RESUMO
Growing evidence demonstrated that cell death pathways including ferroptosis, apoptosis and necroptosis contribute to cardiac ischaemia/reperfusion (I/R) injury. We hypothesized that ferroptosis, apoptosis and necroptosis contribute differently to myocardial damage during acute cardiac I/R injury. Rats underwent cardiac I/R or sham operation. I/R-operated rats were divided into 4 groups: vehicle, apoptosis (Z-vad), ferroptosis (Fer-1) and necroptosis (Nec-1) inhibition. Rats in each cell death inhibitor group were subdivided into 3 different dose regimens: low, medium and high. Infarct size, left ventricular (LV) function, arrhythmias and molecular mechanism were investigated. Cardiac I/R caused myocardial infarction, LV dysfunction, arrhythmias, mitochondrial dysfunction, mitochondrial dynamic imbalance, inflammation, apoptosis and ferroptosis. Infarct size, LV dysfunction, mitochondrial dysfunction, apoptosis and ferroptosis were all reduced to a similar extent in rats treated with Z-vad (low and medium doses) or Fer-1 (medium and high doses). Fer-1 treatment also reduced mitochondrial dynamic imbalance and inflammation. No evidence of necroptosis was found in association with acute I/R injury, therefore Nec-1 treatment could not be assessed. Apoptosis and ferroptosis, not necroptosis, contributed to myocardial damage in acute I/R injury. Inhibitors of these 2 pathways provided effective cardioprotection in rats with I/R injury though modulation of mitochondrial function and attenuated apoptosis and ferroptosis.
Assuntos
Infarto do Miocárdio , Isquemia Miocárdica , Traumatismo por Reperfusão Miocárdica , Disfunção Ventricular Esquerda , Animais , Apoptose , Arritmias Cardíacas/tratamento farmacológico , Inflamação/metabolismo , Mitocôndrias Cardíacas/metabolismo , Isquemia Miocárdica/metabolismo , Traumatismo por Reperfusão Miocárdica/metabolismo , Ratos , Ratos Wistar , Disfunção Ventricular Esquerda/metabolismoRESUMO
OBJECTIVE: Microglial hyperactivation and apoptosis were observed following myocardial infarction and ischemia reperfusion (I/R) injury. This study aimed to test the hypothesis that the apoptosis inhibitor, Z-VAD, attenuates microglial and astrocytic hyperactivation and brain inflammation in rats with cardiac I/R injury. MATERIALS AND METHODS: Rats were subjected to either sham or cardiac I/R operation (30 min-ischemia followed by 120-min reperfusion), rats in the cardiac I/R group were given either normal saline solution or Z-VAD at 3.3 mg/kg via intravenous injection 15 min prior to cardiac ischemia. Left ventricular ejection fraction (% LVEF) was determined during the cardiac I/R protocol. The brain tissues were removed and used to determine brain apoptosis, brain inflammation, microglial and astrocyte morphology. RESULTS: Cardiac dysfunction was observed in rats with cardiac I/R injury as indicated by decreased %LVEF. In the brain, we found brain apoptosis, brain inflammation, microglia hyperactivation, and reactive astrogliosis occurred following cardiac I/R injury. Pretreatment with Z-VAD effectively increased %LVEF, reduced brain apoptosis, attenuated brain inflammation by decreasing IL-1ß mRNA levels, suppressed microglial and astrocytic hyperactivation and proliferation after cardiac I/R injury. CONCLUSION: Z-VAD exerts neuroprotective effects against cardiac I/R injury not only targeting apoptosis but also microglial and astrocyte activation.
