Peripheral vascular structure and function in hypertrophic cardiomyopathy.

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.

Conduit diameter and wall remodeling in elite athletes and spinal cord injury.

PURPOSE: This study aimed to investigate localized and systemic effects of chronic exercise and inactivity on conduit artery remodeling in humans. METHODS: We recruited elite athletes engaged in predominantly lower limb (LL runners/cyclists, n = 10) or upper limb (UL canoe paddlers, n = 12) exercise and matched able-bodied, recreationally active, controls (C, n = 16). We also studied wheelchair controls (spinal cord injury, n = 9) and athletes (spinal cord injury, n = 1; spina bifida, n = 4). Carotid, brachial, and superficial femoral (SF) artery diameter and wall thickness were assessed using high-resolution ultrasound. RESULTS: Brachial diameters were significantly larger in UL and wheelchair users (athletes and controls) compared with C (both P < 0.05). SF artery diameter in wheelchair controls was significantly smaller compared with the other groups, with LL athletes having significantly greater lumen diameter than controls (both P < 0.05). In all arteries, a lower wall thickness was found in able-bodied athletes compared with C, including wheelchair athletes compared with wheelchair controls (P < 0.001). In the SF artery, wall-to-lumen-ratio was significantly lower in able-bodied athletes and higher in wheelchair controls compared with able-bodied controls (P < 0.001). In the brachial and carotid arteries, able-bodied and wheelchair athletes demonstrated lower wall-to-lumen-ratio than less active wheelchair controls and able-bodied controls (P < 0.001). CONCLUSIONS: These findings suggest that remodeling of the arterial wall occurs systemically in response to exercise training and is unrelated to exercise type in humans. Conversely, localized effects are evident with respect to the effect of exercise on arterial diameter. These findings have implications for our understanding of the effects of exercise on arterial structure and function in humans.