Anrep effect

The Anrep effect describes the rapid increase in myocardial contractility in response to the sudden rise in afterload, the pressure the heart must work against to eject blood.^[1][2] This adaptive mechanism allows the heart to sustain stroke volume and cardiac output despite increased resistance. It operates through homeometric autoregulation, meaning that contractility adjustments occur independently of preload (the initial stretch of the heart muscle) or heart rate.^[1][2][3]

The Anrep effect is characterized by a two-step elevation in myocardial contractility, in response to elevated afterload, involving two distinct mechanistic phases: a primary, rapid rise in contractility driven by sarcomeric strain sensing, and a secondary, sustained phase of contraction mediated by post-translational modifications of contractile proteins.^[3][4] First described by Gleb von Anrep in 1912^[5] and further elaborated in the 1960s by Sarnoff et al.,^[1][2] the Anrep effect represents a distinct cardiac regulation mechanism, differing fundamentally from the Frank-Starling mechanism,^[6] the slow force response,^[7][8] and the Gregg effect.^[9]

While traditionally considered a short-term adaptation, recent studies suggest that the Anrep effect may also occur in chronic conditions involving persistent afterload elevation, such as hypertrophic obstructive cardiomyopathy.^[4]