Assuntos
Encefalite , Traumatismo por Reperfusão Miocárdica , Traumatismo por Reperfusão , Animais , Apoptose , Microglia , Ratos , Traumatismo por Reperfusão/tratamento farmacológico , Volume Sistólico , Função Ventricular EsquerdaRESUMO
Erythropoietin (EPO) has been shown to provide protection against ischemia/reperfusion (I/R) injury in various experimental models. However, clinical trials revealed unsatisfactory results when EPO was given to patients with myocardial infarction following reperfusion. The timing of EPO administration and its relation to mitochondrial function may largely involve in this controversy. We hypothesized that EPO given at different time points exert varying cardioprotective effects in terms of myocardial infarct size, left ventricular (LV) function, arrhythmia, apoptosis, mitochondrial function, and mitochondrial dynamics in rats with cardiac I/R injury. Male Wistar rats were subjected to either sham (n = 6) or cardiac I/R operation (n = 48). Rats undergoing cardiac I/R operation (30-min ischemia, followed by 120-min reperfusion) were allotted into 4 subgroups (n = 12/group): vehicle, EPO pretreatment, EPO given during ischemia, and EPO given at reperfusion. EPO was administered intravenously at 5000 unit/kg. Arrhythmia and LV function were monitored throughout the protocol. Next, the hearts were collected to determine infarct size, mitochondrial function, mitochondrial dynamics, gap junction protein, and apoptosis. Cardiac I/R promoted arrhythmias, LV dysfunction, infarct size expansion, apoptosis, mitochondrial dysfunction and increased mitochondrial fission. EPO given either before or during ischemia, but not at reperfusion, attenuated arrhythmia scores, LV dysfunction, infarct size, and apoptosis. Only EPO given either before or during ischemia alleviated mitochondrial swelling, mitochondrial depolarization, and reduced the levels of p-Drp1ser616/Drp1. Data from in vitro study also confirmed that EPO directly attenuated mitochondrial dysfunction in H9c2 cells subjected to hypoxia/reoxygenation. In conclusion, the EPO administration, either before or during ischemia, exerted cardioprotection against I/R injury by attenuating mitochondrial dynamic imbalance, mitochondrial dysfunction, and apoptosis, leading to reduced infarct size and improved LV function.
Assuntos
Eritropoetina , Infarto do Miocárdio , Isquemia Miocárdica , Traumatismo por Reperfusão Miocárdica , Animais , Apoptose , Arritmias Cardíacas/tratamento farmacológico , Arritmias Cardíacas/metabolismo , Eritropoetina/farmacologia , Eritropoetina/uso terapêutico , Masculino , Mitocôndrias/metabolismo , Dinâmica Mitocondrial , Infarto do Miocárdio/tratamento farmacológico , Traumatismo por Reperfusão Miocárdica/metabolismo , Ratos , Ratos WistarRESUMO
Ischemic acute kidney injury (AKI) is a frequent complication resulting from a myriad of conditions that decrease effective arterial blood volume to the kidneys including myocardial ischemia, sepsis, and hypovolemia. Following acute ischemic insult, restoration of renal blood flow inevitably leads to the aggravation of renal injury due to a widely researched condition known as ischemia/reperfusion (I/R) injury. For decades, apoptosis and necrosis have been proposed as being the two cell death pathways responsible for the pathogenesis of renal ischemic AKI. There is recent evidence to show that necrosis could be regulated in a caspase-independent manner. This regulated or programmed necrosis is termed necroptosis. Necroptotic markers such as receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain like pseudokinase (MLKL) have been identified in both in vitro and in vivo models of renal I/R injury, suggesting that necroptosis might be a potential therapeutic target to limit renal I/R injury. In this review, available reports from in vitro, in vivo and clinical reports regarding the association of necroptosis in renal I/R injury, along with its therapeutic potential, has been comprehensively summarized and discussed. Understanding this contributory mechanism could pave ways to improve therapeutic strategies in combating renal I/R injury.
