Plastic hearts still break

By Eleanor McDermid, Senior medwireNews Reporter

Renewal of cells in the human heart occurs throughout life and is boosted by, but cannot prevent, the effects of aging and cardiomyopathy, a study shows.

Researchers carbon-dated cardiac cells obtained from healthy donor hearts and hearts explanted from patients with chronic heart failure. They found that myocyte turnover was rapid during the early years of life, remained fairly constant during adulthood, and increased in old age.

Jan Kajstura (Harvard Medical School, Boston, Massachusetts, USA) and co-workers say that their findings contrast with those of a previous ¹⁴C-dating study, which found minimal cell renewal. They detail several methodologic factors that they believe account for this discrepancy, including the presence of bi- and multinucleated cells, polyploidy, and the variable proportions of different cell types in the heart at different stages of life.

Moreover, they point out that the occurrence of both apoptotic and necrotic cell death in the heart is well accepted.

"Myocyte apoptosis and necrosis occur physiologically, and cell death has to be accompanied by cell formation for the heart to continue to exist," they write in Circulation. "The simple concept of a requisite equilibrium between myocyte death and renewal has often been ignored."

Previous research suggests that 0.006% of cardiomyocytes are lost daily through apoptosis alone, which would account for 95% of the heart over 30 years, were the cells not replaced.

The team found that hearts from children aged 2, 3, and 7 years contained myocytes that averaged 8 months of age, indicating fairly rapid turnover. Myocytes were an average age of 2.8 years in healthy hearts from people aged up to 20 years, 7.9 years for age 33 to 46 years, and 6.5 years for age 49 to 63 years, showing that turnover slowed and then stabilized in adulthood.

In people aged 68 to 78 years, myocytes were younger, at an average age of 2.6 years, indicating that turnover increased in the aging heart.

The entire population of myocytes is replaced about eight times between the ages of 20 and 78 years, say Kajstura et al. They calculated that fibroblasts are also replaced about eight times, but vascular endothelial cells only six.

Cells from hearts affected by post-infarction ischemic cardiomyopathy or idiopathic dilated cardiomyopathy were on average 40-49% younger than those in healthy hearts of a similar age, meaning that turnover was boosted around twofold. In one extreme case, a 22-year-old patient had an annual myocyte renewal rate of 750%, when the expected rate for his age was about 7%.

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