Abstract
Alterations in the coronary vascular system are likely associated with a mismatch between energy demand and energy supply and critical in triggering the cascade of events that leads to symptomatic hypertrophic cardiomyopathy. Targeting the early events, particularly vascular remodeling, may be a key approach to developing effective treatments. Improvement in our understanding of hypertrophic cardiomyopathy began with the results of early biophysical studies, proceeded to genetic analyses pinpointing the mutational origin, and now pertains to imaging of the metabolic and flow-related consequences of such mutations. Microvascular dysfunction has been an ongoing hot topic in the imaging of genetic cardiomyopathies marked by its histologically significant remodeling and has proven to be a powerful asset in determining prognosis for these patients as well as enlightening scientists on a potential pathophysiological cascade that may begin early during the developmental process. Here, we discuss questions that continue to remain on the mechanistic processes leading to microvascular dysfunction, its correlation to the morphological changes in the vessels, and its contribution to disease progression.