Association of severity of menstrual dysfunction with cardiometabolic risk markers among women with polycystic ovary syndrome.

INTRODUCTION: Polycystic ovary syndrome (PCOS) is associated with a wide range of unfavorable cardiometabolic risk factors, including obesity, hypertension, insulin resistance, impaired glucose metabolism, dyslipidemia, and metabolic syndrome. Compared with women with regular menstrual cycles, women with a history of irregular menstrual periods have an increased unfavorable cardiometabolic risk. Recently, the association between the severity of oligomenorrhea and hyperinsulinemia and insulin resistance has been demonstrated. However, evidence linking the severity of menstrual cyclicity with cardiometabolic risk in PCOS women is scarce. MATERIAL AND METHODS: This work was a prospective cross-sectional study. A total of 154 women diagnosed with PCOS by the Rotterdam criteria were recruited from July 2021 to September 2022. PCOS women with eumenorrheic (eumeno group), oligomenorrhea (oligo group), and amenorrhea (ameno group) underwent history and physical examination, gonadal steroid hormone measurement, lipid profile, oral glucose tolerance test, and homeostasis model assessment of insulin resistance. RESULTS: A trend toward an increase in unfavorable cardiometabolic risk markers including obesity, hypertension, prevalence of insulin resistance, prediabetes, dyslipidemia, and metabolic syndrome was observed in the ameno group (n = 57) as compared with the eumeno (n = 24) or oligo group (n = 73). A higher prevalence of insulin resistance (odds ratio [OR]: 3.02; 95% confidence interval [CI]: 1.03-8.81) and prediabetes (OR: 3.94; 95% CI: 1.01-15.40) was observed in the ameno group than in the eumeno group, and a higher proportion of dyslipidemia (OR: 2.44; 95% CI: 1.16-5.15) was observed in the ameno group than in the oligo group in the binary logistic regression analysis after adjusting for confounding factors. CONCLUSIONS: PCOS women with amenorrhea show a higher prevalence of insulin resistance, prediabetes, and dyslipidemia compared with those with oligomenorrhea or eumenorrhea. The severity of menstrual dysfunction could be used as a readily obtainable marker for the identification of PCOS women at greatest risk of cardiometabolic diseases.

Evaluation of left ventricular function in hypertensive athletic patients with different circadian rhythms using stratified strain technique

Purpose:With the stratified strain approach, the changes in the longitudinal mechanical condition of the left ventricular myocardium in hypertensive athleticpatients with a normal left ventricular ejection fraction (LVEF) have been evaluated. Materials and Methods:Based on circadian rhythm, 48 dippers and 53 non-dippers are selected among 103 hypertensionathleticpatients with normal LVEF (LVEF > 50%). The stratified strain approach is used to measure the longitudinal strain (GLS) of the subendocardial, middle,and epicardial myocardium during left ventricular systole. The relationship between the stratified strain and the circadian rhythm in hypertensive individuals has been analysed. Results:show that the levels of IVST, LVPWT, and LVMI in the non-dipper group are considerably higher than those in the dipper group, while there is not statistically significant between the two groups in terms of LVDd, LVDs, LA, or EF. Myocardial strain analysis reveals that the left ventricular long axis strain (GLS) in the non-dipper group is considerably greater than that in the dipper group, And the difference is statistically significant (P< 0.05). But the GLSendo between the non-dipper group and the dipper group did not vary significantly (P<0.05). In GLSMid, GLSepi, there is no significant difference, and the difference is not statistically significant(P>0.05).Conclusion：Ultrasonic stratified strain technique can quantitatively measure and analyze the longitudinal stratified strain of the myocardium in each segment of the left ventricle in hypertensive athleticpatients and evaluate their early left ventricular mechanics changes, providing a better diagnostic method for early clinical determination of myocardial involvement in athleticpatients. (AU)

The triglyceride glucose index predicts short-term mortality in non-diabetic patients with acute heart failure.

