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Abstract Background Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which also improve heart failure and decrease the risk of cardiovascular complications. Epicardial adipose tissue (EAT) dysfunction was suggested to contribute to the development of heart failure. We aimed to elucidate a possible role of changes in EAT metabolic and inflammatory profile in the beneficial cardioprotective effects of SGLT-2i in subjects with severe heart failure. Methods 26 subjects with severe heart failure, with reduced ejection fraction, treated with SGLT-2i versus 26 subjects without treatment, matched for age (54.0 ± 2.1 vs. 55.3 ± 2.1 years, n.s.), body mass index (27.8 ± 0.9 vs. 28.8 ± 1.0 kg/m2, n.s.) and left ventricular ejection fraction (20.7 ± 0.5 vs. 23.2 ± 1.7%, n.s.), who were scheduled for heart transplantation or mechanical support implantation, were included in the study. A complex metabolomic and gene expression analysis of EAT obtained during surgery was performed. Results SGLT-2i ameliorated inflammation, as evidenced by the improved gene expression profile of pro-inflammatory genes in adipose tissue and decreased infiltration of immune cells into EAT. Enrichment of ether lipids with oleic acid noted on metabolomic analysis suggests a reduced disposition to ferroptosis, potentially further contributing to decreased oxidative stress in EAT of SGLT-2i treated subjects. Conclusions Our results show decreased inflammation in EAT of patients with severe heart failure treated by SGLT-2i, as compared to patients with heart failure without this therapy. Modulation of EAT inflammatory and metabolic status could represent a novel mechanism behind SGLT-2i-associated cardioprotective effects in patients with heart failure.

Summary: The Par3 polarity protein is critical for subcellular compartmentalization in different developmental processes. Variants of PARD3, encoding PAR3, are associated with intelligence and neurodevelopmental disorders. However, the role of Par3 in glutamatergic synapse formation and cognitive functions in vivo remains unknown. Here, we show that forebrain-specific Par3 conditional knockout leads to increased long, thin dendritic spines in vivo. In addition, we observed a decrease in the amplitude of miniature excitatory postsynaptic currents. Surprisingly, loss of Par3 enhances hippocampal-dependent spatial learning and memory and repetitive behavior. Phosphoproteomic analysis revealed proteins regulating cytoskeletal dynamics are significantly dysregulated downstream of Par3. Mechanistically, we found Par3 deletion causes increased Rac1 activation and dysregulated microtubule dynamics through CAMSAP2. Together, our data reveal an unexpected role for Par3 as a molecular gatekeeper in regulating the pool of immature dendritic spines, a rate-limiting step of learning and memory, through modulating Rac1 activation and microtubule dynamics in vivo.

Abstract Aims Recipients of left ventricular assist devices (LVAD) are exposed to increased risk of adverse clinical events. One of the potential contributing factors is non‐pulsatile flow generated by LVAD. We evaluated the association of flow patterns in carotid arteries and of increased arterial stiffness with death and cerebrovascular events in LVAD recipients. Methods and results We analysed data from 83 patients [mean age 54 ± 15 years; 12 women; HeartMate II (HMII), n = 34; HeartMate 3 (HM3), n = 49]. Pulsatile and resistive indexes, atherosclerotic changes in carotid arteries (measured by duplex ultrasound), and arterial stiffness [measured by Endo‐PAT 2000 as the augmentation index standardized for heart rate (AI@75)] were evaluated 3 and 6 months after LVAD implantation. Sixteen patients died during follow‐up (27.3 months; interquartile range 15.7–44.3). After adjusting for the main variables examined, the pulsatility index measured at 3 months was positively associated with increased hazard ratios (HR) for death and cerebrovascular events [HR 9.8, 95% confidence interval (CI) 1.62–59.42], with HR increasing after adding AI@75 to the model (HR 18.8, 95% CI 2.44–145.50). In HM3 recipients, HR was significantly lower than in HMII recipients (HR 0.31, 95% CI 0.11–0.91), but the significance disappeared after adding AI@75 to the model (HR 0.33, 95% CI 0.09–1.18). Conclusions The risk of death and cerebrovascular events in LVAD recipients is associated with increased pulsatility index in carotid arteries and potentiated by increased arterial stiffness. The same risk is attenuated by HM3 LVAD implantation, but this effect is weakened by increased arterial stiffness.

