Is Spontaneous Coronary Artery Dissection (SCAD) Related to Vascular Inflammation and Epicardial Fat? Insights from Novel Markers of Computed Tomography Coronary Angiography

Background: Spontaneous coronary artery dissection (SCAD) is increasingly recognised as a cause of myocardial infarction particularly in young women. Vascular inflammation and epicardial fat volume (EFV) are associated with atherosclerotic disease but their relationship with SCAD remains unclear. Pericoronary adipose tissue (PCAT) attenuation is a novel computed tomography coronary angiography (CTCA) marker of vascular inflammation. We seek to evaluate the relationship between PCAT attenuation, EFV and epicardial fat density (EFD) with SCAD. Methods: Asymptomatic patients (control group) and patients with SCAD who had undergone 320-detector CTCA within 2 weeks of acute presentation were studied. Using semi-automated software (AutoPlaque version 2.0), PCAT attenuation was quantified around the proximal 10–50 mm of the right coronary artery by including all voxels between -190 and -30 HU within the predefined volume of interest. PCAT attenuation was defined as the mean CT attenuation within this volume. EFV and EFD were assessed by QFAT software. Results: 11 SCAD and 27 control patients (age 50 vs. 53 years, p = 0.67) were studied. There was no difference in cardiovascular risk factors such as diabetes mellitus (p = 0.13), dyslipidaemia (p = 0.15), hypertension (p = 0.46), smoking status (p = 1.0) and family history of IHD (p = 0.46) between the 2 groups. Median PCAT attenuation (−91.8 vs. −88.4 HU, p = 0.1), EFV (60.5 vs. 54.5 mL, p = 0.5) and EFD (−85.7 vs. −83.0 HU, p = 0.35) were not significantly different between SCAD and control patients. Conclusion: Vascular inflammation may not be implicated as a pathophysiology of SCAD but our findings need confirmation in larger prospective studies.