BACKGROUND: The triglyceride glucose index (TyG) has previously been considered a reliable indicator of insulin resistance (IR) and an independent prognostic predictor in heart failure (HF). OBJECTIVES: To clarify the association between the TyG and short-term death in non-diabetic patients admitted for acute heart failure (AHF). MATERIAL AND METHODS: We examined 886 out of 1620 consecutive AHF patients who were admitted to Shunde Hospital, Southern Medical University, Foshan, China, from June 1, 2014, to June 1, 2022. The median of the patientsf TyG values was used to divide them into 2 groups. The following formula was used to calculate the TyG: ln [fasting triglycerides (mg/dL) ~ fasting glucose (mg/dL)/2]. The data on all-cause mortality of AHF patients during their hospital stay were collected. The 30-day Enhanced Feedback for Effective Cardiac Treatment (EFFECT) death risk score was used to assess the risk of death. RESULTS: The TyG level was positively correlated with a poor AHF prognostic marker (N-terminal B-type natriuretic peptide (NT-proBNP)) (D = 0.207, p < 0.001) and negatively correlated with a protective marker (serum albumin) (D = .0.43, p < 0.001). Higher TyG values were associated with an elevated EFFECT score and hospital mortality (p < 0.001). According to multivariate logistic regression analysis, higher TyG levels raised the risk of death in hospital (odds ratio (OR) = 1.73; 95% confidence interval (95% CI): 1.03.3.27; p = 0.031) after adjusting for multiple variables, including age, EFFECT score and NT-proBNP. The TyG had a greater area under the receiver operating characteristic (ROC) curve (AUC: 0.688) for predicting hospital death compared to NT-proBNP (AUC: 0.506). CONCLUSIONS: Our findings show that the TyG is associated with the short-term mortality rate of non-diabetic patients admitted to the hospital for AHF. The TyG testing could be a useful prognostic indicator for these patients.

Secreted frizzled-related protein 2 ameliorates diabetic cardiomyopathy by activating mitophagy.

OBJECTIVES: Secreted frizzled-related protein 2 (SFRP2), a novel adipokine that used to be considered an inhibitor of the canonical Wnt pathway, may play a protective role in metabolic disorders. However, its effect on diabetic cardiomyopathy was still unclear. Accumulating evidence indicates that mitophagy can protect cardiac function in the diabetic heart. The present study aimed to explore the roles of SFRP2 on diabetic cardiomyopathy, focusing on the effects and mechanisms for regulating mitophagy. METHODS: Wild-type H9c2 cells, Sfrp2 overexpression and knockdown H9c2 cells were exposed to a glucolipotoxic milieu. Reactive oxygen species (ROS) production, cell viability, apoptosis, mitophagy and lysosomal activity were detected. The interaction of SFRP2 with frizzled 5 (FZD5), and its effect on expression and intracellular localization of transcription factor EB (TFEB) and ß-catenin were also explored. Diabetic rats and Sfrp2 overexpression diabetic rats were constructed to further document the findings from the in vitro study. RESULTS: The expression of SFRP2 was low and mitophagy was inhibited in H9c2 cells in a glucolipotoxic milieu. Sfrp2 overexpression activated mitophagy and reduced H9c2 cells injury, whereas Sfrp2 deficiency inhibited mitophagy and worsened this injury. Consistent with the in vitro findings, Sfrp2 overexpression ameliorated the impairment in cardiac function of diabetic rats by activating mitophagy. Sfrp2 overexpression upregulated the expression of calcineurin and TFEB, but did not affect ß-catenin in vitro and in vivo. The calcineurin inhibitor tacrolimus can inhibit mitophagy and worsen cell injury in Sfrp2 overexpression H9c2 cells. Furthermore, we found that FZD5 is required for the SFRP2-induced activation of the calcineurin/TFEB pathway and interacts with SFRP2 in H9c2 cells. Transfection with small interfering RNA targeting FZD5 opposed the effects of Sfrp2 overexpression on mitophagy and cell survival in a glucolipotoxic environment. CONCLUSIONS: SFRP2 can protect the diabetic heart by interacting with FZD5 and activating the calcineurin/TFEB pathway to upregulate mitophagy in H9c2 cells.

Non-alcoholic fatty liver disease is associated with a worse prognosis in patients with heart failure: A pool analysis.

