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Published on: June 14, 2016
Peripheral vascular structure and function in hypertrophic cardiomyopathy
Nicola Jayne Rowley1, Daniel J Green, Keith George
1Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, UK.
Insights
Hypertrophic cardiomyopathy (HCM) patients and athletes show distinct peripheral arterial differences, aiding in distinguishing pathological cardiac enlargement from exercise adaptations. These vascular changes highlight potential diagnostic markers beyond cardiac imaging.
Area of Science:
- Cardiology
- Vascular Biology
- Sports Medicine
Background:
- Hypertrophic cardiomyopathy (HCM) is a primary cause of sudden cardiac death in young athletes.
- Differentiating physiological (athlete's heart) from pathological (HCM) cardiac remodeling is clinically challenging.
- Peripheral vascular adaptations in HCM are poorly understood, despite known effects of training on vasculature.
Purpose of the Study:
- To investigate peripheral vascular differences between HCM patients and athletes.
- To determine if arterial structure and function vary between HCM, athletes, and controls.
- To identify potential non-cardiac markers for differentiating HCM from exercise-induced cardiac changes.
Main Methods:
- High-resolution ultrasound was used to measure carotid and brachial artery diameter and wall thickness.
- Flow-mediated dilation (FMD) of brachial arteries was assessed.
- Age-matched groups of HCM patients (n=18), competitive athletes (n=18), and controls (n=10) were studied.
Main Results:
- Significant differences in carotid and brachial artery wall thickness were observed between athletes and HCM patients.
- Athletes exhibited greater brachial artery peak blood flow response, indicating altered resistance artery remodeling compared to HCM patients.
- No significant differences were found in brachial artery FMD% between the groups.
Conclusions:
- Peripheral arterial structure differs between HCM patients and athletes, despite similar cardiac characteristics.
- These vascular differences may stem from HCM pathology or a general effect of physical activity on arteries.
- Further research is needed to explore artery function and structure in athletic individuals with HCM.
Background:
Hypertrophic cardiomyopathy (HCM) is characterised by idiopathic cardiac enlargement and represents the most frequent cause of sudden cardiac death in athletes under the age of 35 years. Differentiation between physiological (ie, exercise-related) and pathological (ie, HCM-related) cardiac remodelling is challenging. In line with cardiac remodelling, vascular structure and function are altered following training, but little is known about peripheral vascular adaptations in HCM. We hypothesised that, while HCM patients and athletes would exhibit similar cardiac characteristics, differences would be apparent in their brachial and carotid arteries.
Methods:
In age-matched groups of HCM patients (n = 18, 39 ± 15 years), highly competitive athletes (n = 18, 38 ± 12 years) and recreational controls (n = 10, 37 ± 14 years), we used high-resolution ultrasound to assess the diameter and wall thickness of the carotid and brachial arteries, with flow-mediated dilator function (FMD) of the brachial arteries also assessed.
Results:
A significant difference between athletes and HCM was evident in arterial wall thickness (carotid 519 ± 60 vs 586 ± 102 µm, p<0.05; brachial 345 ± 80 vs 456 ± 76 µm, p<0.05) and the brachial artery peak blood flow response following forearm ischaemia, an index of resistance artery remodelling (998 ± 515 vs 725 ± 248 ml/min, p<0.05). Similar differences were noted between athletes and controls, while controls and HCM did not differ. Brachial FMD% was not different between groups.
Conclusions:
Athletes and HCM subjects, who can be difficult to differentiate on the basis of cardiac measures, exhibit differences in indices of arterial structure. While this may be a disease-related effect, we cannot discount a generic impact of physical activity on arterial structure, as the athlete's arteries were also different to untrained control subjects. Future studies should assess artery function and structure in athletic HCM subjects.
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