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PurposeThe aim of the study was to analyze early mortality after continuous-flow left ventricular assist device (LVAD) implantation which remains high.MethodsWe analyzed consecutive (n = 2689) patients from the European Registry for Patients with Mechanical Circulatory Support (EUROMACS) undergoing continuous-flow LVAD implantation. The primary outcome was early (< 90 days) mortality. Secondary outcomes were differential causes of early post-operative death following LVAD implantation.ResultsUnivariable and multivariable analysis as well as regression analysis were used to examine determinants and differential causes of early (< 90 days) mortality after LVAD implantation. During the first 90 days, 2160 (80%) patients were alive with ongoing LVAD support, 40(2%) patients underwent heart transplantation, and 487(18%) deceased. The main causes of early death were MOF (36%), sepsis (28%), cardiopulmonary failure (CPF; 10%), CVA (9%), and right-sided heart failure (RHF, 8%). Furthermore, MOF and sepsis are 70% of causes of death in the first week. Independent clinical predictors of early death were age, female sex, INTERMACS profile 1 to 3, and ECMO. Laboratory predictors included elevated serum creatinine, total bilirubin, lactate, and low hemoglobin. Furthermore, hemodynamic predictors included elevated RA-to-PCWP ratio, pulmonary vascular resistance, and low systemic vascular resistance. Longer total implantation time was also independent predictor of early mortality. A simple model of 12 variables predicts early mortality following LVAD implantation with a good discriminative power with area under the curve of 0.75.ConclusionsIn the EUROMACS registry, approximately one out of five patients die within 90 days after LVAD implantation. Early mortality is primarily dominated by multiorgan failure followed by sepsis. A simple model identifies important parameters which are associated with early mortality following LVAD implantation.

PurposeAcute kidney injury (AKI) frequently occurs after heart transplantation (HTx), but its relation to preoperative right heart hemodynamic (RHH) parameters remains unknown. Therefore, we aimed to determine their predictive properties for postoperative AKI severity within 30 days after HTx.MethodsFrom 1984 to 2016, all consecutive HTx recipients (n = 595) in our tertiary referral center were included and analyzed for the occurrence of postoperative AKI staged by the kidney disease improving global outcome criteria. The effects of preoperative RHH parameters on postoperative AKI were calculated using logistic regression, and predictive accuracy was assessed using integrated discrimination improvement (IDI), net reclassification improvement (NRI), and area under the receiver operating characteristic curves (AUC).ResultsPostoperative AKI occurred in 430 (72%) patients including 278 (47%) stage 1, 66 (11%) stage 2, and 86 (14%) stage 3 cases. Renal replacement therapy (RRT) was administered in 41 (7%) patients. Patients with higher AKI stages had also higher baseline right atrial pressure (RAP; median 7, 7, 8, and in RRT 11 mmHg, p trend = 0.021), RAP-to-pulmonary capillary wedge pressure ratio (median 0.37, 0.36, 0.40, 0.47, p trend = 0.009), and lower pulmonary artery pulsatility index (PAPi) values (median 2.83, 3.17, 2.54, 2.31, p trend = 0.012). Higher RAP and lower PAPi values independently predicted AKI severity [adjusted odds ratio (OR) per doubling of RAP 1.16 (1.02–1.32), p = 0.029; of PAPi 0.85 (0.75–0.96), p = 0.008]. Based on IDI, NRI, and delta AUC, inclusion of these parameters improved the models’ predictive accuracy.ConclusionsPreoperative PAPi and RAP strongly predict the development of AKI early after HTx and can be used as early AKI predictors.