Background and aims: Non-alcoholic fatty liver disease (NAFLD) is associated with a higher risk of heart failure (HF) than those without NAFLD. However, the prognostic impact of NAFLD in HF is still controversial. This meta-analysis aimed to explore the association between NAFLD and the risk of adverse outcomes in patients with HF. Methods: We searched multiple electronic databases (Embase, PubMed, and Google Scholar) for potentially related studies up to June 30, 2022. Cohort studies reported multivariable adjusted relative risks and 95% confidence intervals (CIs) of adverse outcomes in HF patients with NAFLD comparing those without NAFLD were included for analysis. Results: A total of six studies involving 12,374 patients with HF were included for analysis, with a median follow-up duration of 2.5 years. The pooled analysis showed that HF patients with NAFLD were associated with a significantly increased risk of major composite adverse outcomes (HR 1.61, 95% CI 1.25-2.07), all-cause mortality (HR 1.66, 95% CI 1.39-1.98), and HF hospitalization or re-hospitalization (HR 1.71, 95% CI 1.03-2.86). Conclusion: NAFLD is associated with a worse prognosis in patients with HF. Effective screening and treatment strategies are needed to improve the prognosis in HF patients with NAFLD.

Storage duration of vitrified embryos does not affect pregnancy and neonatal outcomes after frozen-thawed embryo transfer.

Background: With the refinement of cryopreservation technology, the number of frozen-warmed embryo transfer (FET) cycles and cryopreserved embryos has increased rapidly. However, studies investigating the effect of storage duration on pregnancy outcomes after vitrification are limited and their results are controversial. Furthermore, the available studies did not take patients' demographic nor clinical treatment characteristics into account and the cryo-storage duration was short. So this study aimed to explore the effect of storage duration of vitrified warmed embryos on pregnancy and neonatal outcomes in patients with good prognosis and long storage duration of vitrified embryos. Methods: This study was a bi-centre, retrospective study including 1037 women undergoing their first FET cycles following a fresh cycle from January 2012 until December 2021. Patients were divided into four storage groups in accordance with the storage duration of transferred embryos (612 patients in group I, with storage duration between 1 and 6 months; 202 patients in group II, with storage duration between 7 and 12 months; 141 patients in group III, with storage duration between 13 and 36 months; and 76 patients in group IV, with storage duration between 37 and 84 months). The pregnancy and neonatal outcomes were compared amongst different storage duration groups. Results: Amongst the different groups, no significant differences were observed in the pregnancy outcomes, including biochemical pregnancy rate, implantation rate, clinical pregnancy rate, ongoing pregnancy rate and live birth rate. In addition, no evidence of differences amongst different storage duration groups was observed in terms of preterm birth, birth length and low birthweight. Conclusions: The pregnancy and neonatal outcomes of embryos after vitrification were not impaired by storage duration up to 7 years.

Treatment of pacemaker-induced superior vena cava syndrome by direct oral anticoagulant.

BACKGROUND: The use of cardiac implantable electronic devices has grown substantially over the past two decades, lead-related vascular issues are commonly encountered in clinical practice. Superior vena cava (SVC) syndrome due to pacemaker leads is an uncommon complication. Anticoagulation remains the mainstay of therapy to restore some degree of patency and relieve swelling. However, there are limited clinical trials on direct oral anticoagulants (DOACs). CASE PRESENTATION: We report a case of an 80-year-old man who developed SVC syndrome after transvenous pacemaker implantation with symptoms of obstruction that were significantly relieved after four months of DOACs. His symptoms had completely resolved nine months later. CONCLUSIONS: DOACs are effective in the treatment of SVC syndrome after pacemaker implantation, representing an important new approach. It is a very good choice for patients who do not want to undergo interventional therapy.

Association between the ratio of serum eicosapentaenoic acid to arachidonic acid and risk of coronary artery disease in young Chinese patients.