Abstract Background Acute Stanford type A aortic dissection (TAAD) is a life-threatening condition. Surgery is usually performed as a salvage procedure and is associated with significant postoperative early mortality and morbidity. Understanding the patient’s conditions and treatment strategies which are associated with these adverse events is essential for an appropriate management of acute TAAD. Methods Nineteen centers of cardiac surgery from seven European countries have collaborated to create a multicentre observational registry (ERTAAD), which will enroll consecutive patients who underwent surgery for acute TAAD from January 2005 to March 2021. Analysis of the impact of patient’s comorbidities, conditions at referral, surgical strategies and perioperative treatment on the early and late adverse events will be performed. The investigators have developed a classification of the urgency of the procedure based on the severity of preoperative hemodynamic conditions and malperfusion secondary to acute TAAD. The primary clinical outcomes will be in-hospital mortality, late mortality and reoperations on the aorta. Secondary outcomes will be stroke, acute kidney injury, surgical site infection, reoperation for bleeding, blood transfusion and length of stay in the intensive care unit. Discussion The analysis of this multicentre registry will allow conclusive results on the prognostic importance of critical preoperative conditions and the value of different treatment strategies to reduce the risk of early adverse events after surgery for acute TAAD. This registry is expected to provide insights into the long-term durability of different strategies of surgical repair for TAAD. Trial registration ClinicalTrials.gov Identifier: NCT04831073 .

Aims: One of the proposed limitations of left ventricular assist device (LVAD) therapy is high degree of sensitization. Apart from human leukocyte antigen (HLA), antibodies against Angiotensin II Type 1 Receptor (AT1R) have been associated with adverse outcomes. The purpose of this study was to compare complications and survival of anti - AT1R positive versus negative Heart Mate II (HMII) recipients. Methods: Altogether 96 patients received HMII at our institution between 2008 and 2012. These were stratified into three groups: antibody positive before implantation (AT1R+), antibody conversion during support (AT1R-/+) and patients who remained antibody negative (AT1R-). Survival, major on-device adverse events and post-transplant rejections were assessed with Kaplan-Meier and log-rank tests. Results: Two year on-device and overall survival was 78 ± 12% and 75 ± 10% in AT1R-, 60 ± 23% and 60 ± 15% in AT1R+ and 92 ± 6% and 87 ± 5% in AT1R-/+ group (P = 0.409, P = 0.185). Freedom from major adverse event at two years for AT1R-, AT1R+ and AT1R-/+ was 49 ± 14%, 53 ± 16% and 41 ± 11% (P = 0.875). Freedom from rejection was 63 ± 17% in patients who were both anti-AT1R and HLA negative and 65 ± 13% in those who were antibody positive (P = 0.788). Conclusion: Patients who were anti-AT1R antibody positive had similar on-device survival and rate of complications in comparison to those who were antibody negative. In transplanted patients, there were no differences in the overall survival and rejection between the groups.

Mechanical circulatory support (MCS) with an implantable left ventricular assist device (LVAD) is an established therapeutic option for advanced heart failure. Most of the currently used LVADs generate a continuous stream of blood that decreases arterial pulse pressure. This study investigated whether a change of the pulse pressure during different pump speed settings would affect cerebral autoregulation and thereby affect cerebral blood flow (CBF). The study included 21 haemodynamically stable outpatients with a continuous-flow LVAD (HeartMate II, Abbott, USA) implanted a median of 6 months before the study (interquartile range 3 to 14 months). Arterial blood pressure (measured by finger plethysmography) was recorded simultaneously with CBF (measured by transcranial Doppler ultrasound) during baseline pump speed (8900 rpm [IQR 8800; 9200]) and during minimum and maximum tolerated pump speeds (8000 rpm [IQR 8000; 8200] and 9800 rpm [IQR 9800; 10 000]). An increase in LVAD pump speed by 800 rpm [IQR 800; 1000] from the baseline lead to a significant decrease in arterial pulse pressure and cerebral blood flow pulsatility (relative change -24 % and -32 %, both p < 0.01), but it did not affect mean arterial pressure and mean CBF velocity (relative change 1 % and -1.7 %, p=0.1 and 0.7). In stable patients with a continuous-flow LVAD, changes of pump speed settings within a clinically used range did not impair static cerebral autoregulation and cerebral blood flow. [ABSTRACT FROM AUTHOR]

