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Figure 16 | Cardiovascular Ultrasound

Figure 16

From: Myocardial contractility in the echo lab: molecular, cellular and pathophysiological basis

Figure 16

Force-frequency curve with stress echo in a subject with dilated cardiomyopathy and depressed baseline left ventricular function (EF% = 30%). 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 at peak exercise is accompanied by no changes in end-systolic volumes (abnormal flat 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). The action potentials are markedly prolonged at baseline and during stress in patients with advanced heart failure; calcium cycling is slow at basal heart rates and even more at higher heart rates. These abnormal patterns are related to a profound derangement of the contractile machinery in the failing myocyte: fewer calcium membrane channels, fewer RNA levels encoding contractile proteins, fewer and dysfunctioning SERCA. A critical alteration of force-frequency relationship occurs, with an inversion of the normal positive to a flat or negative slope.

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