Objective: Long-chain (LC) omega-3 PUFAs, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may play an anti-inflammatory effect and decrease the risk of coronary artery disease (CAD). In contrast, omega-6 PUFA, mainly arachidonic acid (AA), has pro-inflammatory and pro-aggregatory effects, which may increase the risk of CAD. This study evaluated the associations between EPA, DHA, AA, and their ratios (EPA/AA and DHA/AA) with the risk of CAD in young Chinese patients. Methods: A total of 182 young patients with CAD and 143 age-matched controls were included. Traditional cardiovascular risk factors were recorded. Serum EPA, DHA and AA were measured by ultra-performance liquid chromatography-mass spectrometry. Results: The level of AA was significantly higher, while the level of EPA was lower in the CAD group than that in the control group. There was no significant difference in DHA level in the two groups. Both the ratios of EPA/AA and DHA/AA were lower in the CAD group than that in the control. Multivariate logistic regression analysis showed that higher serum AA level was associated with the increased risk of CAD, while EPA was a protective factor for CAD. There was no significant association between DHA level and the risk of CAD. Although both higher ratios of EPA/AA [per tertile increment, adjusted odds ratios (ORs) (OR) 0.356, 95% confidence intervals (CI) 0.247-0.513] and DHA/AA (adjusted OR = 0.465, 95%CI = 0.332-0.653) were associated with a lower risk of CAD in young patients. Receiver operating characteristic (ROC) curve analysis showed that compared with AA, the diagnostic value was increased in EPA/AA, but not in DHA/AA. Conclusion: EPA, but not DHA may play a protective role in CAD, while AA may be associated with the increased risk of CAD in young Chinese patients. The ratio of EPA/AA can increase the predictive value for diagnosing CAD than EPA or AA alone.

Identification of Important Modules and Hub Gene in Chronic Kidney Disease Based on WGCNA.

Chronic kidney disease (CKD) is an ongoing deterioration of renal function that often progresses to end-stage renal disease. In this study, we aimed to screen and identify potential key genes for CKD using the weighted gene coexpression network (WGCNA) analysis tool. Gene expression data related to CKD were screened from GEO database, and expression datasets of GSE66494 and GSE62792 were obtained. After discrete analysis of samples, WGCNA analysis was performed to construct gene coexpression module, and the correlation between the module and disease was calculated. The modules with a significant correlation with the disease were selected for Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Then, the interaction network of related molecules was constructed, and the high score subnetwork was selected, and the candidate key molecules were identified. A total of 882 DEGs were identified in the screening datasets. A subnetwork containing 6 nodes was found with a high score of 12.08, including CEBPZ, IFI16, LYAR, BRIX1, BMS1, and DDX18. DEGs could significantly differentiate CKD and healthy individuals in principal component analysis. In addition, the MEturquiose, MEred, and MEblue in group were significantly correlated with disease in WGCNA. These 6 hub genes were found to significantly discriminate between CKD and healthy controls in the validation dataset, suggesting that they could use these molecules as candidate markers to distinguish CKD from healthy people. Overall, our study indicated that 6 hub genes may play key roles in the occurrence and development of CKD.

Identification and external validation of the hub genes associated with cardiorenal syndrome through time-series and network analyses.

Cardiorenal syndrome (CRS), defined as acute or chronic damage to the heart or kidney triggering impairment of another organ, has a poor prognosis. However, the molecular mechanisms underlying CRS remain largely unknown. The RNA-sequencing data of the left ventricle tissue isolated from the sham-operated and CRS model rats at different time points were downloaded from the Gene Expression Omnibus (GEO) database. Genomic differences, protein-protein interaction networks, and short time-series analyses, revealed fibronectin 1 (FN1) and periostin (POSTN) as hub genes associated with CRS progression. The transcriptome sequencing data of humans obtained from the GEO revealed that FN1 and POSTN were both significantly associated with many different heart and kidney diseases. Peripheral blood samples from 20 control and 20 CRS patients were collected from the local hospital, and the gene expression levels of FN1 and POSTN were detected by real-time quantitative polymerase chain reaction. FN1 (area under the curve [AUC] = 0.807) and POSTN (AUC = 0.767) could distinguish CRS in the local cohort with high efficacy and were positively correlated with renal and heart damage markers, such as left ventricular ejection fraction. To improve the diagnostic ability, diagnosis models comprising FN1 and POSTN were constructed by logistic regression (F-Score = 0.718), classification tree (F-Score = 0.812), and random forest (F-Score = 1.000). Overall, the transcriptome data of CRS rat models were systematically analyzed, revealing that FN1 and POSTN were hub genes, which were validated in different public datasets and the local cohort.