Background Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is increasingly adopted for the treatment of cardiogenic shock (CS). However, a marker of successful weaning remains largely unknown. Our hypothesis was that successful weaning is associated with sustained microcirculatory function during ECMO flow reduction. Therefore, we sought to test the usefulness of microcirculatory imaging in the same sublingual spot, using incident dark field (IDF) imaging in assessing successful weaning from VA-ECMO and compare IDF imaging with echocardiographic parameters. Methods Weaning was performed by decreasing the VA-ECMO flow to 50% (F 50 ) from the baseline. The endpoint of the study was successful VA-ECMO explantation within 48 hours after weaning. The response of sublingual microcirculation to a weaning attempt (WA) was evaluated. Microcirculation was measured in one sublingual area (single spot (ss)) using CytoCam IDF imaging during WA. Total vessel density (TVDss) and perfused vessel density (PVDss) of the sublingual area were evaluated before and during 50% flow reduction (TVDss F50 , PVDss F50 ) after a WA and compared to conventional echocardiographic parameters as indicators of the success or failure of the WA. Results Patients (n = 13) aged 49 ± 18 years, who received VA-ECMO for the treatment of refractory CS due to pulmonary embolism (n = 5), post cardiotomy (n = 3), acute coronary syndrome (n = 2), myocarditis (n = 2) and drug intoxication (n = 1), were included. TVDss F50 (21.9 vs 12.9 mm/mm 2 , p  = 0.001), PVDss F50 (19.7 vs 12.4 mm/mm 2 , p  = 0.01) and aortic velocity–time integral (VTI) at 50% flow reduction (VTI F50 ) were higher in patients successfully weaned vs not successfully weaned. The area under the curve (AUC) was 0.99 vs 0.93 vs 0.85 for TVDss F50 (small vessels) >12.2 mm/mm 2 , left ventricular ejection fraction (LVEF) >15% and aortic VTI >11 cm. Likewise, the AUC was 0.91 vs 0.93 vs 0.85 for the PVDss F50 (all vessels) >14.8 mm/mm 2 , LVEF >15% and aortic VTI >11 cm. Conclusion This study identified sublingual microcirculation as a novel potential marker for identifying successful weaning from VA-ECMO. Sustained values of TVDss F50 and PVDss F50 were found to be specific and sensitive indicators of successful weaning from VA-ECMO as compared to echocardiographic parameters.

Abnormal aortic elasticity serves as a marker for cardiovascular mortality and has a negative impact on the left ventricular (LV) afterload. Noncompaction cardiomyopathy (NCCM) is characterized by hypertrabeculation of the LV endomyocardial wall, with an underdeveloped endocardial helix. This may result in absence of LV twist, disturbed aortic elasticity, LV dysfunction, and ultimately premature heart failure (HF). This study compared the aortic stiffness and clinical outcome in patients with NCCM to that of a control group with dilated cardiomyopathy (DCM). Sixty NCCM patients, matched by age and sex, were compared with 60 DCM controls. Transthoracic echocardiography was performed to measure the systolic (SD) and diastolic diameters (DD) of the ascending aorta. These measurements, along with systolic (SBP) and diastolic blood pressure (DBP), were utilized to calculate the aortic stiffness index defined as ln(SBP/DBP)/[(SD-DD)/DD]. This index was then compared to clinical features and outcome. The mean age was 49 ± 16 years (55% males) in the NCCM group and 49 ± 16 years (55% male) in the DCM group. Aortic stiffness index (ASI) was significantly higher in the NCCM group than in the DCM group (7.0 [5.8–10.2] vs. 6.2 [4.8–7.7], p = 0.011). This difference remained statistically significant after adjustment for established risk factors associated with aortic stiffness (β = 1.771; 95% CI [0.253–3.289], p = 0.023). Patients with NCCM demonstrated increased aortic stiffness when compared to those with DCM, which may reflect the underlying pathophysiological processes. Additional research is necessary to evaluate the impact of aortic stiffness on the advancement of LV dysfunction, the onset of heart failure, and long-term outcomes.

Noncompaction cardiomyopathy (NCCM) is a disease characterized by hypertrabeculation, commonly hypothesized due to an arrest in compaction during fetal development. In 2006, NCCM was classified as a distinct form of cardiomyopathy (CMP) by the American Heart Association. NCCM in childhood is more frequently familial than when diagnosed in adulthood and is associated with other congenital heart diseases (CHDs), other genetic CMPs, and neuromuscular diseases (NMDs). It is yet a rare cardiac diseased with an estimated incidence of 0.12 per 100.000 in children up to 10 years of age. Diagnosing NCCM can be challenging due to non-uniform diagnostic criteria, unawareness, presumed other CMPs, and presence of CHD. Therefore, the incidence of NCCM in children might be an underestimation. Nonetheless, NCCM is the third most common cardiomyopathy in childhood and is associated with heart failure, arrhythmias, and/or thromboembolic events. This state-of-the-art review provides an overview on pediatric NCCM. In addition, we discuss the natural history, epidemiology, genetics, clinical presentation, outcome, and therapeutic options of NCCM in pediatric patients, including fetuses, neonates, infants, and children. Furthermore, we provide a simple classification of different forms of the disease. Finally, the differences between the pediatric population and the adult population are described.

