Pharmacological regression of atherosclerotic plaque in patients with type 2 diabetes

Atherosclerosis of the coronary arteries continues to be one of the major global health burdens and acute coronary syndrome is responsible annually for at least 30 % of all deaths globally. Acute coronary syndrome may be the consequence of thrombus formation after erosion or rupture of obstructive or non-obstructive atherosclerotic plaque. The rupture of plaques is mostly caused by mechanical stress usually called cap fatigue. Vulnerable plaques are characterized by a softer atheromatous core and a thinner fibrous cap, with inflammation and hypercholesterolemia playing a crucial role in the atherothrombotic process. Based on animal studies that extend back to the 1920s, regression of atherosclerotic plaques in humans has just started to be considered and pursued. The idea that the human atherosclerotic plaques could regress at all met an important resistance over the decades; indeed, advanced plaques contain components, such as necrosis, calcification and fibrosis, which are hard to be removed. However, new animal models and imaging technics allowed a more complete and accurate quantitative assessment of plaque volume and are shedding new light on atherosclerosis regression. In this review, we are revisiting the existence of atherosclerosis regression in preclinical and clinical studies, with a focus on the latest mechanistic insights and on the newest pharmacological agents, particularly in patients with diabetes. Interestingly, we suggested that based on literature insights and preclinical studies, a combination of drugs to target hyperglycemia, dyslipidemia and inflammation may be desirable for a fast-track Pharmacological regression of atherosclerotic plaque in patients with type 2 diabetes.