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Published on: August 17, 2022
Coronary Microvascular Dysfunction as a Mechanism of Angina in Severe AS: Prospective Adenosine-Stress CMR Study
Jong-Hwa Ahn1, Sung Mok Kim2, Sung-Ji Park1
1Division of Cardiology, Department of Medicine, Cardiovascular Imaging Center, Heart Vascular Stroke Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Insights
Exertional angina in severe aortic stenosis (AS) without coronary artery disease (CAD) is linked to impaired microvascular function. Cardiac magnetic resonance imaging revealed reduced myocardial perfusion reserve index (MPRI) in patients with angina.
Area of Science:
- Cardiology
- Medical Imaging
- Vascular Biology
Background:
- Exertional angina is common in severe aortic stenosis (AS) without obstructive coronary artery disease (CAD), but its cause is poorly understood.
- Understanding the pathogenesis of angina in this patient group is crucial for effective treatment strategies.
Purpose of the Study:
- To investigate the role of microvascular dysfunction in causing chest pain in patients with severe AS and normal epicardial coronary arteries.
- To utilize adenosine-stress cardiac magnetic resonance (CMR) imaging to assess myocardial perfusion reserve index (MPRI).
Main Methods:
- Prospective enrollment of 117 severe AS patients (without obstructive CAD) and 20 controls.
- Division of AS patients into angina (n=43) and asymptomatic (n=41) groups based on exertional chest pain.
- Calculation of semiquantitative myocardial perfusion reserve index (MPRI) using adenosine-stress CMR.
Main Results:
- Severe AS patients had significantly lower MPRI than controls (0.90 ± 0.31 vs. 1.25 ± 0.21; p < 0.001).
- The angina group exhibited significantly lower MPRI than the asymptomatic group (0.74 ± 0.25 vs. 1.08 ± 0.28; p < 0.001).
- MPRI was the sole independent predictor of angina (OR: 0.003; p < 0.001), with left ventricular mass index (LVMI) being the strongest factor influencing MPRI (β = -0.428; p < 0.001).
Conclusions:
- Angina in severe AS without obstructive CAD is associated with impaired coronary microvascular function.
- Left ventricular hypertrophy, assessed by LVMI, significantly contributes to reduced MPRI.
- Adenosine-stress CMR and semiquantitative MPRI are valuable tools for evaluating angina in this patient population.
Background:
Although a common symptom in patients with severe aortic stenosis (AS) without obstructive coronary artery disease (CAD), little is known about the pathogenesis of exertional angina.
Objectives:
This study sought to prove that microvascular dysfunction is responsible for chest pain in patients with severe AS and normal epicardial coronary arteries using adenosine-stress cardiac magnetic resonance (CMR) imaging.
Methods:
Between June 2012 and April 2015, 117 patients with severe AS without obstructive CAD and 20 normal controls were enrolled prospectively. After exclusions, study patients were divided into 2 groups according to presence of exertional chest pain: an angina group (n = 43) and an asymptomatic group (n = 41), and the semiquantitative myocardial perfusion reserve index (MPRI) was calculated.
Results:
MPRI values were significantly lower in severe AS patients than in normal controls (0.90 ± 0.31 vs. 1.25 ± 0.21; p < 0.001), and were much lower in the angina group than the asymptomatic group (0.74 ± 0.25 vs. 1.08 ± 0.28; p < 0.001). In logistic regression analysis, the only independent predictor for angina was MPRI (odds ratio: 0.003; p < 0.001). Univariate associations with MPRI were identified for diastolic blood pressure, E/e' ratio, left ventricular volume and ejection fraction, cardiac index, presence of late gadolinium enhancement, and left ventricular mass index (LVMI). In multivariate analysis, LVMI was the strongest contributing factor to MPRI (standardization coefficient: -0.428; p < 0.001).
Conclusions:
Our results suggest that, in patients with severe AS without obstructive CAD, angina is related to impaired coronary microvascular function along with LV hypertrophy detectable by semiquantitative MPRI using adenosine-stress CMR.
Clinical Trial Registration:
NCT02575768.
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