Coronary Microvascular Dysfunction as a Mechanism of Angina in Severe AS: Prospective Adenosine-Stress CMR Study

Jong Hwa Ahn, Sung Mok Kim, Sung Ji Park, Dong Seop Jeong, Min Ah Woo, Sin Ho Jung, Sang Chol Lee, Seung Woo Park, Yeon Hyeon Choe, Pyo Won Park, Jae Kuen Oh

Research output: Contribution to journalArticle

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Abstract

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

Original languageEnglish (US)
Pages (from-to)1412-1422
Number of pages11
JournalJournal of the American College of Cardiology
Volume67
Issue number12
DOIs
StatePublished - Mar 29 2016

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Aortic Valve Stenosis
Adenosine
Magnetic Resonance Spectroscopy
Perfusion
Coronary Artery Disease
Chest Pain
Blood Pressure
Gadolinium
Stroke Volume
Hypertrophy
Coronary Vessels
Multivariate Analysis
Logistic Models
Odds Ratio
Regression Analysis
Magnetic Resonance Imaging
Clinical Trials

Keywords

  • cardiac magnetic resonance
  • exertional angina
  • left ventricular mass index
  • myocardial perfusion reserve

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Coronary Microvascular Dysfunction as a Mechanism of Angina in Severe AS : Prospective Adenosine-Stress CMR Study. / Ahn, Jong Hwa; Kim, Sung Mok; Park, Sung Ji; Jeong, Dong Seop; Woo, Min Ah; Jung, Sin Ho; Lee, Sang Chol; Park, Seung Woo; Choe, Yeon Hyeon; Park, Pyo Won; Oh, Jae Kuen.

In: Journal of the American College of Cardiology, Vol. 67, No. 12, 29.03.2016, p. 1412-1422.

Research output: Contribution to journalArticle

Ahn, JH, Kim, SM, Park, SJ, Jeong, DS, Woo, MA, Jung, SH, Lee, SC, Park, SW, Choe, YH, Park, PW & Oh, JK 2016, 'Coronary Microvascular Dysfunction as a Mechanism of Angina in Severe AS: Prospective Adenosine-Stress CMR Study', Journal of the American College of Cardiology, vol. 67, no. 12, pp. 1412-1422. https://doi.org/10.1016/j.jacc.2016.01.013
Ahn, Jong Hwa ; Kim, Sung Mok ; Park, Sung Ji ; Jeong, Dong Seop ; Woo, Min Ah ; Jung, Sin Ho ; Lee, Sang Chol ; Park, Seung Woo ; Choe, Yeon Hyeon ; Park, Pyo Won ; Oh, Jae Kuen. / Coronary Microvascular Dysfunction as a Mechanism of Angina in Severe AS : Prospective Adenosine-Stress CMR Study. In: Journal of the American College of Cardiology. 2016 ; Vol. 67, No. 12. pp. 1412-1422.
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AU - Jeong, Dong Seop

AU - Woo, Min Ah

AU - Jung, Sin Ho

AU - Lee, Sang Chol

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N2 - 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

AB - 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

KW - cardiac magnetic resonance

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KW - left ventricular mass index

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