Spontaneous Coronary Artery Dissection: Advances in Understanding and Management in Women.
Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute myocardial infarction (MI), particularly among young to middle-aged women without traditional cardiovascular risk factors. This review summarizes recent advances in the understanding, diagnosis, and management of SCAD.
SCAD results from an intramural hematoma (IMH) or intimal tear causing separation of the coronary arterial wall and compression of the true lumen. Fibromuscular dysplasia is the most consistently associated arteriopathy, supporting a systemic vascular vulnerability. Genetic studies suggest a predominantly polygenic architecture, with variants such as PHACTR1 implicated in vascular signaling and endothelial regulation. Coronary angiography remains the diagnostic cornerstone, with intracoronary imaging aiding in uncertain cases, while emerging non-invasive modalities such as photon-counting computed tomography may refine non-invasive diagnosis. Conservative management is preferred in most stable patients because spontaneous healing is common and percutaneous coronary intervention carries procedural challenges. Persistent angina, coronary vasospasm, microvascular dysfunction, and psychological distress are increasingly recognized components of recovery. Multidisciplinary follow-up incorporating cardiac rehabilitation and psychological support is essential to address persistent symptoms and recovery after SCAD. SCAD is a distinct non-atherosclerotic cause of MI driven by an underlying arteriopathy and systemic vascular vulnerability, requiring individualized management, vascular screening, and multidisciplinary follow-up. Ongoing randomized trials and genomic studies aim to refine risk stratification, clarify optimal medication strategies, and improve long-term outcomes and recurrences.
SCAD results from an intramural hematoma (IMH) or intimal tear causing separation of the coronary arterial wall and compression of the true lumen. Fibromuscular dysplasia is the most consistently associated arteriopathy, supporting a systemic vascular vulnerability. Genetic studies suggest a predominantly polygenic architecture, with variants such as PHACTR1 implicated in vascular signaling and endothelial regulation. Coronary angiography remains the diagnostic cornerstone, with intracoronary imaging aiding in uncertain cases, while emerging non-invasive modalities such as photon-counting computed tomography may refine non-invasive diagnosis. Conservative management is preferred in most stable patients because spontaneous healing is common and percutaneous coronary intervention carries procedural challenges. Persistent angina, coronary vasospasm, microvascular dysfunction, and psychological distress are increasingly recognized components of recovery. Multidisciplinary follow-up incorporating cardiac rehabilitation and psychological support is essential to address persistent symptoms and recovery after SCAD. SCAD is a distinct non-atherosclerotic cause of MI driven by an underlying arteriopathy and systemic vascular vulnerability, requiring individualized management, vascular screening, and multidisciplinary follow-up. Ongoing randomized trials and genomic studies aim to refine risk stratification, clarify optimal medication strategies, and improve long-term outcomes and recurrences.