Malnutrition and the risk for contrast-induced acute kidney injury in patients with coronary artery disease.

PURPOSE: Malnutrition is a common comorbidity of coronary artery disease (CAD) and is often associated with adverse events. The malnutrition often means lower cholesterol, albumin and high lymphocyte, as risk factors of Contrast-Induced Acute Kidney Injury (CI-AKI). We aim to evaluate the association between malnutrition and CI-AKI following coronary angiography (CAG) in CAD patients. METHODS: We analyzed 3170 CAD patients with variables of nutritional status (Controlling Nutritional Status score (CONUT)) from the prospective multicenter study, REICIN (NCT01402232) including 4,271 consecutive patients undergoing CAG from January 2013 to February 2016. Patients were divided into the normal group (CONUT score 0-1) and malnutrition group (CONUT score > 1). The association of malnutrition and the risk of CI-AKI was examined in all CAD patients using multivariable logistics regression analysis. RESULTS: Among the 3170 patients (mean age: 63.1 ± 10.7 years), 1865 (58.8%) suffered from malnutrition, 111 (3.5%) developed CI-AKI, including 23 (1.76%) in normal group and 88 (4.72%) in malnutrition group (p < 0.01). The malnourished patients were older, and likely had anemia and worse cardiorenal function. After adjustment for confounders, the risk of CI-AKI was 1.04 times higher in the malnutrition group than in the normal group (adjusted OR: 2.04, 95% CI 1.28-3.38, p < 0.01). CONCLUSIONS: Among CAD patients undergoing CAG, malnutrition is extremely common and associated with a double risk of CI-AKI. Further studies are needed to investigate the potential renal protection of intervening malnutrition in CAD patients.

Evolutionary de Winter pattern: from STEMI to de Winter ECG-a case report.

The de Winter electrocardiography (ECG) pattern is a sign that implies proximal left anterior descending coronary artery occlusion in patients with chest pain. We report a case of a 34-year-old man with a history of smoking who presented to the local emergency department with a 49 min history of chest pain. The first ECG of the patient indicated that ST-segment elevation was noted in the lead V2-V4; 57 min later, a second ECG revealed a typical de Winter syndrome when the patient was transferred to the emergency chest pain centre of our hospital. A percutaneous coronary intervention (PCI) was performed approximately 8 h later because the patient initially refused the PCI. Acute coronary artery angiography showed that the proximal left anterior descending coronary artery was completely occluded. Our case suggests that ST-segment elevation myocardial infarction may evolve in the direction of de Winter, which reflects a coronary thrombus in formation, so the de Winter ECG pattern should not be considered static.

SFRP2 Improves Mitochondrial Dynamics and Mitochondrial Biogenesis, Oxidative Stress, and Apoptosis in Diabetic Cardiomyopathy.

BACKGROUND: The mitochondrial dynamics and mitochondrial biogenesis are essential for maintaining the bioenergy function of mitochondria in diabetic cardiomyopathy (DCM). Previous studies have revealed that secreted frizzled-related protein 2 (SFRP2) is beneficial against apoptosis and oxidative stress. However, no research has confirmed whether SFRP2 regulates oxidative stress and apoptosis through mitochondrial function in DCM. METHODS: Exposure of H9C2 cardiomyocytes in high glucose (HG) 25 mM and palmitic acid (PAL) 0.2 mM was used to simulate DCM in vitro. H9C2 cells with SFRP2 overexpression or SFRP2 knockdown were constructed and cultured under glucolipotoxicity or normal glucose conditions. An SD rat model of type 2 diabetes mellitus (T2DM) was generated using a high-fat diet combined with a low-dose STZ injection. Overexpression of SFRP2 in the rat model was generated by using an adeno-associated virus approach. CCK-8, TUNEL assay, and DHE staining were used to detect cell viability, and MitoTracker Red CMXRos was used to detect changes in mitochondrial membrane potential. We used qRT-PCR and western blot to further explore the mechanisms of SFRP2 regulating mitochondrial dynamics through the AMPK/PGC1-α pathway to improve diabetic cardiomyocyte injury. RESULTS: Our results indicated that SFRP2 was significantly downregulated in H9C2 cells and cardiac tissues in T2DM conditions, accompanied by decreased expression of mitochondrial dysfunction. The mitochondrial membrane potential was reduced, and the cells were led to oxidative stress injury and apoptosis. Furthermore, the overexpression of SFRP2 could reverse apoptosis and promote mitochondrial function in T2DM conditions in vitro and in vivo. We also found that silencing endogenous SFRP2 could further promote glucolipotoxicity-induced mitochondrial dysfunction and apoptosis in cardiomyocytes, accompanied by downregulation of p-AMPK. CONCLUSION: SFRP2 exerted cardioprotective effects by salvaging mitochondrial function in an AMPK-PGC1-α-dependent manner, which modulates mitochondrial dynamics and mitochondrial biogenesis, reducing oxidative stress and apoptosis. SFRP2 may be a promising therapeutic biomarker in DCM.

