Abstract
Development of coronary arteriosclerosis has been studied in all life stages of both wild and cultured Atlantic salmon (Salmo salar). Lesions accumulate slowly during juvenile growth in freshwater in both wild and cultured populations and increase sharply during early marine life; much of the progression occurs well before the onset of sexual maturity. Fewer than 5% of sexually mature Atlantic salmon (wild or fast-growing cultivated) were free of coronary lesions. Lesions were distributed over 45–85% of the length of the coronary artery. Lesions were less abundant and less advanced in a cultured strain of salmon that grew more slowly than another cultured, fast-growing strain. We conclude that prevalence and severity of lesions in Atlantic salmon accelerate in parallel with, and possibly in response to, those factors responsible for rapid growth in the sea. We discuss diet, endocrine changes associated with sexual maturation, metabolic aspects of parr–smolt transformation, and physiological stress as factors possibly influencing progression of lesions associated with rapid growth during the marine stage.
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