The last decades have witnessed tremendous progress in preventing and treating cardiovascular disease. Notably, the advent of statin therapy in the 1990s marks one of the victories of contemporary medicine. Yet, in spite of these successes, cardiovascular disease remains the leading cause of death and disability globally. Moreover, the trend of reduced mortality due to cardiovascular disease has flattened in recent years. Fortunately, there may be light at the end of the tunnel. Recent technological advances – most notably in the field of genetics – have enabled leaps in our understanding of the pathophysiological processes that lead to atherosclerosis, and have unveiled new therapeutic targets.This thesis aims to contribute to the translation of pathophysiological insights into improved diagnostic methods and therapies for patients with a high risk of cardiovascular disease. The objectives are threefold:1. Illustrate how “top-down” population studies, combined with “bottom-up” mechanistic studies, can conjointly lead to a better understanding of the path from risk factor exposure to cardiovascular disease;2. Illustrate how population studies can quantify the prevalence of specific manifestations of cardiovascular disease or risk factors, and how assessments of existing diagnostic methods can lead to more appropriate use of those methods;3. Illustrate how more effective use of existing treatment options, combined with novel therapies enabled by rapid scientific advances, can lead to improved therapeutic options for high-risk cardiovascular disease patients
