Prevention of Right Heart Failure After Left Ventricular Assist Device Implantation by Phosphodiesterase 5 Inhibitor

Right ventricular (RV) function immediately after left ventricular assist device (LVAD) implantation is a crucial prognostic factor. RV failure is linked to increased mortality and worse outcome. A phosphodiesterase 5 inhibitor, sildenafil, was shown to decrease pulmonary vascular resistance and pulmonary artery pressure post‐LVAD. We report on a series of heart failure patients, and the effect of sildenafil on the incidence of RV failure after LVAD implantation. We retrospectively analyzed the data of end‐stage heart failure patients who underwent LVAD implantation with pulmonary hypertension and RV dysfunction prior to surgery. Patients were divided into two groups; group 1: patients who received sildenafil perioperatively, and group 2: patients who did not receive sildenafil. Hemodynamic and echographic data were collected before and after surgery. Fourteen patients were included, 8 patients in group 1 and 6 in group 2. Sildenafil was administered with a mean dose of 56.2 ± 9.4 mg in group 1 and was able to significantly reduce right heart failure incidence, and to demonstrate a significant reduction in pulmonary vascular resistance, pulmonary artery pressure, transpulmonary gradient, and a significant increase in cardiac output. In conclusion, sildenafil seems to have a promising role perioperatively in preventing acute RV failure postsurgery in patients with RV dysfunction and pulmonary hypertension, requiring LVAD therapy.     

Preoperative risk factors for right ventricular failure after implantable left ventricular assist device insertion

Background. Implantable left ventricular assist device (LVAD) insertion complicated by early right ventricular (RV) failure has a poor prognosis and is generally unpredictable.

Methods. To determine preoperative risk factors for perioperative RV failure after LVAD insertion, patient characteristics and preoperative hemodynamics were analyzed in 100 patients with the HeartMate LVAD (Thermo Cardiosystems, Inc, Woburn, MA) at the Cleveland Clinic.

Results. RV assist device support was required for 11 patients (RVAD group). RVAD use was significantly higher in younger patients, female patients, smaller patients, and myocarditis patients. There was no significant difference in the cardiac index, RV ejection fraction, or right atrial pressure between the two groups preoperatively. The preoperative mean pulmonary arterial pressure (PAP) and RV stroke work index (RV SWI) were significantly lower in the RVAD group (p = 0.015 and p = 0.011, respectively). Survival to transplant was poor in the RVAD group (27%) and was 83% in the no-RVAD group.

Conclusions. The need for perioperative RVAD support was low, only 11%. Preoperative low PAP and low RV SWI were significant risk factors for RVAD use.     

Clinical Outcomes of Patients Treated With Pulmonary Vasodilators Early and in High Dose After Left Ventricular Assist Device Implantation

Right ventricular failure (RVF) is common after left ventricular assist device (LVAD) implantation and a major determinant of adverse outcomes. Optimal perioperative right ventricular (RV) management is not well defined. We evaluated the use of pulmonary vasodilator therapy during LVAD implantation. We performed a retrospective analysis of continuous‐flow LVAD implants and pulmonary vasodilator use at our institution between September 2004 and June 2013. Preoperative RVF risk was assessed using recognized variables. Sixty‐five patients (80% men, 50 ± 14 years) were included: 52% HeartWare ventricular assist device (HVAD), 11% HeartMate II (HMII), 17% VentrAssist, 20% Jarvik. Predicted RVF risk was comparable with contemporary LVAD populations: 8% ventilated, 14% mechanical support, 86% inotropes, 25% BUN >39 mg/dL, 23% bilirubin ≥2 mg/dL, 31% RV : LV (left ventricular) diameter ≥0.75, 27% RA : PCWP (right atrium : pulmonary capillary wedge pressure) >0.63, 36% RV stroke work index <6 gm‐m/m²/beat. The majority (91%) received pulmonary vasodilators early and in high dose: 72% nitric oxide, 77% sildenafil (max 200 ± 79 mg/day), 66% iloprost (max 126 ± 37 μg/day). Median hospital stay was 26 (21) days. No patient required RV mechanical support. Of six (9%) patients meeting RVF criteria based on prolonged need for inotropes, four were transplanted, one is alive with an LVAD at 3 years, and one died on day 35 of intracranial hemorrhage. Two‐year survival was 77% (92% for HMII/HVAD): transplanted 54%, alive with LVAD 21%, recovery/explanted 2%. A low incidence of RVF and excellent outcomes were observed for patients treated early during LVAD implantation with combination, high‐dose pulmonary vasodilators. The results warrant further investigation in a randomized controlled study.     