Assuntos
Injúria Renal Aguda/patologia , Rim/patologia , Necroptose , Traumatismo por Reperfusão/patologia , Animais , Morte Celular , Fibrose , Humanos , Insuficiência Renal Crônica/patologiaRESUMO
The cancer burden on health and socioeconomics remains exceedingly high, with more than ten million new cases reported worldwide in 2018. The financial cost of managing cancer patients has great economic impact on both an individual and societal levels. Currently, many chemotherapeutic agents are available to treat various malignancies. One of these agents is doxorubicin, which was isolated from Streptomyces peucetius in the 1960s. Doxorubicin is frequently administered in combination with other agents as a mainstay chemotherapeutic regimen in many settings, since there is well-documented evidence that it is effective in eliminating malignant cells. Doxorubicin exerts its anti-tumor properties through DNA intercalation and topoisomerase inhibition. It also contains a quinone moiety which is susceptible to redox reactions with certain intracellular molecules, thereby leading to the production of reactive oxygen species. The oxidative stress following doxorubicin exposure is responsible for its well-documented cardiotoxicity, impairing cardiac contractility, ultimately resulting in congestive heart failure. Despite the cumulative evidence noting its adverse effects on the heart, limited information is available regarding the mechanistic association between doxorubicin and cardiac arrhythmias. There is compelling evidence to suggest that doxorubicin also causes proarrhythmic effects. Several case reports and studies in cancer patients have attributed many arrhythmic events to doxorubicin, some of which are life-threatening such as complete heart block and ventricular fibrillation. In this review, reports regarding the potential arrhythmic complications associated with doxorubicin from previous studies investigating the effects of doxorubicin on cardiac electrophysiological properties are comprehensively summarized and discussed. Consistencies and controversial findings from in vitro, in vivo, ex vivo, and clinical studies are presented and mechanistic insights regarding the effects of doxorubicin are also discussed.
Assuntos
Antibióticos Antineoplásicos/efeitos adversos , Arritmias Cardíacas/induzido quimicamente , Doxorrubicina/efeitos adversos , Coração/efeitos dos fármacos , Neoplasias/tratamento farmacológico , Animais , Arritmias Cardíacas/fisiopatologia , Cardiotoxicidade/tratamento farmacológico , Coração/fisiopatologia , HumanosAssuntos
Injúria Renal Aguda , Síndrome de Hipersensibilidade a Medicamentos , Eosinofilia , Exantema , Injúria Renal Aguda/induzido quimicamente , Injúria Renal Aguda/diagnóstico , Anticonvulsivantes/efeitos adversos , Síndrome de Hipersensibilidade a Medicamentos/diagnóstico , Síndrome de Hipersensibilidade a Medicamentos/etiologia , Eosinofilia/induzido quimicamente , Eosinofilia/diagnóstico , Exantema/induzido quimicamente , Febre/induzido quimicamente , Humanos , Lamotrigina/efeitos adversosRESUMO
Contrast-induced nephropathy (CIN) is a significant complication in patients undergoing coronary angiography, and its development is associated with increased morbidity and mortality. Left ventricular end-diastolic pressure (LVEDP) provides one index of left heart filling status. An elevated LVEDP can reflect volume overload or abnormal diastolic function and indicates a cardiac disorder. Data on the association between an elevated LVEDP and CIN are limited and have had conflicting results. We systematically searched the databases PubMed, Embase, and Scopus for full-text articles from database inception to May 2022. Studies were included if they evaluated the association between a high LVEDP and the incidence of CIN in patients undergoing coronary angiography. The study was registered in the PROSPERO CRD42022334070. A second search in PubMed identified randomized controlled trials using LVEDP to guide fluid administration during coronary procedures. Four studies were identified that used LVEDP to classify patients into groups to determine the association between the level and the development of CIN. In these studies, 240 patients of 2441 patients (9.8%) developed CIN. One study found no association between LVEDP levels and the development of CIN. Two studies found an increased frequency of CIN in patients with elevated levels using 2 cutoff points for LVEDP, ≥20 mm Hg and >30 mm Hg. One study found that lower LVEDP levels (5-14 mm Hg) were associated with the development of CIN. Three randomized control trials used LVDEP levels to manage fluid administration in patients undergoing coronary procedures; only one study found that the use of these levels to guide fluid administration resulted in better outcomes. In patients undergoing coronary angiography, an elevated LVEDP was not consistently associated with increased risk of CIN, and using LVEDP levels to guide fluid administration during these procedures did not always improve outcomes in comparison to other protocols. The use of LVEDP levels can help classify patients with cardiac disorders but does not necessarily provide an adequate description of the hemodynamic patterns in these patients to predict or prevent CIN in patients undergoing angiography.
