Successful treatment of focal renal artery fibromuscular dysplasia by balloon dilatation demonstrated via fractional flow reserve.

We present a rare case of fibromuscular dysplasia (FMD) manifesting in the mid segment of right renal artery, which led to the development of refractory hypertension. The patient received balloon angioplasty to a severe lesion on the middle of right renal artery and subsequently had normalisation of blood pressures. Fractional flow reserve (FFR) detection of the renal artery before and after balloon dilatation was 0.71 and 0.98, respectively. The patient showed renal artery stenosis (RAS) with distal tumour-like dilatation, and multiple tortuosity and stenosis in carotid artery and coronary artery. At follow-up 2 months later, her blood pressures had normalised.

Exploring the Predictors of the Discrepancy Between Quantitative Flow Ratio and Fractional Flow Reserve Measurements.

BACKGROUND: Quantitative flow ratio is a novel technology for the functional assessment of intermediate coronary stenoses. The authors sought to explore the influence of diabetes mellitus on the application of quantitative flow ratio and predictors of discrepancies between quantitative flow ratio and fractional flow reserve. METHODS: Quantitative flow ratio was calculated in 224 patients (317 vessels) who underwent fractional flow reserve measurement by professional technicians blinded to fractional flow reserve value. Patients were divided into the diabetes mellitus group and the non-diabetes mellitus group. The diagnostic performance of quantitative flow ratio was assessed using fractional flow reserve as a reference. RESULTS: Good correlation and agreement between quantitative flow ratio and fractional flow reserve can be found in the diabetes mellitus group (r = 0.834, P <.001; mean difference: 0.007 ± 0.108). Prior myocardial infarction showed a statistically significant association with increased classification discrepancy between quantitative flow ratio and fractional flow reserve (odds ratio 3.16 (95% confidence interval: 1.29-7.75), P =.01). The area under the receiver-operating characteristic curve of quantitative flow ratio showed no significant difference in diabetes mellitus and non-diabetes mellitus groups, hemoglobin A1c ≥ 7% and hemoglobin A1c < 7% groups, diabetic duration ≥ 10 years and diabetic duration < 10 years groups (area under receiver-operating characteristic curve: 0.90 (95% confidence interval: 0.84-0.94) vs. 0.92 (95% confidence interval: 0.87-0.96), P =.54; 0.89 (95% confidence interval: 0.81-0.95) vs. 0.92 (95% confidence interval: 0.81-0.97), P =.65; 0.88 (95% confidence interval: 0.79-0.94) vs. 0.89 (95% confidence interval: 0.79-0.96), P =.83; respectively). CONCLUSIONS: Clinical application of quantitative flow ratio is not limited to diabetic patients. The relationship between prior myocardial infarction and quantitative flow ratio needs to be further developed.

Characteristics of Wellens' Syndrome in the Current PCI Era: A Single-Center Retrospective Study.

Objectives: The goal of this retrospective study was to reveal the prevalence, angiographic characteristics, clinical presentation, and long-term outcomes of non-ST-segment elevation myocardial infarction (NSTEMI) patients with Wellens' syndrome. Background: Procedural results for percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) have improved in recent years. However, there is still a paucity of available clinical trial data for Wellens' syndrome even though it is a well-known high-risk ACS. Methods: Among a total of 3528 patients with ACS who underwent angioplasty from 2017 to 2019 at the Cardiovascular Center of Beijing Friendship Hospital, 476 NSTEMI patients with culprit left anterior descending (LAD) vessels were enrolled in this study. According to electrocardiographic criteria of Wellens' syndrome, the patients were divided into a Wellens group (n = 138) and a non-Wellens group (n = 338). The primary endpoint was cardiac death; the secondary endpoints were main adverse cardiovascular and cerebrovascular events (MACCEs), a composite of all-cause death, cardiac death, heart failure, target lesion revascularization, recurrent myocardial infarction, and stroke. All of the medical and follow-up data were obtained from our institutional database. Results: The incidence of Wellens' syndrome in all ACS patients was 5.7% (200 of 3528). Among the 200 patients with Wellens' syndrome, 138 had NSTEMI, for a proportion of 69%. There was a significant decrease in the percentage of preexisting coronary heart disease (CHD), prior myocardial infarction, and previous PCI (P < 0.05) in the Wellens group compared with the non-Wellens group. On coronary angiography, single-vessel lesions were more common in the Wellens group (11.6% vs. 5.3%, P=0.016), and almost all (97.1%) of these patients received drug-eluting stents. Notably, the Wellens group had a higher proportion of early PCI than the non-Wellens group (71% vs. 61.2%, P=0.044). At 24 months, there was no statistically significant difference in cardiac death (P=0.111) between the two groups, but the MACCEs were comparable (Wellens: 5.1% vs. non-Wellens: 13.3%, P=0.009). Age ≥65 years was the largest independent risk factor for adverse prognosis. Conclusions: With early recognition and aggressive intervention, Wellens' syndrome is no longer a risk factor for adverse prognosis in patients with NSTEMI in the current PCI era.

The Role of Mitochondria in Metabolic Syndrome-Associated Cardiomyopathy.