AKR1C3 and Its Transcription Factor HOXB4 Are Promising Diagnostic Biomarkers for Acute Myocardial Infarction.

Background: A recent study disclosed that ferroptosis was an important myocyte death style in myocardial infarction (MI). However, the diagnostic value of ferroptosis regulators and correlated underlying mechanisms in acute myocardial infarction (AMI) remain unknown. Methods: Bioinformatical analyses were conducted to identify the candidate biomarkers for AMI, and the collected local samples were used to validate the findings via real-time quantitative PCR. Bioinformatical analysis and luciferase reporter assay were implemented to identify the transcriptional factor. Transient transfection and ferroptosis characteristic measurement, including glutathione peroxidase 4, malondialdehyde, iron, and glutathione, was performed to verify the ability of the candidate gene to regulate the ferroptosis of cardiomyocytes. A meta-analysis was conducted in multiple independent cohorts to clarify the diagnostic value. Results: A total of 121 ferroptosis regulators were extracted from previous studies, and aldo-keto reductase family 1 member C3 (AKR1C3) was significantly downregulated in the peripheral blood samples of AMI cases from the analysis of GSE48060 and GSE97320. HOXB4 served as a transcriptional activator for AKR1C3 and could suppress the ferroptosis of the H9C2 cells treated with erastin. Besides this, peripheral blood samples from 16 AMI patients and 16 patients without coronary atherosclerotic disease were collected, where AKR1C3 and HOXB4 both showed a high diagnostic ability. Furthermore, a nomogram including HOXB4 and AKR1C3 was established and successfully validated in six independent datasets. A clinical correlation analysis displayed that AKR1C3 and HOXB4 were correlated with smoking, CK, CK-MB, and N-terminal-pro-B-type natriuretic peptide. Conclusion: Taken together, this study demonstrates that AKR1C3 and HOXB4 are promising diagnostic biomarkers, providing novel insights into the ferroptosis mechanisms of AMI.

Association of Parenteral Anticoagulation Therapy With Outcomes in Non-ST-Segment Elevation Acute Coronary Syndrome Patients Without Invasive Therapy: Findings from the Improving Care for Cardiovascular Disease in China (CCC) project.

Our previous study showed that parenteral anticoagulation therapy (PACT) in the context of aggressive antiplatelet therapy failed to improve clinical outcomes in patients undergoing percutaneous coronary intervention for non-ST-segment elevation acute coronary syndrome (NSTE-ACS). However, the role of PACT in patients managed medically remains unknown. This observational cohort study enrolled patients with NSTE-ACS receiving medical therapy from November 2014 to June 2017 in the Improving Care for Cardiovascular Disease in China-Acute Coronary Syndrome project. Eligible patients were included in the PACT group and non-PACT group. The primary outcomes were in-hospital all-cause mortality and major bleeding. The secondary outcome included minor bleeding. Among 23,726 patients, 8,845 eligible patients who received medical therapy were enrolled. After adjusting the potential confounders, PACT was not associated with a lower risk of in-hospital all-cause mortality (adjusted odds ratio (OR), 1.25; 95% confidence interval (CI), 0.92-1.71; P = 0.151). Additionally, PACT did not increase the incidence of major bleeding or minor bleeding (major bleeding: adjusted OR, 1.04; 95% CI, 0.80-1.35; P = 0.763; minor bleeding: adjusted OR, 1.27; 95% CI, 0.91-1.75; P = 0.156). The propensity score analysis confirmed the primary analyses. In patients with NSTE-ACS receiving antiplatelet therapy, PACT was not associated with a lower risk of in-hospital all-cause mortality or a higher bleeding risk in patients with NSTE-ACS receiving non-invasive therapies and concurrent antiplatelet strategies. Randomized clinical trials are warranted to reevaluate the safety and efficacy of PACT in all patients with NSTE-ACS who receive noninvasive therapies and current antithrombotic strategies.

