ResearchPad - heart https://www.researchpad.co Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[Atherosclerotic spontaneous coronary artery dissection (A-SCAD) in a patient with COVID-19: case report and possible mechanisms]]> https://www.researchpad.co/article/elastic_article_12474 Spontaneous coronary artery dissection (SCAD) may be atherosclerotic (A-SCAD) or non-atherosclerotic (NA-SCAD) in origin. Contemporary usage of the term ‘SCAD’ is typically synonymous with NA-SCAD. COVID-19 could induce a vascular inflammation localized in the coronary adventitia and periadventitial fat and contribute to the development of an A-SCAD of a vulnerable plaque in a susceptible patient.Case summaryIn this report we describe a case of a COVID-19 patient with past cardiac history of CAD who was admitted for acute coronary syndrome (ACS). Coronary angiography demonstrated the culprit lesion in the proximal LAD that presented with a very complex and unusual morphology, indicative of an A-SCAD. The diagnosis of A-SCAD was supported by the presence of a mild stenosis in the same coronary segment in the last angiogram performed 3 years previously. He was successfully treated by PCI, had a favourable course of the COVID-19 with no symptoms of pneumonia, and was discharged from the hospital after two negative tests for SARS-CoV-2.DiscussionA higher index of suspicion of A-SCAD is needed in patients with suspected or confirmed COVID-19 presenting with ACS. The proposed approach with ‘thrombolysis first’ for treating STEMI patients with suspected or confirmed COVID-19 infection could be unsafe in the case of underlying A-SCAD. ]]> <![CDATA[Circulating plasma concentrations of angiotensin-converting enzyme 2 in men and women with heart failure and effects of renin–angiotensin–aldosterone inhibitors]]> https://www.researchpad.co/article/elastic_article_12417 The current pandemic coronavirus SARS-CoV-2 infects a wide age group but predominantly elderly individuals, especially men and those with cardiovascular disease. Recent reports suggest an association with use of renin–angiotensin–aldosterone system (RAAS) inhibitors. Angiotensin-converting enzyme 2 (ACE2) is a functional receptor for coronaviruses. Higher ACE2 concentrations might lead to increased vulnerability to SARS-CoV-2 in patients on RAAS inhibitors.Methods and resultsWe measured ACE2 concentrations in 1485 men and 537 women with heart failure (index cohort). Results were validated in 1123 men and 575 women (validation cohort).The median age was 69 years for men and 75 years for women. The strongest predictor of elevated concentrations of ACE2 in both cohorts was male sex (estimate = 0.26, P < 0.001; and 0.19, P < 0.001, respectively). In the index cohort, use of ACE inhibitors, angiotensin receptor blockers (ARBs), or mineralocorticoid receptor antagonists (MRAs) was not an independent predictor of plasma ACE2. In the validation cohort, ACE inhibitor (estimate = –0.17, P = 0.002) and ARB use (estimate = –0.15, P = 0.03) were independent predictors of lower plasma ACE2, while use of an MRA (estimate = 0.11, P = 0.04) was an independent predictor of higher plasma ACE2 concentrations.ConclusionIn two independent cohorts of patients with heart failure, plasma concentrations of ACE2 were higher in men than in women, but use of neither an ACE inhibitor nor an ARB was associated with higher plasma ACE2 concentrations. These data might explain the higher incidence and fatality rate of COVID-19 in men, but do not support previous reports suggesting that ACE inhibitors or ARBs increase the vulnerability for COVID-19 through increased plasma ACE2 concentrations. ]]> <![CDATA[MitraClip<sup>®</sup> as bridging strategy for heart transplantation in Chagas cardiomyopathy: a case report]]> https://www.researchpad.co/article/elastic_article_10223 Patients with end-stage heart failure, suffering from severe pulmonary hypertension (PH) and elevated pulmonary vascular resistance, are not eligible for heart transplant due to high mortality risk and primary graft dysfunction. Severe PH may be favoured by