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Evaluation of Coronary Flow Reserve After Myocardial Ischemia Reperfusion in Rats
Published on: June 28, 2019
Coronary flow reserve impairment in apical vs asymmetrical septal hypertrophic cardiomyopathy
Hyo-Suk Ahn1, Hyung-Kwan Kim, Eun-Ah Park
1Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
Insights
Coronary flow reserve (CFR) is reduced in hypertrophic cardiomyopathy (HCM) due to impaired stress-induced flow augmentation. Basal coronary flow is a key factor in CFR reduction in both asymmetrical septal hypertrophy and apical HCM.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Medical Imaging
Background:
- Mechanisms of reduced coronary flow reserve (CFR) in hypertrophic cardiomyopathy (HCM), particularly apical HCM (ApHCM), remain unclear.
- This study investigates the underlying mechanisms of CFR reduction in two distinct HCM subtypes.
Purpose of the Study:
- To evaluate the mechanisms responsible for CFR reduction in asymmetrical septal hypertrophy (ASH) and ApHCM.
- To compare CFR reduction mechanisms between ASH and ApHCM subtypes.
Main Methods:
- Transthoracic echocardiography assessed mean diastolic coronary flow velocity (CFmv) before and after adenosine infusion in 31 ASH patients, 43 ApHCM patients, and 27 controls.
- Cardiac MRI evaluated left ventricular mass index and stress myocardial perfusion.
- CFR was calculated as the ratio of post-stress to basal CFmv.
Main Results:
- Post-stress CFmv was lower in both ASH and ApHCM patients compared to controls.
- CFR was significantly reduced in both HCM subtypes versus controls.
- Basal CFmv was identified as the sole independent predictor of CFR reduction in HCM (r2=0.49, P<0.001).
Conclusions:
- Impaired ability to augment coronary flow during stress underlies CFR reduction in both ASH and ApHCM.
- Greater recruitment of vasodilatory capacity at baseline was observed in ASH compared to ApHCM.
Background:
Mechanisms underlying a reduction in coronary flow reserve (CFR) in hypertrophic cardiomyopathy (HCM), especially apical HCM (ApHCM), are elusive. This study set out to evaluate mechanisms underlying a reduction in CFR in 2 HCM subtypes.
Hypothesis:
Mechanisms for CFR reduction in HCM are different between the 2 subtypes of HCM.
Methods:
Thirty-one patients with asymmetrical septal hypertrophy (ASH), 43 with ApHCM, and 27 healthy volunteers were recruited. Mean diastolic coronary flow velocity (CFmv) was monitored before and after adenosine infusion by transthoracic echocardiography in the mid-to-distal left anterior descending coronary artery. Coronary flow reserve was defined as the ratio between CFmv before and after adenosine infusion. Left ventricular mass index and stress myocardial perfusion were assessed by cardiac magnetic resonance imaging.
Results:
Although basal CFmv was higher in ASH patients than in healthy controls (P<0.05), it was similar in ApHCM patients and controls (P=0.85). Poststress CFmv was significantly lower in both HCM subtypes than in controls (P<0.05). Consequently, CFR was higher in controls than in ASH or ApHCM patients (P<0.05). When HCM patients were stratified into 2 groups based on the presence of CFR impairment, no difference was observed between these 2 groups in terms of left ventricular mass index by cardiac magnetic resonance imaging. Multivariate logistic regression analysis identified basal CFmv as the only independent variable associated with CFR reduction in HCM (r2=0.49, P<0.001).
Conclusions:
Whereas the inability to augment coronary flow to its maximal level during stress was found to underlie CFR impairment in both HCM subtypes, the recruitment of vasodilatory capacity at baseline was more prominent in ASH than in ApHCM patients.
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