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Implantation of the coronary sinus reducer for refractory angina due to coronary microvascular dysfunction in the context of apical hypertrophic cardiomyopathy—a case report

BACKGROUND: Refractory angina leads to a poor quality of life and increased healthcare resource utilization. In this growing population of patients, multiple mechanism(s) of ischaemia may co-exist, including functional disorders of the coronary microcirculation. There are few evidence-based effectiv...

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Detalles Bibliográficos
Autores principales: Cheng, Kevin, Keramida, Georgia, Baksi, A John, de Silva, Ranil
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9675594/
https://www.ncbi.nlm.nih.gov/pubmed/36415685
http://dx.doi.org/10.1093/ehjcr/ytac440
Descripción
Sumario:BACKGROUND: Refractory angina leads to a poor quality of life and increased healthcare resource utilization. In this growing population of patients, multiple mechanism(s) of ischaemia may co-exist, including functional disorders of the coronary microcirculation. There are few evidence-based effective therapies resulting in a large unmet clinical need. CASE SUMMARY: A 38-year-old woman with refractory angina was referred with daily chest pain despite multiple anti-anginal medications and previous percutaneous coronary intervention. Cardiac magnetic resonance imaging demonstrated apical hypertrophic cardiomyopathy (HCM). Rubidium-82 positron emission tomography (PET) with regadenoson stress confirmed significant myocardial ischaemia in the apex and apical regions (16% of total myocardium) with a global myocardial perfusion reserve (MPR) of 1.23. Coronary angiography confirmed patent stents and no epicardial coronary artery disease. Therefore, the mechanism of ischaemia was thought attributable to coronary microvascular dysfunction (CMD) in the context of HCM. In view of her significant symptoms and large burden of left-sided myocardial ischaemia, a Coronary Sinus Reducer (CSR) was implanted. Repeat PET imaging at 6 months showed a marked reduction in ischaemia (<5% burden), improvement in global MPR (1.58), symptoms, and quality of life. CONCLUSION: In refractory angina, ischaemia may be due to disorders of both the epicardial and coronary microcirculations. The CSR is a potential therapy for these patients, but its mechanism of action has not been confirmed. This report suggests that CSR implantation may reduce myocardial ischaemia and improve symptoms by acting on the coronary microcirculation. The efficacy of CSR in patients with CMD and its mechanism of action on the coronary microcirculation warrant further investigation.