functional severe mitral regurgitation, which is present in many cardiopathies like end-stage Chagasic cardiomyopathy.Case summaryWe present a case of a young man with end-stage heart failure secondary to Chagas cardiomyopathy with severe functional mitral regurgitation (FMR) and severe PH. The patient received percutaneous correction with MitraClip® system reducing PH and making him a suitable candidate for heart transplant.DiscussionIn patients with advanced heart failure, FMR, and severe PH, optimal treatment according to current guide lines is recommended. MitraClip® therapy appears to be safe and effective for control of severe PH as a bridge measure for cardiac transplantation. ]]> <![CDATA[Impact of myocardial fibrosis on left ventricular remodelling, recovery, and outcome after transcatheter aortic valve implantation in different haemodynamic subtypes of severe aortic stenosis]]> https://www.researchpad.co/article/elastic_article_10049 Myocardial fibrosis (MF) might represent a key player in pathophysiology of heart failure in aortic stenosis (AS). We aimed to assess its impact on left ventricular (LV) remodelling, recovery, and mortality after transcatheter aortic valve implantation (TAVI) in different AS subtypes.Methods and results One hundred patients with severe AS were prospectively characterized clinically and echocardiographically at baseline (BL), 6 months, 1 year, and 2 years following TAVI. Left ventricular biopsies were harvested after valve deployment. Myocardial fibrosis was assessed after Masson’s trichrome staining, and fibrotic area was calculated as percentage of total tissue area. Patients were stratified according to MF above (MF+) or below (MF−) median percentage MF (≥11% or <11%). Myocardial fibrosis burden differed significantly between AS subtypes, with highest levels in low ejection fraction (EF), low-gradient AS and lowest levels in normal EF, high-gradient AS (29.5 ± 26.4% vs. 13.5 ± 16.1%, P = 0.003). In the entire cohort, MF+ was significantly associated with poorer LV function, higher extent of pathological LV remodelling, and more pronounced clinical heart failure at BL. After TAVI, MF+ was associated with a delay in normalization of LV geometry and function but not per se with absence of reverse remodelling and clinical improvement. However, 22 patients died during follow-up (mean, 11 months), and 14 deaths were classified as cardiovascular (CV) (n = 9 arrhythmia-associated). Importantly, 13 of 14 CV deaths occurred in MF+ patients (CV mortality 26.5% in MF+ vs. 2% in MF− patients, P = 0.0003). Multivariate analysis identified MF+ as independent predictor of CV mortality [hazard ratio (HR) 27.4 (2.0–369), P = 0.01].Conclusion Histological MF is associated with AS-related pathological LV remodelling and independently predicts CV mortality after TAVI. ]]> <![CDATA[Right ventricular pressure overload directly affects left ventricular torsion mechanics in patients with precapillary pulmonary hypertension]]> https://www.researchpad.co/article/elastic_article_8470 This study examined the impact of septal flattening on left ventricular (LV) torsion in patients with precapillary pulmonary hypertension (PH). Fifty-two patients with proven precapillary PH and 13 healthy controls were included. Ventricular function was assessed including 4D-measurements, tissue velocity imaging, and speckle tracking analysis. Increased eccentricity index (1.39 vs. 1.08, p<0.001), systolic pulmonary artery pressure (64 vs. 29mmHg, p<0.001) and right ventricular Tei index (0.55 vs. 0.28, p = 0.007), and reduced tricuspid annular plane systolic excursion (19.0 vs. 26.5mm, p<0.001) were detected in PH patients as compared to controls. With increasing eccentricity of left ventricle, LV torsion was both decreased and delayed. Torsion rate paralleled this pattern of change during systole, but not during diastole. In conclusion, right ventricular pressure overload directly affects LV torsion mechanics. The echocardiographic methodology applied provides novel insights in the interrelation of right- and left ventricular function.