RESUMO
Background: Omeprazole, a proton pump inhibitor (PPI), is a widely used and generally safe agent for treating acid-related gastrointestinal conditions. However, drug reaction with eosinophilia and systemic symptoms (DRESSs) syndrome has been reported. Objectives: To report a case of omeprazole-induced rapid DRESS syndrome and to review the literature. Methods: Descriptive analysis of one new case and a case series from literature review. Results: We report a case of 82-year-old woman presenting with rapid-onset of DRESS syndrome. The condition was initially suspected to be caused by antibiotic, but the definite diagnosis was eventually omeprazole-induced DRESS syndrome as suggested by the enzyme-linked immune absorbent spot (ELISpot) assay along with the clinical picture. Previous literatures regarding cases of PPI-induced DRESS syndrome were pooled for descriptive analysis. Among 21 PPI cases pooled, esomeprazole was the most commonly implicated PPI (52.4%), followed by pantoprazole (19.1%), and omeprazole along with lansoprazole (both 14.3%). The issue of cross-reactivities amongst PPIs remains uncertain. Nonetheless, in situations in which a PPIs are deemed necessary, a prudent approach could be considering a switch to an alternative agent with distinct chemical structure. Conclusion: PPI is commonly used safely as an agent for acid-related gastrointestinal conditions. However, PPI-induced rapid DRESS syndrome can occur, particularly with prior exposure history. ELISpot is an in vitro test, useful in identifying the culprit agent in patients with delayed-type hypersensitivity reaction.
RESUMO
BACKGROUND AND AIMS: The burden of alcohol-related complications is high and rising. However, there are notable deficiencies in comprehensive epidemiological study focusing on cardiovascular complications from alcohol, especially among young and middle-aged adults. We thus aimed to determine the burden of these conditions in young and middle-aged adults globally. METHODS AND RESULTS: We used data from the Global Burden of Disease Study 2019 and analysed the mortality and disability-adjusted life years of alcohol-associated cardiovascular complications in young and middle-aged adults. The findings were classified by sex, region, country, and Sociodemographic Index (SDI). The highest age-standardized death rates (ASDR) were observed in stroke 0.84 (95% UI 0.60-1.09), followed by alcoholic cardiomyopathy 0.57 (95% UI 0.47-0.66) per 100,000 population. The overall burden of alcohol-associated cardiovascular complications decreased globally but increased in atrial fibrillation and hypertensive heart disease. Regionally, most regions underwent a decrease in ASDR, but an increase was observed in Southeast Asia (+2.82%), Western Pacific (+1.48%), low-middle (+1.81%), and middle SDI (+0.75%) countries. Nevertheless, the ASDR and ASDALYs were highest in Europe. CONCLUSIONS: The impact of alcohol-associated atrial fibrillation and hypertensive heart disease has increased over the last decades. Regarding region, the burden in Europe and the rising burden in Asia, require immediate public health policy to lessen these cardiovascular complications from alcohol in young and middle-aged adults.
