A drive control method with direct cardiac potential trigger for a ventricular assist device (VAD) was evaluated in various conditions in an experimental model. A pneumatic VAD was implanted as a support bypass between the left ventricular apex and the ascending aorta in eight animals. The hemodynamic parameters and pump output were monitored. Two tips of a bipolar electrode were set on the RV (n = 3) or on the RV and LV (n = 5) for recording direct cardiac potential. The counter-pulsation drive of the VAD was applied by using the R wave in the standard electrocardiogram (ECG) or the direct cardiac potential as an ECG trigger. As special conditions with various artifacts on the ECG, electromusculogram, arrhythmia, irregular ventilation, and passive vibration (simulation of exercise) were set for assessing the ECG trigger modes. Artifacts of irregular ventilation and passive vibration made the drive control poor under standard ECG trigger and caused incomplete control in the case of direct cardiac potential trigger by using the RV bipolar electrode. In contrast, direct cardiac potential trigger by using the RV and LV bipolar electrode maintained the counter-pulsation control of the VAD well in all conditions of this study. The results suggest that this counter-pulsation control with direct cardiac potential trigger might be one of the control methods for various VADs of the next generation.

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A malignant form of non-cardiogenic pulmonary edema (NCPE) that develops soon after the termination of cardiopulmonary bypass support during cardiac surgery is rarely encountered. It sometimes requires immediate management, including venovenous extracorporeal membrane oxygenation (VV-ECMO). In the first case, a 78-year-old female patient experienced fulminating NCPE after mitral valve plasty, which caused severe respiratory failure and hemodynamic instability due to a huge amount of sputum. In the second case, a 47-year-old male patient presented with right-sided unilateral pulmonary edema with a substantial amount of sputum after minimally invasive cardiac surgery for mitral valve repair. In both cases, VV-ECMO and aggressive fluid replacement were promptly initiated. The NCPE resolved on post-operative day 2, resulting in the successful termination of VV-ECMO. NCPE leads to lethal respiratory failure with multifactorial causes during cardiac surgery. However, as NCPE is potentially transient, immediate treatment comprising VV-ECMO and aggressive fluid replacement can improve clinical outcomes.

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Rheumatic tricuspid stenosis has become rare recently. A 54-year-old woman had undergone mitral valve replacement with a Carpentier-Edwards bioprosthesis for mitral stenosis 22 years previously and had undergone repeat mitral valve replacement for prosthetic valve failure 10 years later. She was admitted with severe leg edema. Cardiac catheterization revealed pulmonary hypertension and tricuspid stenosis with a diastolic pressure gradient of 6mmHg across the tricuspid valve. Tricuspid valve replacement was performed with a Hancock bioprosthesis. The postoperative course was uneventful and her edema improved markedly. This case suggested that careful follow-up to detect progression of tricuspid stenosis is necessary in patients with rheumatic valve disease and pulmonary hypertension.