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<![CDATA[Risk of colorectal cancer in patients with alcoholism: A nationwide, population-based nested case-control study]]> https://www.researchpad.co/article/elastic_article_7832 Colorectal cancer (CRC) is regarded as a multifactorial disease and shares many risk factors with alcoholism. However, the association between alcoholism and CRC remains controversial.ObjectivesIn this study, we aimed to evaluate the association between alcoholism and risk of CRC.MethodsWe performed a large-scale, population-based nested case-control study using the Longitudinal Health Insurance Database 2013, derived from Taiwan’s National Health Insurance Research Database, and collected data from 2000 to 2013. There were 49,095 diagnosed cases of CRC defined according to the International Classification of Diseases, Ninth Revision, Clinical Modification. Each case was matched with three controls by sex, age, index date of CRC, and annual medical visits; a total of 147,285 controls were identified. Multiple risk factors of CRC in alcoholism cases were investigated using unconditional multiple logistic regression analysis.ResultsAmong 49,095 cases of CRC, alcoholism was associated with a significantly higher risk of CRC (adjusted odds ratio (OR), 1.631; 95% CI, 1.565–1.699) in multivariate logistic regression, after adjusting other CRC risk factors, and in stratified analysis with multivariate logistic regression. In addition, there was a time-dependent relationship between alcoholism duration and CRC risk in >1 year, > 2 years, >5 years, and > 11 years groups (adjusted ORs, 1.875, 2.050, 2.662 and 2.670; 95% CI, 1.788–1.967, 1.948–2.158, 2.498–2.835, and 2.511–2.989 respectively).ConclusionAn association between alcoholism and risk of CRC was found in this study. Furthermore, patients with longer alcoholism history showed higher likelihood of developing CRC, which indicates a time-dependent relationship between alcoholism exposure and CRC. Further research on colorectal tumorigenesis is needed. ]]> <![CDATA[Association between attending exercise-based cardiac rehabilitation and cardiovascular risk factors at one-year post myocardial infarction]]> https://www.researchpad.co/article/elastic_article_7688 Randomized trials confirm the benefits of exercise-based cardiac rehabilitation on cardiovascular risk factors. Whether exercise-based cardiac rehabilitation provides the same favourable effects in real-life cardiac rehabilitation settings, in the modern era of myocardial infarction treatment, is less well known. We examined the association between attending exercise-based cardiac rehabilitation and improvements in cardiovascular risk factors at one-year post myocardial infarction in patients included in the Swedish heart disease registry, SWEDEHEART.MethodsIn this retrospective registry-based cohort study, we included 19 136 patients post myocardial infarction (75% men, 62.8±8.7 years) who were registered in SWEDEHEART between 2011 and 2013. The association between attending exercise-based cardiac rehabilitation (43% participation rate) and changes in cardiovascular risk profile between baseline and one-year follow-up was assessed using multivariable regression analysis adjusting for age, comorbidities and medication.ResultsAttenders more often reported to have stopped smoking (men 64% vs 50%; women 64% vs 53%, p<0.001 for both, only smokers at baseline considered), be more physically active (men 3.9±2.5 vs 3.4±2.7 days/week; women 3.8±2.6 vs 3.0±2.8 days/week, p<0.001 for both) and achieved a slightly larger reduction in triglycerides (men -0.2±0.8 vs -0.1±0.9 mmol/L, p = 0.001; women -0.1±0.6 vs 0.0±0.8 mmol/L, p = 0.01) at one-year compared to non-attenders. Male attenders gained less weight (+0.0±5.7 vs +0.3±5.7 kg, p = 0.01) while female attenders achieved better lipid control (total cholesterol -1.2±1.4 vs -0.9±1.4 mmol/L, p<0.001; low-density lipoprotein -1.2±1.2 vs -0.9 ±1.2 mmol/L, p<0.001) compared to non-attenders.ConclusionsIn an unselected registry cohort of patients post myocardial infarction, compared to non-attenders those attending exercise-based cardiac rehabilitation achieved significantly larger improvements in cardiovascular risk factors at one-year after the acute event. ]]> <![CDATA[Investigating gene-microRNA networks in atrial fibrillation patients with mitral valve regurgitation]]> https://www.researchpad.co/article/elastic_article_7684 Atrial fibrillation (AF) is predicted to affect around 17.9 million individuals in Europe by 2060. The disease is associated with severe electrical and structural remodelling of the heart, and increased the risk of stroke and heart failure. In order to improve treatment and find new drug targets, the field needs to better comprehend the exact molecular mechanisms in these remodelling processes.ObjectivesThis study aims to identify gene and miRNA networks involved in the remodelling of AF hearts in AF patients with mitral valve regurgitation (MVR).MethodsTotal RNA was extracted from right atrial biopsies from patients undergoing surgery for mitral valve replacement or repair with AF and without history of AF to test for differentially expressed genes and miRNAs using RNA-sequencing and miRNA microarray. In silico predictions were used to construct a mRNA-miRNA network including differentially expressed mRNAs and miRNAs. Gene and chromosome enrichment analysis were used to identify molecular pathways and high-density AF loci.ResultsWe found 644 genes and 43 miRNAs differentially expressed in AF patients compared to controls. From these lists, we identified 905 pairs of putative miRNA-mRNA interactions, including 37 miRNAs and 295 genes. Of particular note, AF-associated miR-130b-3p, miR-338-5p and miR-208a-3p were differentially expressed in our AF tissue samples. These miRNAs are predicted regulators of several differentially expressed genes associated with cardiac conduction and fibrosis. We identified two high-density AF loci in chromosomes 14q11.2 and 6p21.3.ConclusionsAF in MVR patients is associated with down-regulation of ion channel genes and up-regulation of extracellular matrix genes. Other AF related genes are dysregulated and several are predicted to be targeted by miRNAs. Our novel miRNA-mRNA regulatory network provides new insights into the mechanisms of AF. ]]> <![CDATA[Genetic algorithm-based personalized models of human cardiac action potential]]> https://www.researchpad.co/article/elastic_article_7669 We present a novel modification of genetic algorithm (GA) which determines personalized parameters of cardiomyocyte electrophysiology model based on set of experimental human action potential (AP) recorded at different heart rates. In order to find the steady state solution, the optimized algorithm performs simultaneous search in the parametric and slow variables spaces. We demonstrate that several GA modifications are required for effective convergence. Firstly, we used Cauchy mutation along a random direction in the parametric space. Secondly, relatively large number of elite organisms (6–10% of the population passed on to new generation) was required for effective convergence. Test runs with synthetic AP as input data indicate that algorithm error is low for high amplitude ionic currents (1.6±1.6% for IKr, 3.2±3.5% for IK1, 3.9±3.5% for INa, 8.2±6.3% for ICaL). Experimental signal-to-noise ratio above 28 dB was required for high quality GA performance. GA was validated against optical mapping recordings of human ventricular AP and mRNA expression profile of donor hearts. In particular, GA output parameters were rescaled proportionally to mRNA levels ratio between patients. We have demonstrated that mRNA-based models predict the AP waveform dependence on heart rate with high precision. The latter also provides a novel technique of model personalization that makes it possible to map gene expression profile to cardiac function.