RESUMO
Acute myocarditis is a well-recognized condition attributable to a variety of viral illnesses. Common viral aetiologies include enteroviruses including coxsackie, adenovirus, influenza, echovirus, parvovirus B19 and herpesvirus. A high index of suspicion, early diagnosis, and prompt management with supportive anti-failure measures, and in selected cases immunosuppressive therapies including high-dose steroids, might be considered for better outcomes. The authors report a case of sudden onset of acute heart failure complicated by cardiogenic shock caused by viral myocarditis in a patient who initially presented with norovirus gastroenteritis. She had no previous cardiac history or significant cardiovascular risk factors. Prompt medical management for cardiogenic shock for norovirus-induced myocarditis was started, her symptoms gradually improved, and she was discharged safely on regular follow-up. LEARNING POINTS: Viral myocarditis exhibits a wide spectrum of symptoms ranging from non-specific prodromes such as fatigue and myalgia to chest pain, life-threatening arrhythmias, fulminant heart failure, or even sudden cardiac death.Common viral aetiologies for myocarditis include enteroviruses including coxsackie, adenovirus, influenza, echovirus, parvovirus B19 and herpesvirus.A high index of suspicion, early diagnosis, and prompt management with supportive anti-failure measures, and in selected cases immunosuppressive therapies including high-dose steroids, might be considered for better outcomes in cases of acute myocarditis.
RESUMO
Central diabetes insipidus (DI) is an uncommon condition caused by reduced or lack of vasopressin secretion from the posterior pituitary gland, typically caused by gland destruction. Several other causes for central DI have also been proposed. Here we present a case of transient central DI after discontinuation of vasopressin used for septic shock without evidence of overt pituitary damage in a cystic fibrosis patient. The serum sodium concentration peaked at 137 mmol/L in the setting of polyuria within 3 days of vasopressin discontinuation without other identified alternative etiologies. Sodium levels and urine output trended down dramatically with desmopressin administration.
RESUMO
Membranous interventricular septal (MIVS) aneurysm is a rare often asymptomatic, accidentally discovered congenital anomaly, which might be complicated with right ventricular obstruction, rupture, thromboembolism, and conduction abnormalities.
RESUMO
BACKGROUND: An increased heart rate (HR) is deleterious in patients with decompensated heart failure. Ivabradine, an HR lowering agent which acts by inhibiting the If current in the sinoatrial node, is indicated for chronic heart failure with reduced ejection fraction. However, data regarding the safety and efficacy of ivabradine in acute decompensated heart failure is limited. This retrospective observational study aimed to investigate the effects of ivabradine on morbidity and short-term mortality of hospitalized patients with acute decompensated heart failure. METHODS: A total of 998 patients with acute decompensated heart failure on top of a chronic status from 1/5/2014 to 1/5/2019 who were already on guideline-directed treatment including a beta-blocker were included. Patients were divided into two groups, the first group (No-ivabradine) where patients continued the same dose of beta-blocker alone while the second group (ivabradine group) ivabradine 5 mg BID was added in addition to the same dose of beta-blocker. Patients with hemodynamic instabilities were excluded from the study. Propensity matching was performed to exclude confounding factors. RESULTS: There was no significant difference between groups regarding baseline patient characteristics, laboratory, and echocardiographic data. There were significant differences between groups regarding average HR (87 ± 15 and 90 ± 12 bpm in ivabradine and control groups, consecutively, P = 0.0006*) and length of hospital stay (5.3 ± 2.3 and 7.7 ± 5.6 days in ivabradine and control groups, consecutively, P < 0.0001*). However, there were no differences in rehospitalization and mortality rates at 1 month and 6 months. CONCLUSION: In a retrospective cohort study aimed to investigate the effects of ivabradine on morbidity and short-term mortality of hospitalized patients with acute decompensated heart failure. Ivabradine was associated with significantly lower average HR and length of hospital stay. However, there was no benefit in the reduction of rehospitalization and mortality rates at 1- and 6-month follow-ups.
