Molecular imaging agent may halt cell suicide after heart attack
A single intravenous dose of the hormone erythropoietin (EPO) administered immediately after myocardial infarction can drastically reduce or eliminate apoptosis and thereby limit the amount of damage to the heart, according to an article in the October issue of the Journal of Nuclear Medicine.
The purpose of the study was to determine if the area of cell death following acute coronary occlusion could be reduced by a single dose of EPO, according to the study’s co-author H. William. Strauss, MD, physician in the nuclear medicine department at Memorial Sloan Kettering Cancer Center and professor of radiology at Weill Cornell School of Medicine, both located in New York City.
“By administering 99mTc-annexin V, a radiotracer with a high affinity for apoptotic cells, we were able to view the effects of EPO on heart cells immediately following the restriction of blood flow that occurs during MI,” Strauss said.
"In cardiovascular medicine, imaging of apoptosis could be highly useful in managing myocardial infarction, atherosclerotic plaques and cardiac allograft rejection. Because molecular probes such as 99mTc-annexin V are capable of imaging apoptosis in living patients, they are vital to this research," commented Robert W. Atcher, PhD, president of SNM.
In the study, 18 Wistar rats were randomized into two groups; in both groups, arteries were blocked to induce a heart attack; 20 minutes later, they were unblocked.
Immediately afterward, one group received an injection of EPO and the other group of saline. Both groups were then injected with 99mTc-annexin V, and their hearts were examined using autoradiography to evaluate the distribution of the radiotracer.
In the treatment group, EPO therapy caused a 2.7-fold reduction of tracer accumulation, indicating a reduction in apoptosis and, therefore, less damage to heart tissue. The reduction in damage to the heart was also demonstrated by measurement of regional cardiac function, which was significantly better in the EPO-treated group.
The findings suggest that EPO may be useful to prevent long-term heart damage and dysfunction after a heart attack, the authors concluded.
The purpose of the study was to determine if the area of cell death following acute coronary occlusion could be reduced by a single dose of EPO, according to the study’s co-author H. William. Strauss, MD, physician in the nuclear medicine department at Memorial Sloan Kettering Cancer Center and professor of radiology at Weill Cornell School of Medicine, both located in New York City.
“By administering 99mTc-annexin V, a radiotracer with a high affinity for apoptotic cells, we were able to view the effects of EPO on heart cells immediately following the restriction of blood flow that occurs during MI,” Strauss said.
"In cardiovascular medicine, imaging of apoptosis could be highly useful in managing myocardial infarction, atherosclerotic plaques and cardiac allograft rejection. Because molecular probes such as 99mTc-annexin V are capable of imaging apoptosis in living patients, they are vital to this research," commented Robert W. Atcher, PhD, president of SNM.
In the study, 18 Wistar rats were randomized into two groups; in both groups, arteries were blocked to induce a heart attack; 20 minutes later, they were unblocked.
Immediately afterward, one group received an injection of EPO and the other group of saline. Both groups were then injected with 99mTc-annexin V, and their hearts were examined using autoradiography to evaluate the distribution of the radiotracer.
In the treatment group, EPO therapy caused a 2.7-fold reduction of tracer accumulation, indicating a reduction in apoptosis and, therefore, less damage to heart tissue. The reduction in damage to the heart was also demonstrated by measurement of regional cardiac function, which was significantly better in the EPO-treated group.
The findings suggest that EPO may be useful to prevent long-term heart damage and dysfunction after a heart attack, the authors concluded.