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Morphological and Functional Assessment of the Right Ventricle Using 3D Echocardiography
Published on: October 28, 2020
Microvascular dysfunction in nonfailing arrhythmogenic right ventricular cardiomyopathy
Matthias Paul1, Kambiz Rahbar, Joachim Gerss
1Department of Cardiology and Angiology, University Hospital Münster, Münster, Germany. Matthias.Paul@ukmuenster.de
European Journal of Nuclear Medicine and Molecular Imaging
|November 25, 2011
Summary
Arrhythmogenic right ventricular cardiomyopathy (ARVC) patients show impaired blood flow during stress. This study reveals reduced hyperemic myocardial blood flow and increased coronary vascular resistance in nonfailing ARVC, suggesting microvascular dysfunction.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Physiology
Background:
- Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a primary cause of sudden cardiac death in young individuals.
- Microvascular dysfunction, indicated by impaired myocardial blood flow (MBF) response to stress, is observed in other non-ischemic cardiomyopathies and linked to poorer prognosis.
Purpose of the Study:
- To quantify myocardial blood flow (MBF), coronary flow reserve (CFR), and coronary vascular resistance (CVR) in patients with nonfailing ARVC using H(2)(15)O and Positron Emission Tomography (PET).
Main Methods:
- Ten male patients with ARVC underwent H(2)(15)O PET to measure MBF at rest and during adenosine-induced hyperemia.
- Results were compared to 20 age-matched healthy male controls.
Main Results:
- While resting MBF was similar between groups, hyperemic MBF was significantly lower in ARVC patients (2.60 vs. 3.68 ml/min/ml, p=0.005).
- ARVC patients exhibited significantly lower coronary flow reserve (2.41 vs. 3.39, p=0.030) and increased hyperemic coronary vascular resistance (36.79 vs. 26.31 mmHg×ml(-1)×min×ml, p=0.007).
Conclusions:
- This study identified significantly reduced hyperemic MBF and increased coronary vascular resistance in a small cohort of nonfailing ARVC patients.
- These findings suggest a potential new functional aspect of ARVC pathophysiology, warranting further investigation.
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