Effect of left ventricular assist device implantation on right ventricular function: Assessment based on right ventricular pressure–volume curves

Right ventricular (RV) failure is significantly associated with morbidity and mortality after left ventricular assist device (LVAD) implantation. However, it remains unclear whether LVAD implantation could worsen RV function. Therefore, we aimed to investigate the effect of LVAD implantation on RV function by comparing RV energetics derived from the RV pressure–volume curve between before and after LVAD implantation. This exploratory observational study was performed between September 2016 and January 2018 at a national center in Japan. Twenty-two patients who underwent LVAD implantation were included in the analysis. We measured RV energetics parameters: RV stroke work index (RVSWI), which was calculated by integrating the area within the RV pressure–volume curve; RV minute work index (RVMWI), which was calculated as RVSWI × heart rate; and right ventriculo–arterial coupling, which was estimated as RV stroke volume/RV end-systolic volume. We compared RV energetics between before and after LVAD implantation. Although RVSWI was similar [424.4 mm Hg · mL/m² (269.5-510.3) vs. 379.9 mm Hg · mL/m² (313.1-608.8), P = 0.485], RVMWI was significantly higher after LVAD implantation [29 834.1 mm Hg · mL/m²/min (18 272.2-36 357.1) vs. 38 544.8 mm Hg · mL/m²/min (29 016.0-57 282.8), P = 0.001], corresponding to a significantly higher cardiac index [2.0 L/min/m² (1.4-2.2) vs. 3.7 L/min/m² (3.3-4.1), P < 0.001] to match LVAD flow. Right ventriculo–arterial coupling was significantly higher after LVAD implantation [0.360 (0.224-0.506) vs. 0.480 (0.343-0.669), P = 0.025], suggesting that the efficiency of RV performance improved. In conclusion, higher RVMWI with higher cardiac index to match LVAD flow and improved efficiency of RV performance indicate that LVAD implantation might not worsen RV function.     

Impact of Residual Mitral Regurgitation on Right Ventricular Systolic Function After Left Ventricular Assist Device Implantation

Significant mitral regurgitation (MR) is thought to decrease after left ventricular assist device (LVAD) implantation, and therefore repair of mitral valve is not indicated in current practice. However, residual moderate and severe MR leads to pulmonary artery pressure increase, thereby resulting in right ventricular (RV) dysfunction during follow‐up. We examined the impact of residual MR on systolic function of the right ventricle by echocardiography after LVAD implantation. This study included 90 patients (mean age: 51.7 ± 10.9 years, 14.4% female) who underwent LVAD implantation (HeartMate II = 21, HeartWare = 69) in a single center between December 2010 and June 2014. Echocardiograms obtained at 3–6 months and over after implantation were analyzed retrospectively. RV systolic function was graded as normal, mild, moderate, and severely depressed. MR (≥moderate) was observed in 43 and 44% of patients at early and late period, respectively. Systolic function of the RV was severely depressed in 16 and 9% of all patients. Initial analysis (mean duration of support 174.3 ± 42.5 days) showed a statistically significant correlation between less MR and improved systolic function of RV (P = 0.01). Secondary echocardiographic analysis (following a mean duration of support of 435.1 ± 203 days) was also statistically significant for MR degree and RV systolic dysfunction (P = 0.008). Residual MR after LVAD implantation may cause deterioration of RV systolic function and cause right‐sided heart failure symptoms. Repair of severe MR, in selected patients such as those with severe pulmonary hypertension and depressed RV, may be considered to improve the patient's clinical course during pump support.     