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<![CDATA[Identification of miRNA signatures associated with radiation-induced late lung injury in mice]]> https://www.researchpad.co/article/elastic_article_7641 Acute radiation exposure of the thorax can lead to late serious, and even life-threatening, pulmonary and cardiac damage. Sporadic in nature, late complications tend to be difficult to predict, which prompted this investigation into identifying non-invasive, tissue-specific biomarkers for the early detection of late radiation injury. Levels of circulating microRNA (miRNA) were measured in C3H and C57Bl/6 mice after whole thorax irradiation at doses yielding approximately 70% mortality in 120 or 180 days, respectively (LD70/120 or 180). Within the first two weeks after exposure, weight gain slowed compared to sham treated mice along with a temporary drop in white blood cell counts. 52% of C3H (33 of 64) and 72% of C57Bl/6 (46 of 64) irradiated mice died due to late radiation injury. Lung and heart damage, as assessed by computed tomography (CT) and histology at 150 (C3H mice) and 180 (C57Bl/6 mice) days, correlated well with the appearance of a local, miRNA signature in the lung and heart tissue of irradiated animals, consistent with inherent differences in the C3H and C57Bl/6 strains in their propensity for developing radiation-induced pneumonitis or fibrosis, respectively. Radiation-induced changes in the circulating miRNA profile were most prominent within the first 30 days after exposure and included miRNA known to regulate inflammation and fibrosis. Importantly, early changes in plasma miRNA expression predicted survival with reasonable accuracy (88–92%). The miRNA signature that predicted survival in C3H mice, including miR-34a-5p, -100-5p, and -150-5p, were associated with pro-inflammatory NF-κB-mediated signaling pathways, whereas the signature identified in C57Bl/6 mice (miR-34b-3p, -96-5p, and -802-5p) was associated with TGF-β/SMAD signaling. This study supports the hypothesis that plasma miRNA profiles could be used to identify individuals at high risk of organ-specific late radiation damage, with applications for radiation oncology clinical practice or in the context of a radiological incident.

