Key result
CCB therapy linked to ~15 HU reduction in pericoronary adipose tissue attenuation.
Why the study?
Vascular inflammation is linked to vasospastic angina pathogenesis, and pericoronary adipose tissue attenuation on coronary computed tomography angiography can potentially detect coronary inflammation.
Does calcium-channel blocker treatment reduce pericoronary adipose tissue inflammation in a patient with MINOCA and vasospastic angina?
Case Report (n=1)
No
Does calcium-channel blocker treatment reduce pericoronary adipose tissue inflammation in a patient with MINOCA and vasospastic angina?
Noninvasive serial assessment of pericoronary adipose tissue attenuation by coronary CTA is feasible to evaluate disease activity and response to therapy in vasospastic angina.
Answers are grounded in this paper and cite their sources.
May support serial pericoronary adipose tissue monitoring in vasospastic angina; leaves open confirmation beyond this single case.
Vascular inflammation is linked with the pathogenesis of vasospastic angina (VSA). Recent studies reported the potential of pericoronary adipose tissue attenuation as shown on coronary computed tomography angiography to detect coronary inflammation. This report presents a case of myocardial infarction with nonobstructive coronary arteries potentially complicated with VSA that demonstrated reduction of inflammation after symptom improvement with calcium channel-blocker treatment as assessed by serial examination of pericoronary adipose tissue attenuation. This case highlighted the feasibility of a noninvasive assessment of pericoronary adipose tissue attenuation to evaluate the disease activity of VSA and guide patient management.
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Horie et al. (2020) conducted a case report in Myocardial infarction with nonobstructive coronary arteries (MINOCA) and vasospastic angina (VSA) (n=1). Calcium-channel blocker (benidipine) was evaluated on Pericoronary adipose tissue attenuation. Calcium-channel blocker therapy reduced pericoronary adipose tissue attenuation from –62.04 HU at baseline to –77.16 HU at 2-year follow-up, correlating with symptom relief.
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