An enhanced inflammatory state - i.e. "inflammatory/pathogen burden" - in the elderly on the one hand results from physiological immunosenescence and on the other hand is modified by the individual immune history: the latter is determined by sequential infectious/pathogenic events ("multiple hits"). Immunosenescence may prompt ageing of other organs. Cardiac ageing can be assessed by analysing heart rate variability. We present our hypothesis that the increasing "inflammatory/pathogen burden" of each organism during a lifetime significantly contributes to the cardiac ageing process. This hypothesis is grounded on the fact that a characteristic feature of the ageing heart - a narrowed heart rate variability - can be experimentally induced in humans by an inflammatory stimulus (endotoxin).