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Published on: June 28, 2019
Coronary Flow Reserve in Patients With Prior Spontaneous Coronary Artery Dissection and Recurrent Angina
Tara Sedlak1, Andrew Starovoytov1, Karin Humphries2
1Division of Cardiology Vancouver General Hospital Vancouver British Columbia Canada.
Insights
Chronic chest pain after spontaneous coronary artery dissection (SCAD) is often linked to coronary microvascular dysfunction. Invasive testing revealed over 70% of patients had this dysfunction, suggesting underlying vasculopathies like fibromuscular dysplasia contribute to persistent symptoms.
Area of Science:
- Cardiology
- Vascular Biology
- Diagnostic Medicine
Background:
- Spontaneous coronary artery dissection (SCAD) frequently leads to chronic chest pain post-healing.
- The role of coronary microvascular dysfunction (CMD) in persistent post-SCAD pain is not fully understood.
- Investigating CMD is crucial for managing long-term symptoms in SCAD patients.
Purpose of the Study:
- To assess the contribution of coronary microvascular dysfunction to chronic chest pain in SCAD survivors.
- To evaluate coronary reactivity using invasive testing in patients with post-SCAD chest pain.
Main Methods:
- Coronary reactivity testing (CRT) was performed in 18 patients at least 3 months post-SCAD.
- Coronary flow reserve (CFR) and index of microcirculatory resistance (IMR) were measured in SCAD and non-SCAD arteries.
- Coronary microvascular dysfunction was defined as CFR <2.5 or IMR >25.
Main Results:
- Seventy-one percent (12/17) of patients exhibited a CFR <2.5, indicating CMD.
- Seventy-six percent (13/17) had an abnormal IMR (>25), also suggesting CMD.
- No significant difference in CMD prevalence was observed between SCAD and non-SCAD arteries.
Conclusions:
- Over 70% of patients with chronic chest pain post-SCAD demonstrate coronary microvascular dysfunction via invasive CRT.
- The presence of CMD in both SCAD and non-SCAD arteries suggests underlying systemic vasculopathies, such as fibromuscular dysplasia, as a potential cause.
- These findings highlight CMD as a significant contributor to persistent chest pain after SCAD.
Abstract:
Background A significant proportion of patients with spontaneous coronary artery dissection (SCAD) have ongoing chronic chest pain despite healing of their dissection. We sought to determine whether coronary microvascular dysfunction contributes to post-SCAD chronic chest pain by performing coronary reactivity testing in the cardiac catheterization laboratory. Methods and Results Eighteen patients consented to coronary reactivity testing at least 3 months post-SCAD. Coronary flow reserve (CFR) and index of microcirculatory resistance were measured in the previously affected SCAD artery and 1 non-SCAD artery. CFR <2.5 was defined as diagnostic of coronary microvascular dysfunction. An abnormal index of microcirculatory resistance was defined as >25 units. Seventeen women underwent coronary reactivity testing (1 had chronic dissection and was excluded). All presented with myocardial infarction and 2 underwent coronary stenting during the initial SCAD event. Fibromuscular dysplasia was present in 70.6% upon screening renal, iliac, and cerebrovascular arteries. Twelve patients (70.6%) had CFR <2.5 and 13 (76.5%) had an index of microcirculatory resistance >25 in at least 1 artery. There was no difference in the frequency of a low CFR measurement between SCAD and non-SCAD arteries. Conclusions Among patients with chronic chest pain after an SCAD event, >70% had coronary microvascular dysfunction as indicated by abnormal CFR or index of microcirculatory resistance in at least 1 coronary artery on invasive coronary reactivity testing. Presence of coronary microvascular dysfunction in both SCAD and non-SCAD arteries suggests that underlying microvascular abnormalities from vasculopathies such as coronary fibromuscular dysplasia may be the underlying etiology.
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