Left ventricular assist device (LVAD) implantation can be complicated by right ventricular (RV) failure. Several scores have been proposed to predict this event. Our aim was to validate three of these scores in a population which had received a rotary blood pump LVAD. In a consecutive series of 59 full LVAD implantations, preoperative clinical, echocardiographic, laboratory and haemodynamic values were retrospectively collected. Three previously published predictive scores were calculated for all the patients. A logistic regression analysis was used to identify the predictors of RV support after LVAD implantation. Fourteen patients (23.7%) needed additional temporary RV support. The three scores did not present any significant difference between patients treated with LVAD plus right ventricular assist device or LVAD only (45.86 ± 14.02 vs 42.1 ± 17.34, P = 0.46; 4.57 ± 3.37 vs 4.94 ± 2.87, P = 0.69; 2.71 ± 2.11 vs 2.92 ± 2.99m P = 0.81) and they were not predictive for RV failure. High pulmonary vascular resistance and the presence of non-ischaemic cardiomyopathy were the only significant predictors in logistic regression. The use of risk scores failed to predict the need of RV support after LVAD. Stratification of the hazard with these scores should occur with extreme caution.

Background Transplant type for end‐stage pulmonary vascular disease remains debatable. We compared recipient outcome after heart‐lung(HLT) versus double‐lung(DLT) transplantation. Methods Single‐center analysis (38HLT‐30DLT; 1991‐2014] for different causes of pre‐capillary pulmonary hypertension(PH): idiopathic(22); heritable(2); drug‐induced(9); hepato‐portal(1); connective tissue disease(4); congenital heart disease(CHD)(24); chronic thromboembolic PH(6). Results HLT decreased from 91.7% [1991‐1995] to 21.4% [2010‐2014]. Re‐intervention for bleeding was higher after HLT; (p=0.06) while primary graft dysfunction grades 2&3 occurred more after DLT; (p<0.0001). Graft survival at 90 days, 1, 5, 10, and 15 years was 93%, 83%, 70%, 47%, and 35% for DLT versus 82%, 74%, 61%, 48%, and 30% for HLT, respectively (log rank p=0.89). Graft survival improved over time: 100%, 93%, 87%, 72%, and 72% in [2010‐2014] versus 75%, 58%, 42%, 33%, and 33% in [1991‐1995], respectively; p=0.03. No difference in chronic lung allograft dysfunction (CLAD)‐free survival was observed: 80% & 28% for DLT versus 75% & 28% for HLT after 5 and 10 years, respectively; p=0.49. Conclusions Primary graft dysfunction in PH patients was lower after HLT compared to DLT. Nonetheless, overall graft and CLAD‐free survival were comparable and improved over time with growing experience. DLT remains our preferred procedure for all forms of pre‐capillary PH, except in patients with complex CHD.

The aim of this study is to investigate the intravascular application of a micro-electro-mechanical system (MEMS) pressure sensor to directly measure the hemodynamic characteristics of a ventricular assist device (VAD). A bio- and hemo-compatible packaging strategy is implemented, based on a ceramic thick film process. A commercial sub-millimeter piezoresistive sensor is attached to an alumina substrate, and a double coating of polydimethylsiloxane (PDMS) and parylene-C is applied. The final size of the packaged device is 2.6 mm by 3.6 mm by 1.8 mm. A prototype electronic circuit for conditioning and read-out of the pressure signal is developed, satisfying the VAD-specific requirements of low power consumption (less than 14.5 mW in continuous mode) and small form factor. The packaged sensor has been submitted to extensive in vitro tests. The device displayed a temperature-independent sensitivity (12 $\mathsf{\mu }$ V/V/mmHg) and good in vitro stability when exposed to the continuous flow of saline solution (less than 0.05 mmHg/day drift after 50 h). During in vivo validation, the transducer has been successfully used to record the arterial pressure waveform of a female sheep. A small, intravascular sensor to continuously register the blood pressure at the inflow and the outflow of a VAD is developed and successfully validated in vivo.

