Newer-generation ventricular assist devices.

The latest generation of ventricular assist devices has evolved from the pulsatile, volume-displacement pumps of the 1990s to today's non-pulsatile, constant pressure-generating rotary pumps. These pumps include both centrifugal and axial flow devices that are currently being used or are in advanced development. Rotary pumps have the advantage of a much longer and more reliable duty life than pulsatile pumps. They are also considerably smaller than pulsatile pumps, requiring less invasive surgery for implantation and smaller transcutaneous (electrical rather than pneumatic) drivelines. Most of these devices have been approved as a bridge to transplant (BTT) while some are currently in trials for destination therapy (DT) in Europe (Conformité Européenne (CE) mark) or the United States (Food and Drug Administration (FDA)). This article discusses the current generation of pumps, examining particular design features as highlighted by the designers as well as the current approval status of each device in the United States and Europe.

The intravenous anesthetic propofol inhibits human L-type calcium channels by enhancing voltage-dependent inactivation.

Propofol is commonly used to induce anesthesia but has been associated with some negative cardiovascular side effects, including negative inotropy, hypotension, and bradycardia. This study investigated the effect of propofol on L-type calcium current in acutely isolated human atrial myocytes to better understand the mechanism of these side effects. After informed consent was obtained, the atrial appendage was obtained from patients undergoing open-heart surgery who required cardiopulmonary bypass. Atrial myocytes were isolated using enzymatic digestion, and L-type calcium currents were recorded using the whole-cell patch clamp technique. Propofol enhanced the magnitude and speed of voltage-dependent inactivation of L-current. As a result, the propofol-induced inhibition was increased by protocols that increased inactivation such as longer voltage step duration, holding potential depolarization, and increased pulsing frequency. The preferential enhancement of L-channel inactivation by propofol can explain the associated cardiovascular side effects. The depolarized resting potential of arterial smooth muscle may render the L-channels in these cells particularly sensitive to propofol-induced inhibition, which could explain the hypotension observed in some patients. The enhancement of both inactivation kinetics and steady-state inactivation by propofol can also explain the negative inotropic effect. However, the enhanced voltage-dependent inactivation and use dependence could have beneficial effects for patients prone to certain arrhythmias and tachycardia.