Association of Early and Late Contrast-Associated Acute Kidney Injury and Long-Term Mortality in Patients Undergoing Coronary Angiography.

BACKGROUND: Contrast-associated acute kidney injury (CA-AKI) is a common complication in patients undergoing coronary angiography (CAG). However, few studies demonstrate the association between the prognosis and developed CA-AKI in the different periods after the operation. METHODS: We retrospectively enrolled 3206 patients with preoperative serum creatinine (Scr) and at least twice SCr measurement after CAG. CA-AKI was defined as an increase ≥50% or ≥0.3 mg/dL from baseline in the 72 hours after the procedure. Early CA-AKI was defined as having the first increase in SCr within the early phase (<24 hours), and late CA-AKI was defined as an increase in SCr that occurred for the first time in the late phase (24-72 hours). The first endpoint of this study was long-term all-cause mortality. Kaplan-Meier analysis was used to count the cumulative mortality, and the log-rank test was used to assess differences between curves. Univariate and multivariate cox regression analyses were performed to assess whether patients who developed different type CA-AKI were at increased risk of long-term mortality. RESULTS: The number of deaths in the 3 groups was 407 for normal (12.7%), 106 for early CA-AKI (32.7%) and 57 for late CA-AKI (17.7%), during a median follow-up period of 3.95 years. After adjusting for important clinical variables, early CA-AKI (HR = 1.33, 95% CI: 1.02-1.74, P=0.038) was significantly associated with mortality, while late CA-AKI (HR = 0.92, 95% CI: 0.65-1.31, P=0.633) was not. The same results were found in patients with coronary artery disease, chronic kidney disease, diabetes mellitus, and percutaneous coronary intervention. CONCLUSIONS: Early increases in Scr, i.e., early CA-AKI, have better predictive value for long-term mortality. Therefore, in clinical practice, physicians should pay more attention to patients with early renal injury related to long-term prognosis and give active treatment.

The Number of Patients with Acute Myocardial Infarction Decreased and Door-to-Balloon Time Delayed in COVID-19.

BACKGROUND: At present, COVID-19 is sweeping the world, and all countries are actively responding. During the COVID-19 epidemic, the treatment of patients with acute myocardial infarction (AMI) may be affected. METHODS: We reviewed data of patients with AMI from January 23 to April 23, 2020 (2020), and January 23 to April 23, 2019 (2019), who were admitted to two hospitals from Southern China. We collected clinical characteristics, comorbidities, treatment, prognosis, and key time segments to analyze. RESULTS: The total number of patients that had been diagnosed with AMI in the two hospitals was 218 in 2020 and 260 in 2019. The number of AMI patients that were admitted to hospitals per day decreased in 2020. The percentage of patients with AMI who refused hospitalization in 2020 was significantly higher than that in 2019 (5.0% vs 1.5%, p=0.028). There is no statistical difference in symptoms of the first medical contact (S2FMC) time between 2020 and 2019 (p=0.552). Door-to-balloon (D2B) time of ST-elevation myocardial infarction (STEMI) patients who were treated with a primary percutaneous coronary intervention (pPCI) in 2020 was 79 (63.75-105.25) mins, while D2B time in 2019 was 57.5 (41.5-76.5) mins, which was statistically different from the two groups. CONCLUSIONS: COVID-19 had an impact on the number of AMI patients who were admitted to hospitals and the time of treatment. During the COVID-19 epidemic, the number of AMI patients that were admitted to hospitals per day was decreased, while the percentage of AMI patients that refused therapy in these two hospitals increased, and the D2B time of STEMI patients was also delayed.