Ricardo Mori1, Fernando Macaya2, Jaskanwal D Sara3, Takumi Toya4, Hernán Mejía-Rentería1, Nieves Gonzalo1, Amir Lerman3, Javier Escaned1. 1. Hospital Clínico San Carlos, IdISSC and Universidad Complutense, Madrid, Spain. 2. Hospital Clínico San Carlos, IdISSC and Universidad Complutense, Madrid, Spain. Electronic address: fernando@macaya.eu. 3. Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA. 4. Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA; Division of Cardiology, National Defense Medical College, Tokorozawa, Saitama, Japan.
Abstract
BACKGROUND: The physiopathology underlying spontaneous coronary artery dissection remains largely unknown. Endothelial dysfunction is an early feature of many vascular disorders. We sought to determine the endothelial function assessed by reactive hyperemia peripheral arterial tonometry (RH-PAT) in patients with SCAD and compare it to that of non-SCAD patients with similar cardiovascular risk profile. METHODS: This is a case-control study with the participation of 2 centers. Patients (cases) were diagnosed with SCAD between 2008 and 2018. Control subjects were individually matched 2:1 to SCAD cases from a cohort recruited for assessment with RH-PAT between 2006 and 2013. The primary measure variable was the mean difference in the log-transformed reactive hyperemia index (LnRH-PAT Index) between groups. RESULTS: LnRH-PAT data from 23 patients with SCAD and 46 matched controls were analyzed. No significant differences were noted in the matching variables (overall, 95.7% female with mean age 52.7 years). In the SCAD group, more patients reported migraine (61 vs. 21%) and more patients were on betablockers (70 vs 28%), ACE inhibitors (65 vs. 13%) and statins (70 vs. 28%), all differences statistically significant. The mean LnRH-PAT value was 0.55 ± 0.22 in patients with SCAD and 0.77 ± 0.23 in controls (mean difference: 0.22, p < 0.001). CONCLUSIONS: In this observational study, patients with SCAD had a poorer endothelial function than similar subjects without prior SCAD. This finding opens a new venue in the research of the physio pathologic mechanisms underlying SCAD.
BACKGROUND: The physiopathology underlying spontaneous coronary artery dissection remains largely unknown. Endothelial dysfunction is an early feature of many vascular disorders. We sought to determine the endothelial function assessed by reactive hyperemia peripheral arterial tonometry (RH-PAT) in patients with SCAD and compare it to that of non-SCAD patients with similar cardiovascular risk profile. METHODS: This is a case-control study with the participation of 2 centers. Patients (cases) were diagnosed with SCAD between 2008 and 2018. Control subjects were individually matched 2:1 to SCAD cases from a cohort recruited for assessment with RH-PAT between 2006 and 2013. The primary measure variable was the mean difference in the log-transformed reactive hyperemia index (LnRH-PAT Index) between groups. RESULTS:LnRH-PAT data from 23 patients with SCAD and 46 matched controls were analyzed. No significant differences were noted in the matching variables (overall, 95.7% female with mean age 52.7 years). In the SCAD group, more patients reported migraine (61 vs. 21%) and more patients were on betablockers (70 vs 28%), ACE inhibitors (65 vs. 13%) and statins (70 vs. 28%), all differences statistically significant. The mean LnRH-PAT value was 0.55 ± 0.22 in patients with SCAD and 0.77 ± 0.23 in controls (mean difference: 0.22, p < 0.001). CONCLUSIONS: In this observational study, patients with SCAD had a poorer endothelial function than similar subjects without prior SCAD. This finding opens a new venue in the research of the physio pathologic mechanisms underlying SCAD.