Implantation of left ventricular support under extracorporeal membrane oxygenation

Continuous-flow left ventricular assist devices (LVADs) are used to manage patients with end-stage heart failure. Protection of right ventricular (RV) function is important during LVAD implantation, but sometimes patients require temporary RV support. We describe the technique of LVAD implantation under extracorporeal membrane oxygenation (ECMO) we use in our center. This technique allows soft loading of the right ventricle once LVAD is started and even short-term RV support if required.     

The Effect of Left Ventricular Bypass on the Right Ventricular Function: Experimental Analysis of the Effects of Ischemic Injuries to the Right Ventricular Free Wall and Interventricular Septum

The right ventricular (RV) function during left heart bypass (LHB) was examined in open-chest anesthetized mongrel dogs (average weight, 11.8 kg). The LHB was carried out by a left ventricle (LV) to femoral artery bypass using a centrifugal pump for 90 min, and the bypass flow was kept maximum to obtain almost complete decompression of the LV. The RV function was evaluated by hemodynamic parameters and pressure-dimension (sonomicrometry) relationship at pre-LHB (control) and 30, 60, and 90 min after LHB (LHB-30, LHB-60, and LHB-90). The materials were divided into three groups after LHB-30: intact heart (group 1, n = 5), RV free wall ischemia (group 2, n = 5), and interventricular septum (IVS) ischemia group (group 3, n = 8). No significant changes in mean right atrial pressure (mRAP), RV end-diastolic pressure (RVEDP), RV maximum derivative pressure, or RV fractional shortening (RVFS) were found between pre-LHB and post-LHB in groups 1 and 2. On the contrary, group 3 showed significant increases in mRAP and RVEDP, and a decrease in RVFS at LHB-90 compared to both pre-LHB and LHB-30. The RV end-systolic dimension (percentage of pre-LHB) showed significant increases at LHB-90 compared to LHB-30 in groups 2 and 3. These results indicate that the LHB itself does not depress the RV function in the intact heart and in the RV free wall ischemic heart, while the impairment of the IVS during LHB appears to lead to RV dysfunction.     

左心室及双心室辅助装置对缺血心肌的影响

目的 比较左心室辅助装置（LVAD）和双心室辅助装置（BVAD）对缺血心肌再灌注后心脏血流动力学、心肌能量代谢物质和心肌超微结构中线粒体形态的影响。方法 将16只绵羊随机分为LVAD组和BVAD组,每组8只,常温阻断升主动脉25分钟,造成双心室缺血损伤的动物模型。结扎右颈内动脉远端,在心脏复跳后应用转子泵分别行LVAD（左心室－右颈内动脉径路）和BVAD（左心室－右颈内动脉和右心室－肺动脉径路）辅助循环120分钟,测定血流动力学,心肌三磷酸腺苷、磷酸肌酸、观察心肌超微结构变化。结果 施行BVAD或LVAD辅助循环的同时增加容量负荷能够显著改善心脏血流动力学,但LVAD组右心房压显著高于BVAD组（P＜0．05）;BVAD组右心室心肌三磷酸腺苷、磷酸肌酸含量和心肌线粒体比表面值均高于LVAD组（P＜0．05）。结论 BVAD与LVAD更有助于促进双心室缺血损伤心肌的功能恢复。     

Systematic Review of Phosphodiesterase‐5 Inhibitor Use in Right Ventricular Failure Following Left Ventricular Assist Device Implantation

Our aim was to identify relevant literature supporting the use of phosphodiesterase‐5 (PDE5) inhibitors in patients with persistent pulmonary hypertension with signs of postprocedural right ventricular (RV) dysfunction following left ventricular assist device (LVAD) implantation. We searched MEDLINE, SCOPUS, and Web of Science from inception through November 27, 2014 for citations evaluating patients with end‐stage heart failure necessitating LVAD, continuous and pulsatile, who received a PDE5 inhibitor to prevent RV failure. Outcomes of interest included changes in mean pulmonary artery pressure, pulmonary vascular resistance, central venous pressure, cardiac index, and mean arterial pressure. Results are presented qualitatively. Four citations (n = 83 patients) were included. These included a single case report, two retrospective case series, and a prospective open‐label study with a historical control. All four studies utilized the PDE5 inhibitor sildenafil with various doses for up to 3 months. Sildenafil routinely reduced mean pulmonary artery pressures as soon as 90 min after administration. Reductions in pulmonary vascular resistance were also seen shortly after the procedure and maintained through 12–15 weeks. While one study saw improvements in postoperative central venous pressures, another did not. Evidence supporting PDE5 inhibitor use to attenuate RV failure in patients requiring an LVAD is weak.     

