A study from our group and another recent review of 2196 patients in The Society of Thoracic Surgeons National Database found that tricuspid valve (TV) procedures in LVAD patients with moderate to severe tricuspid valve regurgitation failed to reduce early mortality or the need for an RV assist device (RVAD) but was associated with more postoperative renal failure and prolonged intensive care unit and hospital lengths of stay [10, 26]. Therefore, we don’t consider TV repair procedures at the time of LVAD surgery. As previously described in the preoperative management, aggressive diuresis is among important preoperative measures to prevent postoperative RVF. Our experience and experience of several other groups have shown that tricuspid valve regurgitation can be significantly reduced with aggressive diuresis prior to LVAD implantation.

Pharmacological therapies of RV dysfunction include inhalative and intravenous agents. The role of pulmonary vasodilators (inhaled nitric oxide (NO) or prostacyclin) or a phosphodiesterase inhibitor such as sildenafil is still the subject of current investigation. Current evidence suggests that pulmonary hemodynamics may be improved in some patients with LVAD therapy receiving inhaled NO. In the study by Argenziano et al. including 11 patients with LVAD and pulmonary hypertension were randomized to receive either inhaled NO at 20 ppm (n = 6) or nitrogen (n = 5). In that study, the use of inhaled NO was associated with a decrease in mean PAP and improvement in LVAD flow compared with the placebo group [27]. However, Kukucka et al. investigated in a randomized trial the effects of inhaled nitric oxide on the hemodynamics of LVAD patients with PVR above 200 dyne s/cm⁵ [28]. In their study, no significant difference in hemodynamics was found between groups, although hemodynamics improved after LVAD implantation in both groups. In another small study including seven patients with RV dysfunction after LVAD insertion, inotropes, inhaled NO (10 ppm), and iloprost (10 g) in repeated doses were evaluated [29]. The authors conclude that inhaled vasodilators mainly affected the pulmonary vasculature. Furthermore, combination treatment with inhaled NO and iloprost sufficiently decreased PVR and mean PAP on the basis of an additive effect, improved RV function, and avoided the need for RVAD.

The effect of inhaled milrinone was prospectively evaluated in ten postoperative LVAD patients with a mean INTERMACS profile of 2.5 ± 0.8 [30]. Inhaled milrinone was delivered into a ventilator circuit for 24 hours. Tolerability, efficacy, pharmacokinetics, and cost data were evaluated. Invasive mean PAP from baseline to during milrinone therapy was improved. The authors conclude that inhaled milrinone delivery after cf-LVAD implantation was well tolerated and feasible and demonstrated favorable hemodynamic, pharmacokinetic, and cost profiles.

Considering inotropic agents for RV support, it is important to consider supporting the RV with inotropes that allow some pulmonary vasodilatation (dobutamine or milrinone) while maintaining adequate systolic blood pressure (epinephrine) for coronary perfusion. Ideally, inotropic support can be withdrawn in the first few days after surgery as volume status is optimized and RV function recovers. The most commonly used inotropes are milrinone, dobutamine, and epinephrine depending on center preference. Milrinone is a phosphodiesterase- 3 inhibitor that has inotropic and vasodilatory effects. Dobutamine directly stimulates β1-adrenergic receptors resulting in increased contractility. While dobutamine provides some peripheral vasodilation, its systemic hypotensive effects are substantially less pronounced compared to milrinone. Therefore, dobutamine may be the inotrope of choice in a patient with systemic hypotension and/or postoperative vasoplegic syndrome. In addition, milrinone has a half-life of more than 2 h in patients with normal renal function but substantially longer in patients with renal dysfunction. The longer half-life of milrinone compared with dobutamine (which has a half-life of minutes) may be an advantage when inotropes are being slowly weaned, but may be a disadvantage in patients with significant renal dysfunction [23]. Epinephrine and dopamine do have inotropic effects, but they produce dose-dependent increases in PVR (epinephrine at doses of >0.05 μg/kg/min and dopamine at doses of >5 μg/kg/min). Therefore, these agents are usually used as adjuncts when systemic vasopressor support is needed to maintain coronary perfusion [23, 31].