Figure 14

Force-frequency curve with stress echo in a normal subject. 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). An increased heart rate is accompanied by an increased systolic pressure with smaller end-systolic volumes (normal up sloping force-frequency relation). Lower panel: 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 the normal heart increase in heart rate is accompanied by an increase in myocardial contractile performance (up-sloping FFR). At higher heart rates more and faster "cascade" calcium is released from the SR: more calcium is available in the cytoplasm for C troponin interaction and contraction. Equally calcium reuptake is more and faster in diastole. Both action potential and calcium transient are rapidly peaking in systole at each stress step.