The hemocompatible HeartMate3 (HM3) LVAD has demonstrated near-elimination of pump thrombosis but bleeding adverse events (AE) persist. We previously demonstrated safety of lower intensity anticoagulation targetsin the MAGENTUM 1 study and now explored complete withdrawal of anticoagulation in the MAGENTUM 2 trial. The prospective, single-center study was designed as a trial of vitamin K antagonist (VKA) withdrawal in HM3 patients. Stable patients who did not suffer a hemocompatibility event at 6 months post implant were enrolled. Exclusion criteria included absence of aortic valve opening, presence of intracardiac/aortic root thrombosis or a functional left atrial appendage with atrial fibrillation. Patients were transitioned to monotherapy with Aspirin.The primary endpoint was survival free of pump thrombosis, ischemic stroke and major bleeding at 6 months after VKA withdrawal. We enrolled 11 HM3 LVAD patients (mean age 62.3 (45-72) years, 10 men, 8 ischemic etiology [72%]) with 5 as bridge to transplant, 5 destination therapy (DT) and in 1 as bridge to candidacy. All patients met the primary endpoint for success at a median follow-up of 551 days (73-1168) accruing 16.6 pt years of experience. No mortality or hemocompatibility AE occured during follow-up. One patient with recurrent driveline infection developed abrupt pump flow drop after 319 days suspected as outflow graft twist however perioperatively, deep pump pocket infection was observed and pump inspection revealed obstructive Streptococcus vegetations corroborated by histology and microbiology. After pump exchange, VKA was resumed and uneventful transplant ensued. The MAGENTUM 2 Study supports the potential safety of VKA withdrawal in highly selected patients pointing to a signal of intrinsic thromboresistence with the HM3 pump. These observations set the stage for exploring a use of alternative strategies or novel anticoagulant regimens with the HM 3 LVAD. [ABSTRACT FROM AUTHOR]

Aims. One of the proposed limitations of left ventricular assist device (LVAD) therapy is high degree of sensitization. Apart from human leukocyte antigen (HLA), antibodies against Angiotensin II Type 1 Receptor (AT1R) have been associated with adverse outcomes. The purpose of this study was to compare complications and survival of anti - AT1R positive versus negative Heart Mate II (HMII) recipients. Methods. Altogether 96 patients received HMII at our institution between 2008 and 2012. These were stratified into three groups: antibody positive before implantation (AT1R+), antibody conversion during support (AT1R-/+) and patients who remained antibody negative (AT1R-). Survival, major on-device adverse events and post-transplant rejections were assessed with Kaplan-Meier and log-rank tests. Results. Two year on-device and overall survival was 78 ± 12% and 75 ± 10% in AT1R-, 60 ± 23% and 60 ± 15% in AT1R+ and 92 ± 6% and 87 ± 5% in AT1R-/+ group (P = 0.409, P = 0.185). Freedom from major adverse event at two years for AT1R-, AT1R+ and AT1R-/+ was 49 ± 14%, 53 ± 16% and 41 ± 11% (P = 0.875). Freedom from rejection was 63 ± 17% in patients who were both anti-AT1R and HLA negative and 65 ± 13% in those who were antibody positive (P = 0.788). Conclusion. Patients who were anti-AT1R antibody positive had similar on-device survival and rate of complications in comparison to those who were antibody negative. In transplanted patients, there were no differences in the overall survival and rejection between the groups. [ABSTRACT FROM AUTHOR]

Microparticles are small circulating vesicles originating from circulatory system and vascular wall cells released during their activation or damage. They possess different roles in regulation of endothelial function, inflammation, thrombosis, angiogenesis, and in general, cellular stress. Microparticles are the subject of intensive research in pulmonary hypertension, atherosclerotic disease, and heart failure. Another recently emerging role is the evaluation of the status of vasculature in end-stage heart failure patients treated with implantable ventricular assist devices. In patients implanted as destination therapy, assessment of the long-term effect of currently used continuous-flow left ventricular assist devices (LVADs) on vasculature might be of critical importance. However, unique continuous flow pattern generated by LVADs makes it difficult to assess reliably the vascular function with most currently used methods, based mainly on ultrasound detection of changes of arterial dilatation during pulsatile flow. In this respect, the measurement of circulating microparticles as a marker of vascular status may help to elucidate both short- and long-term effects of LVADs on the vascular system. Because data regarding this topic are very limited, this review is focused on the advantages and caveats of the circulating microparticles as markers of vascular function in patients on continuous-flow LVADs. [ABSTRACT FROM AUTHOR]

