Stress cardiomyopathy is a unique heart syndrome that is characterized by reversible left ventricular apical wall motion abnormalities and is commonly known as Takotsubo syndrome. In transient left ventricular apical ballooning, myocardium lengthening stress is in a high energy-demand state. The increased passive tension and force enhancement conducted asynergically are associated with severe hypokinesis on the ventricular wall and reduced the blood ejection fraction. Ventricular myocardial deformation and global longitudinal strain have significant mechanotemporal alteration characteristics. Membrane potential dominant mechanisms related to akinesia are considered from multiple effects of variation of calcium transients, myocardium metabolism, which is relative to the ST segment lift in an ECG, and in the weakness of contraction of the ventricular muscle. Ventricular filling, not pressure,-determine the strengthening from stretching; thus, in stress cardiomyopathy, ventricular apical ballooning (takotsubo-shaped ventricle) strengthens the mechanical stress on the wall. Muscle fiber tolerance of lengthening is a high energy consumption process. Ventricular apical akinesia further aggravates passive tension. Depleted ATP and high inorganic phosphate inhibit Ca 2+-activated development, terminates the crossbridge detachment process in its early stage, and facilitates the occurrence of myogenic force enhancement. Comprehensive analysis of the above mechanisms, in lengthening stress, increased cardiac fibers energy demand, and Ca 2+ transient variation interruption of the diastolic cycle, delayed the onset of systole and aggravated the occurrence of apical ballooning in stress cardiomyopathy.