In Vitro Evaluation of the Influence of Pulsatile Intraventricular Pumping on Ventricular Pressure Patterns

Abstract: The Pulsatile catheter (PUCA) pump consists of a single port membrane pump connected to an indwelling valved catheter. This so–called transarterial blood pump was originally designed to be introduced through a superficial artery into the left ventricular cavity to pump blood from the left ventricle into the ascending aorta. By introducing the catheter directly into the thoracic aorta or the pulmonary artery, the possibility is created of applying large–diameter catheter PUCA pumps as left, right, or biventricular assist devices (LVAD, RVAD, or BIVAD) without damaging any of the structures of the heart. The pump performance of an 8 mm PUCA pump prototype (internal diameter catheter, 8 mm; catheter length, 40 cm; stroke volume, 80 ml) was studied in a mock circulation to investigate the influence of pulsatile intraventricular pumping on ventricular pressure patterns. The pumping mode of the PUCA pump was changed from approximately 1: 1 ([n + l]: n) to 1: 2 ([1/2n + l]: n) and 1: 3 ([1/3n + l]: n) in relation to the frequency of a ventricle–simulating membrane pump. Apart from the pumping mode, timing of the PUCA pump driving system (ejection phase) seems to be crucial in obtaining optimal unloading of the ventricle.     

Effects of Cardiomyoplasty on Right Ventricular Filling During Volume Loading

Background. Although cardiomyoplasty (CMP) is thought to improve ventricular systolic function, its effects on ventricular diastolic function are not clear. Especially the effects on right ventricular diastolic filling have not been fully investigated. Because pericardial influences are more pronounced in the right ventricle than in the left ventricle, CMP with its external constraint may substantially impair right ventricular diastolic filling.

Methods. Fourteen purebred adult beagles were used in this study. Seven underwent left posterior CMP, and 7 underwent a sham operation with a pericardiotomy and served as controls. Four weeks later, the hemodynamic effects of CMP were evaluated by heart catheterization before and after volume loading (central venous infusion of 10 mg/kg of 4.5% albumin solution for 5 minutes).

Results. In the CMP group, mean right atrial pressure and right ventricular end-diastolic pressure increased significantly from 3.1 ± 1.2 mm Hg to 6.1 ± 2.0 mm Hg (p < 0.001) and from 4.0 ± 1.8 mm Hg to 9.6 ± 2.5 mm Hg (p < 0.001), respectively. Volume loading in the control group did not significantly increase either variable. Right ventricular end-diastolic volume and stroke volume did not change significantly (from 53 ± 9.3 mL to 60 ± 9.0 mL and from 20 ± 2.3 mL to 21 ± 3.2 mL, respectively) in the CMP group. In the control group, however, right ventricular end-diastolic volume and stroke volume increased significantly from 45 ± 7.7 mL to 63 ± 14 mL (p < 0.05) and from 18 ± 4.3 mL to 22 ± 4.2 mL (p < 0.05), respectively.

Conclusions. These results suggest that CMP may reduce right ventricular compliance and restrict right ventricular diastolic filling in response to rapid volume loading because of its external constraint.     