Left ventricular assist devices (LVAD), currently used in treatment of terminal heart failure, are working on principle of rotary pump, which generates continuous blood flow. Non-pulsatile flow is supposed to expose endothelial cells to high stress and potential damage. Therefore, we investigated longitudinal changes in concentration of circulating endothelial microparticles (EMP) as a possible marker of endothelial damage before and after implantation of LVAD. Study population comprised 30 patients with end-stage heart failure indicated for implantation of the Heart Mate II LVAD. Concentrations of microparticles were measured as nanomoles per liter relative to phosphatidylserine before and 3 months after implantation. At 3 months after implantation we observed significant decrease in concentration of EMP [5.89 (95% CI 4.31-8.03) vs. 3.69 (95% CI 2.70-5.03), p=0.03] in the whole group; there was no difference observed between patients with ischemic etiology of heart failure (n=18) and with heart failure of non-ischemic etiology (n=12). In addition, heart failure etiology had no effect on the rate of EMP concentration decrease with time. These results indicate possibility that LVAD do not cause vascular damage 3 months after implantation. Whether these results suggest improvement of vascular wall function and of endothelium is to be proved in long-term studies. [ABSTRACT FROM AUTHOR]

Pumps inflow cannula design considerably impacts thrombus formation proclivity that translates to a risk of thrombotic events. Long-term performance of the HeartMate3 (HM3; Abbott, USA) fully textured conic infundibulum cannula is incompletely understood given limited systematic analysis at time of transplant. Evidence of reduced anticoagulation impact on cannula thromboresistance absents completely. Consecutive HM3 patients (n= 46) undergoing transplant (2017-2021) were subject to comprehensive apical area analysis of explanted native heart. Makro- and detailed microscopic examination of the tissue surrounding the inflow cannula was performed. Mean time on support was 586 ±297 days (144-1351). Cut-then-sew technique was used in 13 pts while sew-then-cut dominated in 33 pts (71.7 %). One HM3 was implanted off-pump. Nine patients were till transplant on pre-specified long-term modified anticoagulation given dedicated study participation (6 pts INR range 1.5-1.9; complete warfarin withdrawal 3 pts; mean duration 504 (229-1028) days and 257 (73-526) days respectively). No pump thrombosis or thromboembolic events were revealed on support. Of 46 pts, we confirmed on histology only one (2.2 %) small spheric thrombus firmly adherent to the base of the cannula in sew-then-cut off-pump implanted pt with complete warfarin withdrawal for 73 days pre-transplant (see photo below). Our analysis suggests consistent pattern of mitigated thrombus formation with HM3 cannula contributing its hemocompatibility. The effect persists irrespective of the implant technique. Observations may signal preserved thromboresistant profile even in long-term low-intensity anticoagulation domain. However, complete withdrawal of warfarin and off-pump strategy mandate extreme caution. [ABSTRACT FROM AUTHOR]

Attenuation of physiological pulsatility after continuous flow left ventricular assist device (LVAD) implantation has been reported as a contributor to alteration of aortic wall morphology and function. MicroRNAs are non-coding RNAs that act to regulate translation of messenger RNA (mRNA) into proteins and are fine-tuners of gene expression in response to pathophysiological stimuli. Differences in gene expression (mRNA) and in post-transcriptional regulators (microRNAs) could reflect biological response to exposure to the low pulsatile environment. We hypothesized that pulsatility deficit caused by LVAD may influence miRNA/mRNA expression in aortic tissue. The aim of the study was to detect miRNA/mRNA associations in the aortic tissue during LVAD support. Aortic samples were collected at the time of LVAD implant and at heart transplantation in 16 patients (mean age 49.6±16.8 years; 3 females) and examined for miRNA/mRNA profiling. QuantSeq 3′ mRNA-Sequencing was used to examine differences in gene expression. Using human miRNome panels a profile of 752 miRNAs was identified. A total of 277 mRNAs were dysregulated after LVAD support (p adj <0.05). 5 most up-regulated genes (all p<0.0001) were COL1A2, CMKLR1, S100A4, ELN, and COL3A1. The most down-regulated genes (all p<0.0001) included SLC12A2, PDK4, ID1, ARGLU1 and MALAT1. Of 68 differently expressed miRNAs the most increased were let-7, miR-181, -29, 149 and -99 (all p<0.01), decrease was found in miR-19-, -654, -664, -885, and -511 (all p<0.01). Gene analysis identified genes involved in extracellular matrix (ECM) and collagen organization. MiRNA/mRNA analysis showed that miRNA downregulated in explanted samples affected expression of genes involved in myeloid leukocyte activation and cell activation during immune response. The study provides additional insight in pathophysiology of vascular changes after LVAD implantation. A significant regulation of mRNAs involved in ECM and collagen fibers organization in response to implantation of LVAD was observed, which may suggest infliction of ECM homeostasis resulting in changes of intrinsic properties of vascular wall and arterial stiffness. Downregulation of miRNAs involved in molecular processes related to immune response, could implicate dysregulation in inflammatory processes after LVAD implantation. [ABSTRACT FROM AUTHOR]

