In accordance with the Frank–Starling law of the heart, the myocardium contracts more powerfully as the end-diastolic<unk> lume increases. Stretching of the myofibrils in cardiac muscle causes them to contract more powerfully due to a greater number of cross-bridges being formed between the myofibrils within cardiac myocytes. This is true up to a point, however beyond this there is a loss of contractile ability due to loss of connection between myofibrils; see figure. Various pathologies, listed below, can lead to<unk> . Different mechanisms are involved depending on the cause, however the common theme is that of a high cardiac output with a low or normal afterload. The output may be high due to the inefficiency in valve disease, or it may be high due to shunting of blood in left-to-right shunts and arteriovenous malformations. Left ventricular<unk>  may produce inverted u waves on the electrocardiogram.
Volume overload
Allostatic load
Dehydration
Exercise addiction
Cardiac fibrosis
Digoxin toxicity
Cholemia
Monofixation syndrome