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Cardiovascular ageing represents a major burden for elderly patients and healthcare providers. The current impressive increase of life expectation highlights the need to understand the (patho)physiology of ageing in order to define potential therapeutic strategies to confront this challenge. Among many unresolved issues, the age-related progressive reduction of myocardial efficiency certainly represents one of the most fascinating.
Age-related reduction of cardiac cellular metabolic reserve
In normal myocardium, the concentrations of the high-energy phosphate compounds ATP and phosphocreatine (PCr) are tightly controlled over a range of performance because ATP production by mitochondrial oxidative phosphorylation is closely coupled to ATP utilisation by cytosolic adenosine triphosphatases. ATP is the direct energy source for energy-consuming reactions in the cell, while PCr acts as an energy storage compound and, in addition, as an energy transport molecule in the ‘creatine kinase-PCr energy shuttle’. Previous clinical studies using phosphorus-31 magnetic resonance spectroscopy (31P-MRS) to measure PCr/ATP ratios in human myocardium have shown that this ratio is reduced in hypertrophied and, even more so, in failing human myocardium. In their Heart manuscript, Nathania1 investigated a possible relation between age and PCr/ATP ratio and cardiac power in healthy women by cardiac MRS with 31P spectroscopy and maximal graded cardiopulmonary exercise testing.1 PCr/ATP ratio, peak cardiac power, diastolic function and peak exercise oxygen consumption were significantly lower in old compared with young age group. PCr/ATP ratio showed a significant positive relationship with diastolic function, peak cardiac power output and peak oxygen consumption. These results indicate that high-energy phosphate metabolism and peak power of the heart decline with age. Additionally, based on the positive relationship between …
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