Increased nerve fibers and decreased perivascular adipose tissue in coronary arteries of acute myocardial infarction patients indicate structural changes before AMI episode
Authors: Fiet M D , Krijnen P A J , Niessen J W M ,   Cardio Pathology
Published: October 2021

Acute myocardial infarction (AMI) is caused by ruptured atheroslerotic plaques. The influence of nerves on both plaque formation and vascular tone might play a role in AMIs. Nerve sprouting can occur following AMI throughout the myocardium and coronary arteries. High densities of sympathetic nerves are associated with cardiac arrhythmias, occurring most often in the first month following an AMI. The imbalance of the nervous system is caused by the upregulation of nerve growth factor from diseased cardiomyocytes. In addition to cardiomyocytes, adipose tissue activates nerves as well.

Neural remodelling in the ventricle occurs one week following AMI in dogs. In humans, however, it is unknown how much time passes following an AMI before neural remodelling. In addition, the role of adipose tissue in neural remodelling is largely unknown and the amount of nerve fibres in coronary arteries in AMI patients has not been examined yet. The purpose of this study is determining both the amount of neural remodelling and changes in adipose tissue at different time points following an AMI.

Coronary arteries were obtained at autopsy from AMI patients (N=23) and controls who did not have any kind of heart disease (N=7). The infarct related area from the heart was also obtained from AMI patients. AMI patients were subdivided based on time passed following infarction. Nerve fibres were visualised by immunohistochemistry, using a S100 antibody. Activation of nerves was visualised by neuropeptide Y (NPY). Adipose tissue was visualised by use of a Elastica Von Gieson (EvG) staining. In the coronary arteries, S100+ nerve fibres and NPY+ nerve fibres were quantified by using a light microscope and then calculated per mm2 of the adventitia surface areas. Fat tissue was quantified by measuring the total area, intima and media of blood vessels.

AMI patients had an increase of nerves in their coronary arteries compared to control patients. Comparing the different phases of AMI, an increase in AMI patients with phase 1 infarctions was found compared to AMI patients with phase 3 infarctions. No differences were found based on the specific coronary arteries. Next we looked at the ventricles, which had no increase of nerves in AMI patients. A significant decrease of PVAT was found in both the left ventricle and coronary arteries of AMI patients.

As AMI patients have an increase of S100+ nerves during the early stage of infarction, these nerves are presumably upregulated before the MI episode. All coronary arteries, including those not related to the infarction, have an increase of S100+ nerves, hinting at activated arteries during MI. Decrease of PVAT is associated with vascular dysfunction and occurs during aging. Whether the increase of nerves and a decrease of PVAT cause an AMI is unknown. As there is little time following an phase 1 infarct for upregulation of nerves, however, it can be assumed nerves are atleast increased before the AMI episode.

Funding Acknowledgement

Type of funding sources: None.