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Updated: May 6, 2026
In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
Myocardial perfusion imaging in Takayasu arteritis
Cloé Comarmond1, Odile Dessault, Jean-Yves Devaux
1From the Assistance Publique-Hôpitaux de Paris (AP-HP), Groupe Hospitalier Pitié Salpétrière, Department of Internal Medicine, Université Pierre et Marie Curie; AP-HP, Groupe Hospitalier Saint-Antoine, Department of Nuclear Medicine, Université Pierre et Marie Curie; AP-HP, Hôpital Saint-Louis, Department of Biostatistics, Université Denis Diderot; AP-HP, Groupe Hospitalier Pitié Salpétrière, Department of Cardiology, Université Pierre et Marie Curie; AP-HP, Groupe Hospitalier Pitié Salpétrière, Department of Vascular Surgery, Université Pierre et Marie Curie, Paris, France.
Insights
Takayasu arteritis (TA) often causes myocardial perfusion defects. Dipyridamole (DPM) improved these defects in most patients, suggesting microcirculatory dysfunction plays a key role in TA-related myocardial ischemia.
Area of Science:
- Cardiology
- Vascular Medicine
- Nuclear Cardiology
Background:
- Takayasu arteritis (TA) is associated with myocardial perfusion defects, even without coronary stenosis.
- Assessing coronary microcirculation in TA patients is crucial for understanding cardiac involvement.
Purpose of the Study:
- To evaluate coronary microcirculation in Takayasu arteritis (TA) patients.
- To investigate the effect of dipyridamole (DPM) on myocardial perfusion in TA using thallium-201 (201Tl) scintigraphy.
Main Methods:
- Prospective recruitment of 25 asymptomatic TA patients.
- 201Tl myocardial scintigraphy performed at rest and after DPM-induced vasodilation.
- Analysis of factors associated with improved myocardial perfusion post-DPM.
Main Results:
- 84% of TA patients exhibited myocardial perfusion defects at rest.
- DPM significantly improved perfusion in 61% of patients.
- Coronary stenoses were found in only 18.2% of examined patients, indicating microvascular issues.
Conclusions:
- A high prevalence of myocardial perfusion defects, largely reversible with DPM, was observed in TA.
- Microcirculatory dysfunction is likely a major contributor to myocardial ischemia in Takayasu arteritis.
Objective:
Myocardial perfusion defects using scintigraphy have been frequently observed in patients with Takayasu arteritis (TA) without coronary stenosis. The aim of our study was to evaluate coronary microcirculation in TA using thallium-201 (201Tl) myocardial scintigraphy and dipyridamole (DPM) as vasodilator agent.
Methods:
Twenty-five consecutive patients with TA were prospectively recruited. They were asymptomatic for cardiac issues and examined using 201Tl myocardial scintigraphy at rest and after coronary artery vasodilation with intravenous DPM. Factors associated with improvement in myocardial perfusion after DPM were identified in patients with TA.
Results:
Among 25 patients with TA, 21 (84%) had 201Tl myocardial perfusion defects and 4 (16%) had normal resting myocardial perfusion. Using a 17-segments model for quantitative image analysis, DPM significantly improved resting 201Tl myocardial perfusion in 14 patients (61%) versus 9 patients without improvement (39%). We were able to examine coronary artery stenoses in 11 patients, including 10 patients with thallium perfusion defects, and significant coronary artery stenoses were present in only 2 patients (18.2%). No significant difference was found in traditional cardiovascular risk factors between TA patients with or without improvement of myocardial perfusion after DPM. The absence of improvement in myocardial perfusion after DPM tended to be closely associated with specific features and prognostic factors of TA, such as aortic regurgitation at diagnosis, renovascular hypertension, longer duration of TA disease, and male sex.
Conclusion:
We found the significantly high prevalence of myocardial perfusion defects mostly improved after vasodilation with DPM, which may indicate the major role of microcirculatory dysfunction in myocardial ischemia in TA.
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