Right ventricular performance during hypotension induced by prostaglandin E1, nicardipine HCl, glycerine trinitrate, and isosorbide dinitrate

This study investigated right ventricular (RV) performance during hypotensive anesthesia and compared the effect of the vasodilators prostaglandin E₁ (PGE₁), nicardipine HCl (Nic), glycerin trinitrate (GTN), and isosorbide dinitrate (ISDN) on RV function. Fifty patients were allocated into four groups [PGE₁ (n=20), Nic (n=10), GTN (n=10), and ISDN (n=10)] in random order. Pulmonary and RV hemodynamics were measured using a rapid-response thermodilution catheter before and during induced hypotension, when systolic arterial pressure was maintained at 80 mmHg. In the PGE₁, GTN, and ISDN groups, RV end-diastolic volume (RVEDV) and pulmonary vascular resistance were reduced in a similar manner. However, RV ejection fraction increased only in the PGE₁ group, and as a consequence, RV stroke volume (RVSV) was maintained. Nic did not change the RV parameters observed, but reduced only systemic vascular resistance (SVR). PGE₁ enhanced RV function during induced hypotension. Nic was a useful alternative agent for hypotensive anesthesia. GTN and ISDN reduced RV preload and RVSV; however, cardiac output was maintained by increasing heart rate (HR). Therefore, such nitrates should be used under an adequate RV preload.     

A Right Ventricular Hemopump Restores Right Ventricular Function with Pulmonary Artery Banding

Abstract: We investigated the ability of the Hemopump to support the right ventricle during acute, partial, pulmonary artery obstruction. In 6 pigs, a 14 Fr size Hemopump was placed through the pulmonary artery into the right ventricle. Control measurements were made. A band around the pulmonary artery proximal to the outflow port of the Hemopump was tightened, and measurements were repeated with the Hemopump at minimum and then maximum speed. With banding, right ventricular stroke volume and output decreased (43 [SD,7] to 28 [SD,8] ml, p < 0.001; 4.9 [SD,0.8] to 3.7 [SD,1.0] L/min, p < 0.01 respectively), but they were restored with the Hemopump (38 [SD,5] ml and 4.5 [SD,0.6] L/min; both p = NS vs control). Increases in right ventricular peak systolic (28 [SD,10] to 42 [SD,17] mm Hg; p < 0.01) and end-diastolic pressure (2 [SD,1] to 12 [SD,6] mm Hg; p < 0.02) were reversed by the Hemopump (29 [SD,8] and 4 [SD,2] mm Hg; both p = NS vs control). Right ventricular pressure rate product almost doubled with banding (3,199 [SD,1,252] to 5,962 [SD,2,796] mm Hg; p < 0.01), but it decreased with the Hemopump (3,368 [SD,767] mm Hg; p = NS vs control). With acute partial pulmonary artery banding, a right ventricular Hemopump restores output from and offloads the right ventricle.     

Stem cells improve right ventricular functional recovery after acute pressure overload and ischemia reperfusion injury

