Force-frequency curve with stress echo in a subject with latent LV dysfunction without dilation. Upper panel. On the left, systolic blood pressure by cuff sphygmomanometer (SP, first row); left ventricular end-systolic volumes calculated with biplane Simpson method (ESV, second row); heart rate increase during stress (bpm, third row); in the lowest row, the force-frequency curve built off-line with the values recorded at baseline (second column), and at different steps (third, fourth, fifth column) up to peak stress (sixth column). The force-frequency relation is biphasic, with an initial up-sloping trend followed by a later down-sloping trend. Lower panel: hypothetical molecular basis (first row), action potential (second row) and calcium transient (third row) of myocytes at baseline (first column), intermediate stress (second column) and peak stress (third column). In latent failing myocytes calcium transient can be normal at baseline, but abnormal at higher heart contraction rates: compared with a normal baseline pattern (first column), at intermediate stress (second column) delayed cytosolic Ca2+ diastolic removal occurs; further dysfunction (cytolsolic Ca2+ attenuated rise with depolarization and a markedly delayed return to baseline) occurs at higher heart rates. When the heart beats at frequencies beyond the CHR, when calcium is extruded from the myocyte instead of re-entry in the SR, the O2 consumption for each unit of force developed is doubled; the combination of decreased cardiac force development and increased oxygen uptake indicates decreased efficiency of cardiac work.