This pathological stew, which is self-reinforcing in many ways, is typically triggered by chronic mechanical strain—induced by uncontrolled hypertension, volume overload, valvular stenosis or failure, or loss of viable myocardium following myocardial infarctions or infections—and neurohormonal stimuli associated with the systemic stress reaction and/or kidney failure, such as adrenergic activity, angiotensin II, endothelin, and fibroblast growth factor 23 (FGF23). Here, FGF23 is linked to infection.