BACKGROUND: In many clinical scenarios, a relatively untrained right ventricle may be subjected to acute elevations in pulmonary artery and right ventricular pressures. The right and left heart are distinctly different in this regard and there is currently no in vivo model to study right ventricular ischemia in the setting of acute pressure overload. In acute injury, cardiomyocytes produce tumor necrosis factor, which mediates a proinflammatory pathway, eventually leading to myocardial dysfunction. Stem cells have been shown to reduce the production of proinflammatory mediators by the ischemic myocardium and protect the myocardium. Pretreatment with stem cells has been shown to protect the left ventricle. The effect of acute pressure overload to the untrained right ventricle is still not well understood. Furthermore, it is unclear whether pretreatment with stem cells would protect the right ventricle when it is subjected to acute pressure overload and concomitant ischemia reperfusion injury. The purpose of this study was (1) to create a simple model of acute pressure overload for the study of concomitant right ventricular ischemia and reperfusion, and (2) to evaluate the effect of pretreatment with stem cells prior to ischemia reperfusion injury. MATERIALS AND METHODS: Isolated rat hearts were perfused with the modified Langendorff technique with the latex balloon in the right ventricle instead of the left, with a pressure-transduced balloon being used to create an acute elevation in right ventricular pressure before ischemia. In the first of a two-series experiment, there were two experimental groups (N = 8 per group): one with right ventricular balloon end-diastolic pressure (EDP) of 5 mmHg (physiological), and the other with an EDP of 40 mmHg (pathologic). In the second series, the hearts with the higher balloon pressure (EDP 40 mmHg) were divided into two experimental groups (N = 5 per group). The control group was not pretreated. One group was pretreated with human mesenchymal stem cells 5 min immediately prior to ischemia reperfusion injury. Right ventricular developed pressure (RVDP), contractility (+dP/dt), and compliance (-dP/dt) were continuously assessed. Additionally, mesenchymal stem cells (MSCs) in culture were stressed by hypoxia and activation was determined by measuring vascular endothelial growth factor-A (VEGF) and hepatocyte growth factor (HGF) production by enzyme-linked immunosorbent assay. RESULTS: Recovery of RVDP, +dP/dt, and -dP/dt was significantly higher (P < 0.001) in the group with lower EDP compared to the group with the higher EDP [RVDP: 79.53 +/- 6.34 versus 54.28 +/- 10.76%; +dP/dt: 76.54 +/- 8.79 versus 38.75 +/- 19.74%; -dP/dt: 72.29 +/- 7.02 versus 30.54 +/- 12.44%]. In the higher EDP groups, pretreatment with human mesenchymal stem cells significantly improved myocardial function recovery (P < 0.01) when compared to controls [RVDP: 75.76 +/- 7.97 versus 59.10 +/- 11.18%; +dP/dt: 71.78 +/- 10.36 versus 54.93 +/- 12.64%; -dP/dt: 77.38 +/- 11.09 versus 59.30 +/- 15.20%]. Further, hypoxic MSCs demonstrated significantly greater VEGF and HGF release than controls. CONCLUSION: This compounded injury model allowed the study of right ventricular dysfunction in the setting of acute pressure overload and ischemia. Additionally, we have also demonstrated that pretreatment with stem cells of an acutely pressure overloaded right ventricle prior to ischemia reperfusion injury improves functional recovery. This is the first report of a modified Langendorff technique to study right ventricular function in the setting of acute pressure overload and ischemia and the effect of pretreatment with stem cells.     

Intraaortic Balloon Counterpulsation Improves Right Ventricular Failure Resulting From Pressure Overload

Background. Right ventricular (RV) dysfunction is common after heart transplantation, and myocardial ischemia is considered to be a significant contributor. We studied whether intraaortic balloon counterpulsation would improve cardiac function using a model of acute RV pressure overload.

Methods. In 10 anesthetized sheep, RV failure was induced using a pulmonary artery constrictor. Baseline measurements included mean systemic blood pressure, RV peak systolic pressure, cardiac index, and RV ejection fraction. Myocardial and organ perfusion were measured using radioactive microspheres.

Results. After pulmonary artery constriction, there was an increase in RV peak systolic pressure (32 ± 2 to 60 ± 3 mm Hg; p < 0.01) and a decrease in mean systemic blood pressure (68 ± 4 to 49 ± 2 mm Hg; p < 0.01), RV ejection fraction (0.51 ± 0.04 to 0.16 ± 0.02; p < 0.01), and cardiac index (2.48 ± 0.04 to 1.02 ± 0.11; p < 0.01). Blood flow to the RV did not change significantly, but there was a significant reduction in blood flow to the left ventricle. The initiation of intraaortic balloon counterpulsation (1:1) using a 40-mL intraaortic balloon inserted through the left femoral artery resulted in an increase in mean systemic blood pressure (49 ± 2 to 61 ± 3 mm Hg; p < 0.01), cardiac index (1.02 ± 0.11 to 1.45 ± 0.14; p < 0.05), RV ejection fraction (0.16 ± 0.02 to 0.23 ± 0.02; p < 0.01), and blood flow to the left ventricle.

Conclusions. In a model of right heart failure, the institution of intraaortic balloon counterpulsation caused a significant improvement in cardiac function. Although RV ischemia was not demonstrated, the augmentation of left coronary artery blood flow by intraaortic balloon counterpulsation and subsequent improvement in left ventricular function suggest that left ventricular ischemia contributes to RV dysfunction, presumably through a ventricular interdependence mechanism. Therefore, study of the safety and efficacy of intraaortic balloon counterpulsation in the management of patients with acute right heart dysfunction is warranted.     