A pulsatility decrement caused by implantation of continuous flow left ventricular assist device (LVAD) has been corroborated as an additive factor further compromising aortic wall morphology and function. MicroRNAs (miRNAs) are important post-transcriptional regulators of gene expression which could reflect individual biologic adaptation to exposure to the low pulsatile environment. We hypothesized that pulsatility deficit caused by CF-LVAD implantation may influence miRNAs expression in aortic wall and that the miRNA profiles may differ between devices with different pulsatility profiles, such as speed modulated artificial pulse wave in HeartMate3. Paired aortic samples obtained at the time of LVAD implantation and at the time of Heart transplantation from CF-LVAD patients were examined for miRNA profiling in ten patients (3 females; mean age 55±13.8 years, ischemic cardiomyopathy 40%; HeartMateII(n=4), HeartMate3 (n=6). Human miRNome profile (miRCURY LNA miRNA PCR panels) of 752 miRNAs using qPCR on QuantStudio6 RT-PCR instrument was performed in all samples. The mean support duration was 383.5±222.4 days (range 162 to 887 days). 25 differently expressed multifunctional miRNAs that contribute to the regulation of multiple signaling pathways were identified. The most significant differences in miRNAs expression between implant/explant samples were found in miR-99b-5p; -144-3p; -23b-3p; -30e-3p and let-7d-5p (all p<0.002) which all play important role in differentiation of endothelial cells, vascular smooth muscle cells, or inflammation. No differences were observed between different types of CF-LVAD. The study provides additional evidence on a negative effect of suppressed physiologic pulsatility amplitude in CF-LVAD patients. Negative changes predominantly in miRNAs participating in vascular tissue engineering in aortic wall and pro-inflammatory changes of miRNA profiles during LVAD duration were observed. Our observations suggest that a programmed artificial pulsatility in HeartMate3 does not provide mitigation of continuous flow effect on aortic wall. Moreover, the most up-expressed miR-99b which target ENO2 gene, a marker of neuronal injury, was detected after explant of LVAD. Larger scale adverse events matched clinical trials are warranted. [ABSTRACT FROM AUTHOR]

Summary of Objectives The HeartMate 3 Left Ventricular Assist System has demonstrated absence of confirmed de-novo pump thrombosis and reduction in stroke. However, bleeding related adverse events persist under standard anticoagulation targeting a INR range of 2.0-3.0. In an initial experience we demonstrated safety of transition to low intensity anticoagulation (INR target 1.5-1.9, n=15, follow up of at least 6 months). Whether complete cessation of anticoagulation maintains "thromboresistance" in the HeartMate 3 pump remains unknown. Methods We previously reported on a strategy of low-intensity warfarin anticoagulation in patients implanted with HeartMate 3 (J Heart Lung Transplant. 2018;37(5):579-586). Following completion of this study phase, a staged trial was approved by the single site's ethics committee and registered as NCT03704220. All patients enrolled in the low intensity warfarin study (target INR of 1.5-1.9) were considered eligible for enrollment in the "anticoagulation withdrawal" study, if they were continuing on long-term support. All patients had to meet safe eligibility criteria including pump speed reduction to facilitate aortic valve opening (to avoid root thrombus), absence of thrombus in the pre-pump cardiac system, and absence of signs of poor unloading at reduced device speed. Careful surveillance for pump thrombosis was algorithmically mandated with biomarker and serial pump log file analyses. If enrolled, they were withdrawn from warfarin therapy and followed for survival free of pump thrombosis, disabling stroke or major bleeding for at least 3 months as the primary safety end point. Endpoints Enrollment and follow up in the low intensity anticoagulation study has been reported (n=15); 13 men, mean age 57 years (18-72) , with intended goal of therapy of either BTT or DT, INTERMACS Profile mean 3 (2-5), Cardiac Index mean 1.62 l/min/m2. Of 10 patients followed beyond 1 year on reduced anticoagulation, 5 patients have qualified for complete withdrawal of anticoagulation and the safety endpoint analysis will be completed prior to the ISHLT meeting in March 2019. This pivotal study is the first indication-independent anticoagulation withdrawal study in the HeartMate 3 designed to establish thrombo-resistance for the device and form the rationale for a large scale multicenter trial. [ABSTRACT FROM AUTHOR]