Background: Exertional intolerance is a limiting and often crippling symptom in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Traditionally the pathogenesis has been attributed to central factors, including ventilation/perfusion mismatch, increased pulmonary vascular resistance, and right heart dysfunction and uncoupling. Pulmonary endarterectomy and balloon pulmonary angioplasty provide substantial improvement of functional status and hemodynamics. However, despite normalization of pulmonary hemodynamics, exercise capacity often does not return to age-predicted levels. By systematically evaluating the oxygen pathway, we aimed to elucidate the causes of functional limitations in patients with CTEPH before and after pulmonary vascular intervention. Methods: Using exercise cardiac magnetic resonance imaging with simultaneous invasive hemodynamic monitoring, we sought to quantify the steps of the O ₂ transport cascade from the mouth to the mitochondria in patients with CTEPH (n=20) as compared with healthy participants (n=10). Furthermore, we evaluated the effect of pulmonary vascular intervention (pulmonary endarterectomy or balloon angioplasty) on the individual components of the cascade (n=10). Results: Peak V o ₂ (oxygen uptake) was significantly reduced in patients with CTEPH relative to controls (56±17 versus 112±20% of predicted; P <0.0001). The difference was attributable to impairments in multiple steps of the O ₂ cascade, including O ₂ delivery (product of cardiac output and arterial O ₂ content), skeletal muscle diffusion capacity, and pulmonary diffusion. The total O ₂ extracted in the periphery (ie, ΔAV o ₂ [arteriovenous O ₂ content difference]) was not different. After pulmonary vascular intervention, peak V o ₂ increased significantly (from 12.5±4.0 to 17.8±7.5 mL/[kg·min]; P =0.036) but remained below age-predicted levels (70±11%). The O ₂ delivery was improved owing to an increase in peak cardiac output and lung diffusion capacity. However, peak exercise ΔAV o ₂ was unchanged, as was skeletal muscle diffusion capacity. Conclusions: We demonstrated that patients with CTEPH have significant impairment of all steps in the O ₂ use cascade, resulting in markedly impaired exercise capacity. Pulmonary vascular intervention increased peak V o ₂ by partly correcting O ₂ delivery but had no effect on abnormalities in peripheral O ₂ extraction. This suggests that current interventions only partially address patients’ limitations and that additional therapies may improve functional capacity.

Preventive antireflux surgery (ARS) at the moment of congenital diaphragmatic hernia (CDH) repair has been suggested by some authors, particularly in subgroups with a liver herniated in the chest or patch requirement. We evaluated the incidence and associated factors of gastro-oesophageal reflux disease (GERD) and the need for subsequent ARS in our CDH patients. We retrospectively reviewed our CDH database. Demographics, prenatal assessment of severity, prenatal treatment, type of repair, intraoperative findings and incidences of gastro-oesophageal reflux and ARS were recorded. CDH repair was performed in 77 infants between July 1993 and November 2009. Eight died after repair. Seven were lost to follow-up. The median follow-up was 4.0 (0.16–14.88) years. Fourteen of these 62 patients were prenatally treated with fetoscopic endoluminal tracheal occlusion (FETO) because of severe pulmonary hypoplasia. After CDH repair, GERD was diagnosed in 31 patients. In all of them, medical antireflux treatment was started. Thirteen (42%) patients needed ARS at a median age of 64 (37–264) days. One year after starting medical treatment, 14 (45%) patients were completely off antireflux medication. In CDH subgroups with patch repair, liver herniated in the chest or previous FETO, the incidences of gastro-oesophageal reflux and ARS were 61 and 32%, 73 and 38% and 71 and 43%, respectively. Univariable analysis of associated potentially predisposing factors shows that patch repair, liver herniated in the chest, pulmonary hypertension, high-frequency oscillatory ventilation and FETO are associated with subsequent ARS. On multivariable analysis, liver herniated in the chest was the only independent predictor for both gastro-oesophageal reflux and ARS. Of all CDH patients, 50% developed gastro-oesophageal reflux and 21% required ARS. For both, liver in the chest was the only independent predictor. Routine ARS in certain subgroups at the time of CDH repair seems not to be justified. Foetal endoluminal tracheal occlusion creates a new cohort of survivors with an increased risk for undergoing ARS. The surgical group, in particular, reflects a more complex gastro-oesophageal reflux physiopathology.