Chronic Effects of a Cardiac Assist Device on the Bulk and Regional Mechanics of the Failed Left Ventricle in Goats

Abstract: Pneumatically driven, diaphragm-type left ventricular assist devices (LVADs) were implanted into 8 goats with profound induced infarction to the left ventricle by using multiple ligations of the left anterior descending (LAD) coronary artery as well as small arteries in the LAD distribution area. Left ventricular diameters, regional myocardial segment lengths, and wall thicknesses were measured by sono-micrometers. After left ventricular function seemed to be recovered, the goats were weaned off the LVADs after a gradual decrease of pump bypass flow over several days. Thereafter, hemodynamic and cardiac parameters were observed for about I month more. Three animals recovered successfully owing to the LVAD pumping. Before starting pump-weaning procedures, the bulk mechanical work (BMW) done by the left ventricle during LVAD pumping and under temporary pump-off conditions was 0.08 ± 0.01 (mean ± SE) and 0.22 ± 0.01 W/100 g left ventricular weight (LVW), respectively, while the regional mechanical work done by the normal myocardium (RMWn) was 1.5 ± 0.4 and 4.3 ± 0.9 mW/cm³ during pumping and under temporary pump-off conditions, respectively. BMW and RMWn values obtained under pump-on conditions both increased gradually during the weaning process. Even after pump removal, they continued to increase and reached constant values of about 0.3 W/100 g LVW and 10 mW/cm³, respectively, around 2 weeks after pump removal. Although the myocardium in the infarction area did no work for the first several days after surgery, it recovered to do some external work with the aid of LVAD pumping. However, recovery of left ventricular function owed more to compensatory increases in pumping ability of the remaining normal myocardium than to recovery of the damaged myocardium. The LVAD could salvage severely damaged hearts unless the infarction area exceeded 50% of the left ventricular wall.     

Cadaver fitting study of the DexAide right ventricular assist device

The DexAide right ventricular assist device (RVAD) has been developed to provide an implantable RVAD option to surgeons. The aim of this study was to determine the optimal cannula design and optimal implantation location of the DexAide RVAD in preparation for its clinical use. Separately, a HeartMate XVE left ventricular assist device (LVAD) and CorAide LVAD models were implanted into the preperitoneal and right thoracic space, and the anatomical fit of the DexAide RVAD was evaluated in five preserved human cadavers. The DexAide RVAD inflow cannula was inserted through the diaphragmatic surface of the right ventricle and the outflow was directed to the pulmonary artery. Right thoracic implantation of the DexAide RVAD provided an excellent fit with either the HeartMate or CorAide LVAD in all cadavers. The results of this study will guide improvements in the designs of cannulae and implantation of the DexAide RVAD in future clinical applications.     

The effect of incremental positive end-expiratory pressure on right ventricular hemodynamics and ejection fraction

The effects of incremental positive end-expiratory pressure (PEEP) on right ventricular (RV) function were evaluated in 36 (n = 36) ventilated patients. Positive end-expiratory pressure was increased from 0 (baseline) to 20 cm H2O in 5-cm H2O increments and RV hemodynamics and thermally derived right ventricular ejection fraction (RVEF), right ventricular end-diastolic volume index (RVEDVI), and right ventricular end-systolic volume index (RVESVI) were computed. Right ventricular contractility was determined from the analysis of RV systolic pressure-volume relations. Right ventricular ejection fraction declined from 42 +/- 8% at baseline to 30 +/- 9% at 20 cm H2O PEEP. Right ventricular end-diastolic volume index declined between 0 and 5 cm H2O PEEP (103 +/- 42 to 92 +/- 34 ml.m-2) and then increased to 113 +/- 40 at 20 cm H2O PEEP. Right ventricular end-systolic volume index increased from 60 +/- 31 ml.m-2 at baseline to 79 +/- 34 ml.m-2 at 20 cm H2O PEEP. The slope (E) of the relation of RV peak systolic pressure to RV end-systolic volume index decreased from 0.26 mm Hg.m2.ml-1 between PEEP of 0-15 cm H2O to 0.05 mm Hg.m2.m-1 at PEEP greater than 15 cm H2O. It is concluded that low levels of PEEP have a predominant preload reducing effect on the RV. Above 15 cm H2O PEEP, RV volumes increase and E decreases, consistent with increased RV afterload and a decline in RV contractility.     

