FIGURE LEGENDS
Figure 1. Long-axis view on echocardiography on admission. Echocardiography showed diffuse severe hypokinesis, increased left ventricular end-diastolic diameter, and moderate mitral regurgitation.
Figure 2. Clinical course. Dobutamine and pimobendane promoted adequate diuresis at the beginning, but gradually result in poor diuresis with HR elevation (120 bpm). After oral ivabradine, the HR decreased and blood pressure increased.
SBP; systolic blood pressure, HR; heart rate, BW; body weight
Figure 3. Echocardiographic changes before (left) and after (right) ivabradine administration. Before ivabradine, echocardiography shows an extreme overlap between the E- and A-waves, low LVOT-VTI, and low SV. After ivabradine, the overlap decreased and LVOT-VTI and SV increased.
HR; heart rate, LVOT-VTI; velocity-time integral at the left ventricular outflow tract, SV; stroke volume
Figure 4. Long-axis view on echocardiography at the time of discharge. Echocardiography showed diffuse severe hypokinesis, but LVEF and mitral regurgitation had improved compared to the time of admission.
Figure 5. The plausible mechanism of an increase of SV by ivabradine. The increased SV by ivabradine is derived from alterations in hemodynamics such as pre-and afterload and myocardial contractility.
HR; heart rate, SV; stroke volume, SERCA2a; sarcoplasmic/endoplasmic reticulum calcium ATPase 2a
Figure 6. HR optimization from the viewpoint of echocardiography.
A: Normal. B: LV diastolic dysfunction prolongs LV relaxation time. C: In higher heart rate, LA systole could interfere with LV complete relaxation. D: Prevention of the E and A waves from overlapping using echocardiographic monitoring might help LV complete relaxation.
LV; left ventricle, LA; left atrial, TMF; trans mitral flow, IRT; isovolumic relaxation time, RF; rapid filling, SF; slow filling, AS; atrial systole, the red line indicates the overlap between the E and A waves