RESUMO
BACKGROUND: A wide range of cardiac arrhythmias were reported in the setting of active infection or as a complication of COVID-19. The main pathophysiology can be attributed to dysautonomia or autonomic nervous system dysfunction. Postural orthostatic tachycardia syndrome (POTS) is a complex, multisystemic disorder affecting usually younger age with tachycardia at rest or with minimal effort being the main symptom. Data regarding the safety and efficacy of ivabradine in POTS treatment is limited to small studies and case reports. METHODS: This prospective observational study included a total of 55 COVID-19-associated POTS patients after the exclusion of other causes of tachycardia. Ivabradine 5 mg twice daily was initiated. Re-assessment of patients' symptoms, heart rate, and heart rate variability (HRV) parameters' changes after 3 days of ivabradine therapy was done. RESULTS: The mean age of the included patients was 30.5±6.9 years with 32 patients being males (58.2%). 43 of 55 (78%) of the included patients reported significant improvement of the symptoms within 7 days of ivabradine therapy. 24-hour heart rate (minimum, average, and maximum) was significantly lower (p-value < 0.0001*, = 0.001*, < 0.0001* consecutively) with a significant difference in HRV time-domain parameters (SDNN, rMSSD) (p-value < 0.0001*) after ivabradine therapy. CONCLUSION: In a prospective study that evaluated the effects of ivabradine in post-COVID-19 POTS, patients treated with ivabradine reported improvement of their symptoms within 7 days of ivabradine treatment with a significant reduction of 24-hour average, minimum, and maximum heart rate, and improvement of HRV time domains parameters. Ivabradine might be a useful option to relieve symptoms of tachycardia in COVID-19 POTS. Further research is required to confirm the safety and efficacy of ivabradine in POTS treatment.
RESUMO
Key Clinical Message: In suspected cases of systemic vasculitis, imaging studies should include the pulmonary artery. This is a rare case of Takayasu arteritis with a large pulmonary aneurysm. Medical management is the first line and vascular intervention if fails prior. Abstract: Takayasu arteritis (TA) should be suspected in young women presented with hypertension, carotidynia, and claudications. Pulmonary artery involvement is frequent, occurring in 20%-50% of patients with TA. However, this case highlights the rare presentation of TA with a large pulmonary aneurysm and minimal aortic involvement. Medical management including immunosuppressive agents and biological therapies remains an important role, with vascular intervention remains as an option if medical therapy failed.
RESUMO
Key Clinical Message: Infective endocarditis should be considered in any febrile individual with acute onset neurological symptoms. If suspicion is high, a negative brain computed tomography does not virtually exclude embolism, and magnetic resonance imaging is warranted. Abstract: A diagnosis of infective endocarditis (IE) is often delayed, particularly in those infected with unusual organisms. Hereby, we report a case of a female patient presented with dysarthria, confusion, and altered mental status after being treated for Escherichia coli bacteremia. Computed tomography of the brain was unrevealing; however, scattered embolic phenomena were visualized on magnetic resonance imaging (MRI). The case underscores the importance of clinical awareness, particularly in the setting of unusual microorganisms, and the role of brain MRI in the diagnosis of IE.
RESUMO
BACKGROUND: Promising results with the CHA2DS2-VASc risk score (CVRS) have been reported for the prediction of contrast-induced nephropathy (CIN). The aim of this study is to consolidate all the data available and examine the association between elevated CVRS and the incidence of CIN in patients undergoing percutaneous coronary intervention (PCI). METHODS: We systematically searched PubMed, Embase, and Scopus for abstracts and full-text articles from inception to May 2022. Studies were included if they evaluated the association between a high CVRS and the incidence of CIN in patients undergoing PCI. Data were integrated using the random-effects, generic inverse variance method of DerSimonian and Laird. Prospero registration: CRD42022334065. RESULTS: Seven studies from 2016 to 2021 with a total of 7,401 patients were included. In patients undergoing PCI, a high CVRS (≥2: Odds ratio [OR]:2.98, 95% confidence interval [95% CI] 2.25-3.94, p < .01, I2 = 1%, ≥3: OR 4.46, 95% CI 2.27-8.78, p < .01, I2=56% and ≥4: OR:2.75, 95% CI 1.76-4.30, p < .01, I2 = 11%) was significantly associated with an increase incidence for CIN. Subgroup analyses were done in patients with acute coronary syndrome, and association with CIN remained statistically significant (≥2: OR 2.93, 95% CI 2.11-4.07, p < .01, I2=22%and ≥4: OR:2.24, 95% CI 1.36-3.69, p < .01, I2 = 0%,). CONCLUSION: In patients undergoing PCI, an elevated CVRS is associated with an increased risk for CIN. More rigorous studies are needed to clarify this association and to identify strategies to reduce CIN.