Initial experience with Impella RP in a quaternary transplant center

Right ventricular failure is one of the most common complications encountered after left ventricular assist device implantation and heart transplantation. It has been reported to have an incidence up to 30%. It increases morbidity and short-term mortality. Impella RP is a small pump that can provide up to 4L/min of flow. We analyzed all the patients with right ventricular failure that were treated with Impella RP in our institution. The Impella RP was implanted percutaneously in the catheterization laboratory guided by fluoroscopy. Overall, 7 patients required the implantation of an Impella RP due to right ventricular failure: 2 after long-term LVAD, 3 presented with acute right ventricular failure immediately after LVAD implantation, and 2 needed it after heart transplantation. Regarding complications, we report 2 patients with hemolysis. Hemodynamic parameters as well as end-organ perfusion and inotropic requirements improved after the insertion of the Impella. Overall, 30-day survival is 58%. Median time of support was 9 (5–19) days. RV failure is one of the most challenging complications after LVAD implantation and heart transplantation. The major challenge is the timing of implantation. The minimally invasive nature of the Impella RP facilitates de-escalation of treatment and paves the road to recovery. Impella RP proved useful in facilitating ECMO wean. Used in a prompt manner alongside the ease of implantation and the minimal rate of complications, Impella RP seems to be an appropriate device to tackle RV failure providing enough flow to allow for recovery or escalation decision-making.     

Mechanisms of transplant right ventricular dysfunction.

OBJECTIVE: Right ventricular (RV) dysfunction remains the leading cause of early mortality after cardiac transplantation. The effect of brain death and subsequent hypothermic cardioplegic arrest and storage on subsequent post-transplant right ventricular function was examined. SUMMARY BACKGROUND DATA: Right ventricular dysfunction in the donor heart usually is attributed to failure of the donor right ventricle to adapt to the sudden increase in afterload (pulmonary vascular resistance) in the recipient. Strategies to improve ventricular mechanics in the postoperative period are aimed at reducing pulmonary vascular resistance with vasodilators or augmenting right ventricular contractility with inotropic agents. Events occurring in the donor heart (brain death, hypothermic cardioplegic arrest, and storage) also may be directly related to post-transplant RV dysfunction. METHODS: A canine model of brain death and orthotopic cardiac transplantation was used. A dynamic pressure-volume analysis of RV mechanics was performed using micromanometers and sonomicrometric dimension transducers. Systolic function was assessed by measurement of preload recruitable stroke work (PRSW). Brain death was induced in 17 dogs by inflation of an intracranial balloon. Right ventricular function then was assessed serially to 6 hours (PRSW). Right ventricular adrenergic beta receptor density and function was sampled at control and after 6 hours of brain death. The effect of cardioplegic arrest and hypothermic storage was assessed in a second group of 17 dogs, using the same instrumentation and method of RV analysis. RESULTS: A significant decrease in right ventricular PRSW occurred after brain death, with the average decrease being 37% +/- 10.4% from the control. The RV myocardial beta adrenergic receptor density did not significantly change (253 +/- 34 fmol/ng control vs. 336 +/- 54 fmol/ng after brain death). The adenylyl cyclase activity of the RV beta receptor was assessed and was not altered by brain death. Orthotopic transplantation after cardioplegic arrest and hypothermic storage significantly decreased RV PRSW from 23.6 +/- 2.0 x 10(3) erg to 13.5 +/- 1.4 x 10(3) erg. CONCLUSIONS: These data indicate that the donor right ventricle is exposed to factors significantly detrimental to its mechanical performance well before facing an increased afterload in the recipient. Strategies to reduce RV dysfunction associated with brain death and hypothermic storage could positively impact post-transplant survival.