Acute-phase administration of ivabradine supported by intra-aortic balloon pump induces myocardial recovery without significant haemodynamic worsening in a patient with acute fulminant myocarditis: a case report

Figures

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  Figure 1. Chest X-ray (A), 12-lead electrocardiography (B), and histopathology (C) on Day 1. Histopathology of the right-ventricular endomyocardial specimen taken on admission (haematoxylin and eosin staining ×400). Marked and diffused infiltration of lymphocytes (arrow) within the myocardium is observed, while eosinophilic infiltration is absent. The findings are consistent with acute lymphocytic myocarditis.

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  Figure 2. Changes in haemodynamics and the treatment. Ivabradine was initiated on Day 2 because guideline-directed medications combined with intra-aortic balloon pump did not improve haemodynamic parameters and the sinus tachycardia continued. ‘Supported ivabradine’ induced favourable changes in the parameters. HR, heart rate; BP, blood pressure; BNP, brain natriuretic peptide; CI, cardiac index; IVA, ivabradine; IABP, intra-aortic balloon pump; hANP, human atrial natriuretic peptide; MIL, milrinone; DOB, dobutamine.

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  Figure 3. The illustration of changes of the cardiac output curve under ‘supported ivabradine’. The circulatory equilibrium framework consists of the cardiac output curve, representing ventricular pumping ability, and venous return. The patient in acute heart failure with left-ventricular dysfunction has a lower cardiac output curve than normal (thin line). The heart rate is a major determinant of the slope in cardiac output curve. The bradycardia by ivabradine might decrease cardiac output curve further (dashed line). Intra-aortic balloon pump support preserved the decrease of cardiac output curve within acceptable haemodynamic level (bold line). LV, left ventricle; IVA, ivabradine; IABP, intra-aortic balloon pump.