Purpose Heart failure is associated with impaired endothelial function including peripheral vessels. A pulsatility decrement once continuous flow left ventricular assist device (CF-LVAD) implanted has been consistently corroborated as an additive factor further compromising peripheral vascular function in such patients. EndoPAT 2000 is a FDA approved, operator independent device for assessment of endothelial function allowing for serial examination of reactive hyperemia index (RHI; as a measure of endothelial responsiveness; cutoff < 1.67 indicative of an endothelial dysfunction) and peripheral augmentation index (AI; as a measure of arterial stiffness). We hypothesized that a documented detrimental impact of a pulsatility deficit may be mitigated by a presence of speed modulated artificial pulse wave in fully magnetically levitated CF-LVAD HeartMate3. Methods Thirty-two patients implanted with HeartMate3 LVAS (5 females; mean age 55±13.8 years, ischemic cardiomyopathy 43.75%) were longitudinally examined by EndoPAT 2000 prior to the procedure and subsequently at 3rd and 6th month after implantation. Results Mean RHI was substantially impaired and below the norm already at a baseline (1.33±0.63). Temporal analysis revealed highly significant worsening at 3rd (RHI = 0.5±0.64) and 6th (RHI = 0.67±0.59) month post implantation (both p < 0.0001). Conversely, the arterial stiffness expressed as AI significantly increased at 3rd [(-3.4)±27.1] and 6th [(-0.9)±34.5] month after implantation relative to baseline [(-32.2)±25.2]; (p = 0.003 and p <0.0001 respectively). Additive functional worsening was most prominent within the first time interval and plateaued within a pre-specified follow up (RHI p=0.58; AI p=0.55). Conclusion The study provides additional evidence on a negative effect of suppressed physiologic pulsatility amplitude in CF-LVAD patients. Despite restored central hemodynamics, peripheral vascular function after implantation is further compromised based on serial assessment by EndoPAT 2000. Our observations suggest that a novel feature of programmed artificial pulsatility in HeartMate3 does not provide a sufficient pulse amplitude to avert further progression of peripheral vascular dysfunction due to continuous flow circulatory pattern. Larger scale adverse events matched clinical trials are warranted. [ABSTRACT FROM AUTHOR]

Left ventricular assist devices (LVADs) play a fundamental role in treating end-stage heart failure. Outflow graft stenosis (OGS) represents a serious complication that can occur at a variable time point after the implantation, although typically of the order of months to years. Different types of OGS, both intrinsic and external, were described. Notwithstanding the etiology, this clinical scenario poses a life and health-threatening complication requiring timely and precise diagnosis followed by appropriate intervention. We present a case of a 72-years-old woman on LVAD HeartMate II (HM II) support. Three years after the index implantation, she presented with clinical symptoms of outflow graft stenosis. The patient was admitted to the hospital due to"low-flow" alarms of HMII. The CT scan revealed distal outflow graft stenosis suggestive of kinking of the graft. Subsequent percutaneous transluminal stenting of the graft was performed. However, after the intervention, signs of hemodynamic compromise persisted. Both angiography and repeated CT scans verified peculiar pattern of the proximal shift of the stenotic segment relative to the implanted stent. Given this specific feature, a diagnosis was reclassified as a previously reported pattern of the outflow graft twist scenario, and surgical subxiphoid approach reexploration was indicated. On inspection, after disconnecting the bend relief from the pump body massive"gelly mass" plasma transudate located in the interspace between the graft and the bend relief was observed. Immediately after removing compressing gelly mass, hemodynamic and pump parameters promptly resolved, and the bend relief was re-attached. Further patient follow-up remains uneventful to the date. Our observation suggests that the diagnostic assessment of the outflow graft stenosis may be confusing and challenging. As plasma transudate likely develops over an extended period of time once a distal orifice of the bend relief already gets entrapped within the adjacent adhesion, the outflow graft may become contained within incompressible interspace while limited by tight connection to the pump body. That said, the graft constriction migration upon stenting can easily get misdiagnosed as a pattern suggestive of the intrinsic twist instead of correct"pseudotwist" diagnosis associated with the external contained compartment compression. [ABSTRACT FROM AUTHOR]