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<![CDATA[Comprehensive assessment of coronary pulse wave velocity in anesthetized pigs]]> https://www.researchpad.co/article/elastic_article_8025 Four methods for measuring coronary pulse wave velocity (CoPWV) were compared in animal (n = 10) using two regular pressure guidewires. During decompression phase a trend exists for higher CoPWV and repeatability is better than during compression phase. When coronary blood flow is reduced, known methods assessing CoPWV are not applicable and only the template matching and a new “backward wave” method yields reliable results.

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<![CDATA[Model based estimation of QT intervals in non-invasive fetal ECG signals]]> https://www.researchpad.co/article/elastic_article_7659 The end timing of T waves in fetal electrocardiogram (fECG) is important for the evaluation of ST and QT intervals which are vital markers to assess cardiac repolarization patterns. Monitoring malignant fetal arrhythmias in utero is fundamental to care in congenital heart anomalies preventing perinatal death. Currently, reliable detection of end of T waves is possible only by using fetal scalp ECG (fsECG) and fetal magnetocardiography (fMCG). fMCG is expensive and less accessible and fsECG is an invasive technique available only during intrapartum period. Another safer and affordable alternative is the non-invasive fECG (nfECG) which can provide similar assessment provided by fsECG and fMECG but with less accuracy (not beat by beat). Detection of T waves using nfECG is challenging because of their low amplitudes and high noise. In this study, a novel model-based method that estimates the end of T waves in nfECG signals is proposed. The repolarization phase has been modeled as the discharging phase of a capacitor. To test the model, fECG signals were collected from 58 pregnant women (age: (34 ± 6) years old) bearing normal and abnormal fetuses with gestational age (GA) 20-41 weeks. QT and QTc intervals have been calculated to test the level of agreement between the model-based and reference values (fsECG and Doppler Ultrasound (DUS) signals) in normal subjects. The results of the test showed high agreement between model-based and reference values (difference < 5%), which implies that the proposed model could be an alternative method to detect the end of T waves in nfECG signals.

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<![CDATA[The left ventricle undergoes biomechanical and gene expression changes in response to increased right ventricular pressure overload]]> https://www.researchpad.co/article/N51034a10-0d22-497f-84f8-cbd530e51603 Right ventricular (RV) failure is a common endpoint in pulmonary hypertension. While most clinical and research efforts are focused on the RV, our research shows that the left ventricle undergoes bio‐mechanical and gene‐expression changes in response to RV pressure overload.

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<![CDATA[Long-term Outcome of Pulmonary Vein Isolation Versus Amiodarone Therapy in Patients with Coexistent Persistent AF and Congestive Heart Failure]]> https://www.researchpad.co/article/N82af611f-ef65-4e29-b44f-6f02ecd6d4a9 Although pharmacological rhythm control of AF in patients with heart failure with reduced ejection fraction (HFrEF) does not seem to provide any benefit over rate control, catheter ablation of AF has been shown to improve clinical outcomes. These results can be explained with higher success rates of catheter ablation in restoring and maintaining sinus rhythm compared with antiarrhythmic drugs. In addition, pharmacotherapy is not void of side-effects, which are thought to offset its potential antiarrhythmic benefits. Therefore, efforts should be made towards optimisation of ablation techniques for AF in patients with HFrEF.

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<![CDATA[Asymptomatic Left Ventricle Systolic Dysfunction]]> https://www.researchpad.co/article/Na50cd32d-233b-4933-9bea-963a8b862395 Heart failure is a common debilitating illness, associated with significant morbidity and mortality, rehospitalisation and societal costs. Current guidelines and position statements emphasise the management of patients with overt symptomatic disease, but the increasing prevalence of congestive heart failure underscores the need to identify and manage patients with early left ventricular dysfunction prior to symptom onset. Asymptomatic left ventricular systolic dysfunction (ALVSD), classified as stage B heart failure, is defined as depressed left ventricular systolic function in the absence of clinical heart failure. Early initiation of therapies in patients with presumed ALVSD has been shown to lead to better outcomes. In this article, the authors clarify issues surrounding the definition and natural history of ALVSD, outline clinical tools that may be of value in identifying patients with ALVSD and highlight potential opportunities for future investigations to better address aspects of our understanding of this complex syndrome.

