No abstract

Vasospastic angina (VSA) is an under-appreciated cause of chest pain. It is characterised by transient vasoconstriction of the coronary arteries and plays a significant role in the pathogenesis of stable angina and acute coronary syndromes. Complex mechanistic pathways characterised by endothelial dysfunction and smooth muscle hypercontractility lead to a broad spectrum of clinical manifestations ranging from recurrent angina to fatal arrhythmias. Invasive provocation testing using intracoronary acetylcholine or ergonovine is considered the current gold standard for diagnosis, but there is a wide variation in protocols amongst different institutions. Conventional pharmacological therapy relies on calcium channel blockers and nitrates; however, refractory VSA has limited options. This review evaluates the pathophysiology, diagnostic challenges, and management strategies for VSA. We believe global efforts to standardise diagnostic and therapeutic guidelines will improve the outcomes for affected patients.

Clonal expansion is a process that can drive pathogenesis in human diseases, with atherosclerosis being a prominent example. Despite advances in understanding the etiology of atherosclerosis, clonality studies of vascular cells remain in an early stage. Recently, several paradigm-shifting preclinical studies have identified clonal expansion of progenitor cells in the vasculature in response to atherosclerosis. This review provides an overview of cell clonality in atherosclerotic progression, focusing particularly on smooth muscle cells and macrophages. We discuss key findings from the latest research that give insight into the mechanisms by which clonal expansion of vascular cells contributes to disease pathology. The further probing of these mechanisms will provide innovative directions for future progress in the understanding and therapy of atherosclerosis and its associated cardiovascular diseases.