Most middle-aged and elderly people in the developed world have atherosclerosis and a quarter of this group will die of it making atherosclerosis the number one cause of death worldwide. Advanced atherosclerosis, through thrombosis, often leads to ischemic heart disease and ischemic stroke. Much progress has been made in the prevention of these conditions, but once a patient has suffered a coronary occlusion the outcome is still often fatal.

  • The ruling paradigm within atherosclerosis is that vulnerable plaques are the main cause of thrombosis in man. Plaques are defined by possessing a lipid-rich core which by rupture of its fibrous cap allows the lipid-rich atheromatous core to get in contact with the flowing blood exposing the thrombogenic core to platelets whereby fibrin and eventually a thrombus is formed.
  • Thus the rupture of vulnerable atherosclerotic plaques is central to the disease in man and for obvious rea-sons very difficult to study in the living human being. Much information about vulnerable plaques has been accumulated from post mortems of patients who have died from the disease and there is no doubt that a good animal model would help to understand how rupture occurs in vivo and eventually to develop treatments to prevent it from happening.


Animal models of atherosclerosis

Many animal models of atherosclerosis have been developed over time. The question is how well they mimic the human condition. Atherosclerosis is a disease that really only affects man and a few other species and for that reason animal models have been induced in various ways in other species.

  • Probably the most common one is by feeding an atherogenic diet which increases the plasma cholesterol levels. The diet is most often enriched in both cholesterol and saturated fat and sometimes also containing cholate to inhibit the up-regulation of a cholesterol eliminating enzyme. 
  • More than 90 years ago rabbits with atherosclerosis-like symptoms were generated by feeding a cholesterol rich diet. However, the model only had limited resemblance to the human condition and did not provide a suitable model for plaque rupture.
  • Also other methods including physical and chemical injury of the arteries have been developed. Some of these models develop plaques; but the characteristics of the plaques might differ from what is seen in man.
  • Several genetically modified mouse models of atherosclerosis have been developed – also plaque forming ones. It has however been claimed that the composition of the plaques and the rupture of the fibrous cap are different from those of man and much discussion about the usefulness of these models in this respect has taken place.


Some pig strains are naturally prone to develop atherosclerosis with time. However, large pig strains are not practical as they become larger than man before they show the symptoms. Large pigs are furthermore very costly to house. These issues have been solved by generating our mini pig models of human like atherosclerosis.