Background Post-transplant diabetes mellitus (PTDM) affects up to 34% of heart transplant recipients (HTR) within five years, increasing the risk of adverse outcomes. Although the oral glucose tolerance test (OGTT) is the most sensitive method for detecting prediabetes and diabetes, it is burdensome. This study evaluates the diagnostic accuracy of exhaled breath analysis using an electronic nose (eNose) as a non-invasive alternative for detecting prediabetes or PTDM. Methods HTR > one year post-transplant undergoing OGTT were included, along with fasting HTR with known PTDM as a control group. Exhaled breath was analyzed before glucose loading using the SpiroNose. Diagnostic performance of eNose parameters alone and combined with clinical variables was assessed using multivariate logistic regression. Results Seventy-six HTR were included (29% female, median age 56 years, median 7.8 years post-transplant). Of these, 18 had normal glucose tolerance, 33 had prediabetes, and 25 had PTDM (including 8 newly diagnosed). Overall, 76% had prediabetes or PTDM. eNose alone differentiated normal from abnormal glucose tolerance (prediabetes or PTDM) with an AUROC of 0.70 (95% CI 0.57–0.83), 68% accuracy, 69% sensitivity, 67% specificity, 40% negative predictive value (NPV), and 87% positive predictive value (PPV). Combining eNose with clinical parameters improved diagnostic performance (AUROC 0.88, 95% CI 0.81–0.96), achieving 78% accuracy, 71% sensitivity, 100% specificity, 51% NPV, and 100% PPV. Conclusions Prediabetes or PTDM is common in HTR. eNose technology, especially when combined with clinical data, shows promise as a non-invasive screening tool with high specificity and PPV. This approach may reduce OGTT burden, pending further confirmation. Graphical abstract

Aims Sufficient myocardial recovery with the subsequent explantation of a left ventricular assist device (LVAD) occurs in approximately 1–2% of the cases. However, follow‐up data about this condition are scarcely available in the literature. This study aimed to report the long‐term outcomes and clinical management following LVAD explantation. Methods and results An analysis of the European Registry for Patients with Mechanical Circulatory Support was performed to identify all adult patients with myocardial recovery and successful explantation. Pre‐implant characteristics were retrieved and compared with the non‐recovery patients. The follow‐up data after explantation were collected via a questionnaire. A Kaplan–Meier analysis for freedom of the composite endpoint of death, heart transplantation, LVAD reimplantion, or heart failure (HF) relapse was conducted. A total of 45 (1.4%) cases with myocardial recovery resulting in successful LVAD explantation were identified. Compared with those who did not experience myocardial recovery, the explanted patients were younger (44 vs. 56 years, P < 0.001), had a shorter duration of cardiac disease (P < 0.001), and were less likely to have ischaemic cardiomyopathy (9% vs. 41.8%, P < 0.001). Follow‐up after explantation could be acquired in 28 (62%) cases. The median age at LVAD implantation was 43 years (inter‐quartile range: 29–52), and 23 (82%) were male. Baseline left ventricular ejection fraction was 18% (inter‐quartile range: 10–20%), and 60.7% of the patients had Interagency Registry for Mechanically Assisted Circulatory Support Profile 1 or 2. Aetiologies of HF were dilated cardiomyopathy in 36%, myocarditis in 32%, and ischaemic in 14% of the patients, and 18% had miscellaneous aetiologies. The devices implanted were HeartMate II in 14 (50%), HVAD in 11 (39%), HeartMate 3 in 2 (7%), and 1 unknown with a median duration of support of 410 days (range: 59–1286). The median follow‐up after explantation was 26 months (range 0.3–73 months), and 82% of the patients were in New York Heart Association Class I or II. Beta‐blockers were prescribed to 85%, angiotensin‐converting enzyme inhibitors to 71%, and loop diuretics to 50% of the patients, respectively. Freedom from the composite endpoint was 100% after 30 days and 88% after 2 years. Conclusions The survival after LVAD explantation is excellent without the need for heart transplantation or LVAD reimplantation. Only a minority of the patients suffer from a relapse of significant HF.

