Fe (iron) or 1H (proton) irradiation + aging of 1, 3, and 10 months. We also investigated mice after 56Fe or 1H irradiation + aging of 1, 3, and 10 months, and 3 days after an induced acute myocardial infarct (AMI). Western blot analyses were performed for proteins involved in cardiac function and cardiac recovery. Results indicated that 56Fe irradiation impaired cardiac function significantly during aging and continued to worsen with age. AMI results were less straightforward. The younger, 56Fe irradiated mice revealed a significant decrease in the expression of proteins associated with survival of cardiac tissue. The older, 1H irradiated mice group revealed a significantly decreased expression of proteins associated with survival of cardiac tissue. The 10 month 56Fe irradiated mice did not show compensatory mechanisms and the cardiac protein expression levels were attributed to aging. While the 10 month 1H irradiated mice compensated and required less repair activation.