Coronary endothelial function and spontaneous coronary artery dissection
Thomas M Waterbury1, Marysia S Tweet1, Sharonne N Hayes1
1Department of Cardiovascular Diseases, Mayo Clinic, USA.
Insights
Endothelial dysfunction does not appear to be the main cause of spontaneous coronary artery dissection (SCAD). This study found no predominant epicardial or microvascular dysfunction in SCAD patients.
Area of Science:
- Cardiology
- Vascular Biology
- Endothelial Function
Background:
- Mechanisms of spontaneous coronary artery dissection (SCAD) are not well understood.
- The potential role of endothelial dysfunction in SCAD requires further investigation.
Purpose of the Study:
- To assess endothelial function in patients with a history of spontaneous coronary artery dissection.
- To determine if endothelial dysfunction is a primary factor in SCAD.
Main Methods:
- Retrospective analysis of 10 patients with prior SCAD undergoing invasive endothelial function testing.
- Assessment of coronary epicardial and microvascular responses to acetylcholine, adenosine, and nitroglycerine.
- Comparison with a control group of 232 individuals with normal endothelial function.
Main Results:
- No predominant coronary epicardial or microvascular vasomotor dysfunction was observed in SCAD patients.
- Acetylcholine response in SCAD patients was similar to controls, suggesting normal microvascular function.
- Abnormal microvascular response to acetylcholine was seen in 40% of SCAD patients, often associated with left anterior descending artery or multivessel SCAD.
Conclusions:
- Endothelial dysfunction is not the principal underlying mechanism in spontaneous coronary artery dissection.
- Coronary epicardial and microvascular vasomotor function appear largely preserved in SCAD patients.
Objectives:
To investigate the role of endothelial function in patients with previous spontaneous coronary artery dissection.
Background:
Mechanisms underlying spontaneous coronary artery dissection, including a possible contribution from endothelial dysfunction, remain poorly understood.
Methods:
This was a single center, retrospective study of patients with a prior spontaneous coronary artery dissection episode who underwent invasive endothelial function testing in the cardiac catheterization laboratory for evaluation of recurrent chest pain. Coronary epicardial and microvascular responses to acetylcholine, adenosine, and nitroglycerine were assessed. Findings were compared to a reference group of normal controls (n=232).
Results:
A total of 10 patients with prior angiographically confirmed spontaneous coronary artery dissection were referred for coronary endothelial function testing. The median coronary flow reserve was 2.8 (interquartile range (IQR) 2.3, 3.6). The median change in coronary diameter with acetylcholine was -0.9% (IQR -23.9, 4.2). The median increase in peak coronary blood flow following acetylcholine administration was 91.4% (IQR 9.1, 105.7), which was similar to the response observed in a reference group of patients (median age 51 years, 96% women) from our laboratory with normal microvascular responses to acetylcholine: 107.4% (IQR 75.5, 165.7; P=0.20). Four patients (40%) had an abnormal microvascular response to acetylcholine, with less than a 50% increase in coronary blood flow, and all but one patient had left anterior descending artery or multivessel spontaneous coronary artery dissection.
Conclusion:
Coronary epicardial and microvascular vasomotor dysfunction is not a predominant feature of spontaneous coronary artery dissection. Endothelial dysfunction is not implicated as the principal underlying mechanism.
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