Spontaneous Coronary Artery Dissection

Spontaneous coronary artery dissection (SCAD) accounts for approximately 1–4% of all acute coronary syndrome cases. Although rare overall, it is responsible for up to 25–40% of myocardial infarctions in women under the age of 50, who comprise ~90% of SCAD patients, underscoring its strong female predominance. 

SCAD is characterized by a sudden separation of the coronary arterial wall layers, either due to an intimal tear or intramural haemorrhage. This creates a false lumen that compresses the true lumen, leading to impaired coronary blood flow and myocardial infarction. 

Despite its clinical impact, the mechanisms underlying SCAD remain poorly understood. Unlike atherosclerotic coronary artery disease, SCAD typically occurs in the absence of traditional cardiovascular risk factors such as obesity, hypertension, or diabetes, pointing to a fundamentally different disease biology. 

Our laboratory, in collaboration with an international consortium, aims to elucidate the molecular and genetic determinants of SCAD. By integrating genomic analyses with vascular biology, we seek to identify susceptibility pathways and circulating biomarkers that enable earlier and more accurate diagnosis. Ultimately, this work aims to improve patient stratification and support the development of mechanism-based, targeted therapies. 

Funded by the Dutch Heart Foundation, the German Centre for Cardiovascular Research (DZHK) and the Lefoulon-Delalande Foundation (LDF) and the Vrienden van het UMC Utrecht.