Aims Many heart transplant recipients will develop end‐stage renal disease in the post‐operative course. The aim of this study was to identify the long‐term incidence of end‐stage renal disease, determine its risk factors, and investigate what subsequent therapy was associated with the best survival. Methods and results A retrospective, single‐centre study was performed in all adult heart transplant patients from 1984 to 2016. Risk factors for end‐stage renal disease were analysed by means of multivariable regression analysis and survival by means of Kaplan–Meier. Of 685 heart transplant recipients, 71 were excluded: 64 were under 18 years of age and seven were re‐transplantations. During a median follow‐up of 8.6 years, 121 (19.7%) patients developed end‐stage renal disease: 22 received conservative therapy, 80 were treated with dialysis (46 haemodialysis and 34 peritoneal dialysis), and 19 received a kidney transplant. Development of end‐stage renal disease (examined as a time‐dependent variable) inferred a hazard ratio of 6.45 (95% confidence interval 4.87–8.54, P < 0.001) for mortality. Tacrolimus‐based therapy decreased, and acute kidney injury requiring renal replacement therapy increased the risk for end‐stage renal disease development (hazard ratio 0.40, 95% confidence interval 0.26–0.62, P < 0.001, and hazard ratio 4.18, 95% confidence interval 2.30–7.59, P < 0.001, respectively). Kidney transplantation was associated with the best median survival compared with dialysis or conservative therapy: 6.4 vs. 2.2 vs. 0.3 years (P < 0.0001), respectively, after end‐stage renal disease development. Conclusions End‐stage renal disease is a frequent complication after heart transplant and is associated with poor survival. Kidney transplantation resulted in the longest survival of patients with end‐stage renal disease.

Background Studies focusing on sex differences in circulating proteins in patients with heart failure with reduced ejection fraction (HFrEF) are scarce. Insight into sex-specific cardiovascular protein profiles and their associations with the risk of adverse outcomes may contribute to a better understanding of the pathophysiological processes involved in HFrEF. Moreover, it could provide a basis for the use of circulating protein measurements for prognostication in women and men, wherein the most relevant protein measurements are applied in each of the sexes. Methods In 382 patients with HFrEF, we performed tri-monthly blood sampling (median follow-up: 25 [13–31] months). We selected all baseline samples and two samples closest to the primary endpoint (PEP: composite of cardiovascular death, heart transplantation, left ventricular assist device implantation, and HF hospitalization) or censoring. We then applied an aptamer-based multiplex proteomic assay identifying 1105 proteins previously associated with cardiovascular disease. We used linear regression models and gene-enrichment analysis to study sex-based differences in baseline levels. We used time-dependent Cox models to study differences in the prognostic value of serially measured proteins. All models were adjusted for the MAGGIC HF mortality risk score and p -values for multiple testing. Results In 104 women and 278 men (mean age 62 and 64 years, respectively) cumulative PEP incidence at 30 months was 25% and 35%, respectively. At baseline, 55 (5%) out of the 1105 proteins were significantly different between women and men. The female protein profile was most strongly associated with extracellular matrix organization, while the male profile was dominated by regulation of cell death. The association of endothelin-1 (P interaction  < 0.001) and somatostatin (P interaction  = 0.040) with the PEP was modified by sex, independent of clinical characteristics. Endothelin-1 was more strongly associated with the PEP in men (HR 2.62 [95%CI, 1.98, 3.46], p  < 0.001) compared to women (1.14 [1.01, 1.29], p  = 0.036). Somatostatin was positively associated with the PEP in men (1.23 [1.10, 1.38], p  < 0.001), but inversely associated in women (0.33 [0.12, 0.93], p  = 0.036). Conclusion Baseline cardiovascular protein levels differ between women and men. However, the predictive value of repeatedly measured circulating proteins does not seem to differ except for endothelin-1 and somatostatin. Highlights Baseline levels of circulating proteins related to extracellular matrix organization were dominant in women, while those related to regulation of cell death were dominant in men. A significant interaction is present between sex and the circulating proteins endothelin-1 and somatostatin, in the longitudinal associations with adverse cardiovascular outcome. Even if circulating proteins entail similar risk in women and men, the use of the same thresholds in both sexes to ascertain the risk of future cardiovascular events may not result in equitable risk stratification, because of sex differences in baseline levels combined with underlying differences in risk of adverse events. Altogether, inherent sex differences in baseline levels may reflect sex differences in disease risk, suggesting that a sex-specific interpretation could be beneficial when circulating proteins are used for risk prediction in patients with chronic HF.