Assuntos
Síndrome Coronariana Aguda , Nefropatias , Intervenção Coronária Percutânea , Humanos , Meios de Contraste/efeitos adversos , Intervenção Coronária Percutânea/efeitos adversos , Intervenção Coronária Percutânea/métodos , Fatores de Risco , Síndrome Coronariana Aguda/etiologia , Valor Preditivo dos Testes , Angiografia Coronária , Nefropatias/induzido quimicamente , Medição de Risco/métodosRESUMO
Several studies have shown that elevated serum ferritin level is associated with a higher risk of coronary artery disease. Recently, it has been shown that high serum ferritin levels in men are independently correlated with an increased risk of cardiovascular mortality. This study aimed to investigate the possible correlation between the initial serum ferritin level and in-hospital mortality in patients presenting with ST-elevation myocardial infarction (STEMI). This retrospective cohort study included 890 patients who presented with acute STEMI and underwent successful primary percutaneous coronary intervention (PPCI) according to the standard techniques during the period from 1 May 2020 to 1 May 2021. At the time of admission, an initial serum ferritin level was measured in all patients. Comparison between initial ferritin levels was made between two groups: died and survived. Propensity matching was performed to exclude confounding factors effect. Forty-one patients had in-hospital mortality. There was no significant difference between both groups regarding baseline clinical characteristics. Initial serum ferritin levels were higher in deceased patients, even after propensity matching. In conclusion, even after propensity matching, initial ferritin levels were significantly higher in patients who died after being admitted for STEMI.
RESUMO
Introduction: Posttransplant anemia is a common finding after kidney transplantation. A previous meta-analysis reported an association between anemia and graft loss. However, data on cardiovascular outcomes have not yet been reported. Objective: We conducted an updated meta-analysis to examine the association between posttransplant anemia and outcomes after transplantation including cardiovascular mortality in adult kidney transplant recipients. Methods: We comprehensively searched the databases of MEDLINE and EMBASE from inception to November 2021. Data from each study were combined using the random-effects model. Generic inverse variance method of DerSimonian and Laird was employed to calculate the risk ratios and 95% CIs. Results: Seventeen studies from August 2006 to April 2019 were included (16 463 kidney transplantation recipients). Posttransplant anemia was associated with overall mortality (pooled risk ratio = 1.72 [1.39, 2.13], I2 = 56%), graft loss (pooled risk ratio = 2.28 [1.77, 2.93], I2 = 94%), cardiovascular death (pooled risk ratio = 2.06 [1.35, 3.16], I2 = 0%), and cardiovascular events (pooled risk ratio = 1.33 [1.10, 1.61], I2 = 0%). Early anemia (≤6 months), compared with late anemia (>6 months), has higher risk of overall mortality and graft loss with a pooled risk ratio of 2.63 (95% CI 1.79-3.86; I2 = 0%) and 2.96 (95% CI 2.29-3.82; I2 = 0%), respectively. Discussion: In addition to increased risk of graft loss, our updated meta-analysis demonstrated that posttransplant anemia was significantly associated with poor outcomes after kidney transplantation including overall mortality, graft loss, cardiovascular death, and cardiovascular events. Future studies are required to assess the effects of treatment strategies for posttransplant anemia on posttransplant outcomes including cardiovascular mortality.