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<![CDATA[Coronary Artery Spasm: The Interplay Between Endothelial Dysfunction and Vascular Smooth Muscle Cell Hyperreactivity]]> https://www.researchpad.co/article/N2a546849-7f84-4ff0-bc4c-d7be3a4f0899 Patients with angina pectoris, the cardinal symptom of myocardial ischaemia, yet without significant flow-limiting epicardial artery stenosis represent a diagnostic and therapeutic challenge. Coronary artery spasm (CAS) is an established cause for anginal chest pain in patients with angiographically unobstructed coronary arteries. CAS may occur at the epicardial level and/or in the microvasculature. Although the underlying pathophysiological mechanisms of CAS are still largely unclear, endothelial dysfunction and vascular smooth muscle cell (VSMC) hyperreactivity seem to be involved as major players, although their contribution to induce CAS is still seen as controversial. This article will look at the role and possible mechanistic interplay between an impaired endothelial and VSMC function in the pathogenesis of CAS.

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<![CDATA[Heart Failure Treatment by Device]]> https://www.researchpad.co/article/N4092ce6f-ef0a-4213-ba3d-5028a913919b <![CDATA[Effects of Statin Treatment on Patients with Angina and Normal or Nearly Normal Angiograms]]> https://www.researchpad.co/article/N5f35d569-d5b5-4b61-b35a-2e4e4b321af9 This article offers an updated and comprehensive overview of major findings on the effects of statin treatment in patients with chronic angina but without any epicardial coronary artery with obstructive lesion.

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<![CDATA[MEF2C Silencing Attenuates Load-Induced Left Ventricular Hypertrophy by Modulating mTOR/S6K Pathway in Mice]]> https://www.researchpad.co/article/5989daeaab0ee8fa60bbee3f

Background

The activation of the members of the myocyte enhancer factor-2 family (MEF2A, B, C and D) of transcription factors promotes cardiac hypertrophy and failure. However, the role of its individual components in the pathogenesis of cardiac hypertrophy remains unclear.

Methodology/Principal Findings

In this study, we investigated whether MEF2C plays a role in mediating the left ventricular hypertrophy by pressure overload in mice. The knockdown of myocardial MEF2C induced by specific small interfering RNA (siRNA) has been shown to attenuate hypertrophy, interstitial fibrosis and the rise of ANP levels in aortic banded mice. We detected that the depletion of MEF2C also results in lowered levels of both PGC-1α and mitochondrial DNA in the overloaded left ventricle, associated with enhanced AMP:ATP ratio. Additionally, MEF2C depletion was accompanied by defective activation of S6K in response to pressure overload. Treatment with the amino acid leucine stimulated S6K and suppressed the attenuation of left ventricular hypertrophy and fibrosis in the aforementioned aortic banded mice.

Conclusion/Significance

These findings represent new evidences that MEF2C depletion attenuates the hypertrophic responses to mechanical stress and highlight the potential of MEF2C to be a target for new therapies to cardiac hypertrophy and failure.

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<![CDATA[Long-term outcomes after extracorporeal membrane oxygenation in patients with dialysis-requiring acute kidney injury: A cohort study]]> https://www.researchpad.co/article/5c92b361d5eed0c4843a3f31

Background

Acute kidney injury (AKI) is a common complication of extracorporeal membrane oxygenation (ECMO) treatment. The aim of this study was to elucidate the long-term outcomes of adult patients with AKI who receive ECMO.

Materials and methods

The study analyzed encrypted datasets from Taiwan’s National Health Insurance Research Database. The data of 3251 patients who received first-time ECMO treatment between January 1, 2003, and December 31, 2013, were analyzed. Characteristics and outcomes were compared between patients who required dialysis for AKI (D-AKI) and those who did not in order to evaluate the impact of D-AKI on long-term mortality and major adverse kidney events.

Results

Of the 3251 patients, 54.1% had D-AKI. Compared with the patients without D-AKI, those with D-AKI had higher rates of all-cause mortality (52.3% vs. 33.3%; adjusted hazard ratio [aHR] 1.82, 95% confidence interval [CI] 1.53–2.17), chronic kidney disease (13.7% vs. 8.1%; adjusted subdistribution HR [aSHR] 1.66, 95% CI 1.16–2.38), and end-stage renal disease (5.2% vs. 0.5%; aSHR 14.28, 95% CI 4.67–43.62). The long-term mortality of patients who survived more than 90 days after discharge was 22.0% (153/695), 32.3% (91/282), and 50.0% (10/20) in the patients without D-AKI, with recovery D-AKI, and with nonrecovery D-AKI who required long-term dialysis, respectively, demonstrating a significant trend (Pfor trend <0.001).

Conclusion

AKI is associated with an increased risk of long-term mortality and major adverse kidney events in adult patients who receive ECMO.

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