Right heart failure (RHF) is a major cause of morbidity and mortality in patients supported with durable left ventricular assist devices (LVADs). While right coronary artery infarction is a recognized cause of acute RHF, the ventricular consequences of left coronary system infarction in LVAD-supported patients are not well characterized. We describe two patients supported with HeartMate III LVADs who developed acute RHF within 24–48 hours after successful revascularization of acute left coronary system occlusions (mid-left anterior descending artery and left main coronary artery). Both had previously stable LVAD function and no evidence of advanced RHF. After revascularization, each developed hypotension, rising central venous pressure, reduced LVAD flows, and echocardiographic evidence of severe right ventricular (RV) dilation and dysfunction with septal shift toward the left ventricle. Hemodynamic deterioration reversed with inotropic support, diuresis, and LVAD speed adjustment, without mechanical RV support. These cases suggest left coronary acute myocardial infarction (AMI) may precipitate acute RHF in LVAD-supported patients through septal ischemia with impaired ventricular interdependence, acute increases in RV afterload, and relative RV ischemia despite patent right coronary arteries. Heightened surveillance and early echocardiographic assessment after left-sided AMI in LVAD recipients may enable prompt recognition and timely intervention.
Ventricular assist devices (VADs) have become an established therapy for children with end-stage heart failure, yet multinational data describing pediatric VAD programs remain limited. We conducted a 12 question survey through the Advanced Cardiac Therapies Improving Outcomes Network (ACTION) involving 74 international healthcare professionals from pediatric VAD programs outside North America. The survey assessed device and resource availability, multidisciplinary team composition, program challenges, and future priorities. Fifteen responses representing 15 centers from 14 countries were received, including 13 centers with established pediatric VAD programs. Most centers (91%, 10/11) managed 1–5 pediatric VAD patients annually. Berlin Heart EXCOR and HeartMate 3 were available in 85% (11/13) of centers, while only 46.7% (7/15) had a dedicated VAD coordinator. Major barriers included inadequate education for intensive care unit (ICU) and nursing staff and patients (69%, 9/13), financial constraints (54%, 7/13), limited device availability (46%, 6/13), and lack of outpatient VAD experience, with 31% (4/13) of centers reporting no experience discharging patients on VAD support. Substantial variation in device availability, multidisciplinary resources, and program experience exists across regions. These findings highlight important gaps in pediatric VAD care and support international collaboration to improve education, infrastructure, and access to advanced heart failure therapies.
Cardiac output (CO) monitoring is challenging during venovenous extracorporeal membrane oxygenation (VV ECMO), as thermodilution techniques are unreliable. Cardiac output from right ventricular pressure (RVP) waveforms has recently been considered. We evaluated whether RVP-derived CO (CO RV ) accurately reflects cardiac output measured by echocardiography (CO US ) during VV ECMO. Ten anesthetized pigs underwent femoro-jugular VV ECMO implantation. A Swan-Ganz IQ catheter provided continuous CO RV monitoring throughout the experiment. Cardiac output was modulated using either dobutamine (5–20 µg/kg/min) or landiolol (10–40 µg/kg/min) infusions. Agreement between CO RV and CO US was assessed using Pearson correlation and Bland–Altman analysis. Overall, 596 paired CO measurements were performed in seven animals. Cardiac output ranged from 1.05 to 9.46 L/min. Correlation between CO RV and CO US was poor ( R = 0.24; R 2 = 0.057; p < 0.05). Bland–Altman analysis showed a mean bias of +1.94 L/min with wide limits of agreement (−1.44 to +5.32 L/min). Correlations between individual right ventricular pressure waveform components and CO US were heterogeneous and weak to moderate (diastolic RVP, R = 0.36; right ventricle +d P /d t [delta pressure/delta time] R = 0.40; systolic RVP R = 0.60). CO RV is not reliable during VV ECMO in our experiment. Further studies are needed to assess CO RV performances.
Although baseline renal impairment and post-heart transplantation (HT) dialysis are established clinical predictors, the prognostic impact of pre-HT renal decline in patients bridged with left ventricular assist devices (LVADs) remains unclear. We retrospectively analyzed patients from the United Network for Organ Sharing registry who underwent HT following LVAD support between 2009 and 2024. Renal decline was defined as a greater than or equal to 40% reduction in estimated glomerular filtration rate (eGFR) from listing to HT. Among 10,454 patients, 624 (6.0%) experienced pre-HT renal decline. Patients with renal decline had longer waitlist durations (median 297 vs. 197 days; p < 0.001), lower eGFR at HT (42.0 vs. 70.6 ml/min/1.73 m 2 ; p < 0.001), and higher rates of post-HT dialysis (23.7 vs. 12.8%; p < 0.001). Independent predictors of renal decline included longer waitlist time and perioperative blood transfusions, whereas HeartMate 3 LVAD use was protective. Renal decline was independently associated with an increased risk of post-HT dialysis (adjusted odds ratio [aOR]: 2.64) and all-cause mortality (adjusted hazard ratio [aHR]: 1.16), with post-HT dialysis strongly predicting mortality (aHR: 3.48). Renal deterioration is a significant predictor of post-HT dialysis and mortality in LVAD-bridged patients. Incorporating renal trajectory into risk stratification may enhance candidate selection and promote perioperative renal protection strategies.
