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In a related study that assessed the heart size and function of sixty non-élite Boston marathoners, Malissa Wood and Tom Neilan found that, immediately following the race, a percentage of runners had evidence of heart-chamber enlargement and increased stiffness.
Pulmonary hyperinflation in COPD affects pulmonary haemodynamics and consequently heart size and function.
Observational studies often have different endpoints (e.g. advanced magnetic resonance imaging of heart size and function) that may not have been studied in an RCT, longer follow-up, unique populations, or some other inherent practical advantage for examining certain associations.
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Pulmonary hyperinflation can significantly affect heart size and its function.
It has been shown that both heart size and cardiac function are angiogenesis dependent, and disruption of coordinated cardiac muscle growth and angiogenesis in the heart contributes to the progression from adaptive cardiac hypertrophy to heart failure [ 99, 108].
Whether the improved function, small heart size and decreased wall stress were responsible for a reduction in apoptosis is not known.
GGA led to reduction in heart size and inhibition of interstitial fibrosis, and recovery of cardiac function as well as improved survival.
Furthermore, R120G TG mice treated with GGA exhibited decreased heart size and less interstitial fibrosis, as well as improved cardiac function and survival compared to untreated R120G TG mice.
Hyperinflation may play an important role regarding heart size and heart dysfunction in patients with COPD.
Large animal models such as the dog, sheep, or pig have greater physiologic resemblance to humans with similar body size, heart size, and heart rate.
Thickening of the heart muscle, which results in increased heart size and decreased chamber size.
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