With the rapid development of society, the incidence of metabolic syndrome (MS) is increasing rapidly. Evidence indicated that patients diagnosed with MS usually suffered from cardiomyopathy, called metabolic syndrome-associated cardiomyopathy (MSC). The clinical characteristics of MSC included cardiac hypertrophy and diastolic dysfunction, followed by heart failure. Despite many studies on this topic, the detailed mechanisms are not clear yet. As the center of cellular metabolism, mitochondria are crucial for maintaining heart function, while mitochondria dysfunction plays a vital role through mechanisms such as mitochondrial energy deprivation, calcium disorder, and ROS (reactive oxygen species) imbalance during the development of MSC. Accordingly, in this review, we will summarize the characteristics of MSC and especially focus on the mechanisms related to mitochondria. In addition, we will update new therapeutic strategies in this field.

Abiotrophia Defectiva as a Rare Cause of Mitral Valve Infective Endocarditis With Mesenteric Arterial Branch Pseudoaneurysm, Splenic Infarction, and Renal Infarction: A Case Report.

Introduction: Abiotrophia defectiva (A. defectiva) is a rare species leading to infective endocarditis (IE) with a poor prognosis. We describe a previously healthy patient with mitral valve infective endocarditis caused by A. defectiva. Case report: A young man was admitted with intermittent fever. Echocardiography confirmed vegetation on the mitral valve with evidence of valve perforation and severe mitral regurgitation. Three sets of blood cultures became positive for A. defectiva. As he presented with manifestations of mesenteric arterial branch pseudoaneurysm, splenic and renal infarction, mitral valve replacement, and embolization of superior mesenteric aneurysm were operated during 8 weeks' targeted antibiotic therapy. Conclusion: This case study emphasizes the importance of considering A. defectiva as a rare but important cause of IE and of performing blood culture to make its accurate diagnosis and timely anti-infective treatment. Early surgical management and active prevention of complications have been associated with a favorable prognosis.

Wellens' syndrome: incidence, characteristics, and long-term clinical outcomes.

BACKGROUND: Few studies with large sample sizes are available regarding patients with Wellens' syndrome. Therefore, we sought to assess the current incidence, risk factors, clinical presentation and long-term outcomes of this population. METHODS: Among a total of 3528 patients with ACS who underwent angioplasty from 2017 to 2019 in our centre, 2127 NSTE-ACS patients with culprit LAD vessels were enrolled in this study. According to electrocardiographic criteria, the patients were divided into a Wellens' group (n = 200) and non-Wellens' group (n = 1927). The primary endpoint was cardiac death; the secondary endpoint was MACCE, a composite of all-cause death, cardiac death, recurrent myocardial infarction, target lesion revascularization, heart failure and stroke. RESULTS: The incidence of Wellens' syndrome was 5.7% (200 of 3528) of all ACS patients. Wellens' syndrome more often manifested as NSTEMI (69% vs. 17.5%, P < 0.001). The percentages of preexisting coronary heart disease (39.6% vs. 23%) and previous PCI (19.5% vs. 9%) were significantly higher in the non-Wellens' group than in the Wellens' group (all P < 0.001). More importantly, the proportion of early PCI was higher in the Wellens' group (68% vs. 59.3%, P = 0.017). At a median follow-up of 24 months, Wellens' syndrome was not associated with an increased risk of MACCE (P = 0.05) or cardiac death (P = 0.188). CONCLUSIONS: The presence of Wellens' syndrome is not definitively associated with adverse prognosis in patients with NSTE-ACS. Age ≥ 65 years, diabetes, NSTEMI, eGFR < 60 ml/min and left main disease are associated with the incidence of cardiac death. Early recognition and aggressive intervention are critical, as they may help to attenuate adverse outcomes.

Impact of COVID-19 pandemic on STEMI undergoing primary PCI treatment in Beijing, China.

OBJECTIVE: Strict control measures under the COVID epidemic have brought an inevitable impact on ST-segment elevation myocardial infarction (STEMI)'s emergency treatment. We investigated the impact of the COVID on the treatment of patients with STEMI undergoing primary PCI. METHODS: In this single center cohort study, we selected a time frame of 6 month after declaration of COVID-19 infection (Jan 24-July 24, 2020); a group of STEMI patients in the same period of 2019 was used as control. Finally, a total of 246 STEMI patients, who were underwent primary PCI, were enrolled into the study (136 non COVID-19 outbreak periods and 110 COVID-19 outbreak periods). The impact of COVID on the time of symptom onset to the first medical contact (symptom-to-FMC) and door to balloon (D-to-B) was investigated. Moreover, the primary outcome was in-hospital major adverse cardiac events (MACE), defined as a composite of cardiac death, heart failure and malignant arrhythmia. RESULTS: Compared with the same period in 2019, there was a 19% decrease in the total number of STEMI patients undergoing primary PCI at the peak of the pandemic in 2020. The delay in symptom-to-FMC was significantly longer in COVID Outbreak period (180 [68.75, 342] vs 120 [60,240] min, P = 0.003), and the D-to-B times increased significantly (148 [115-190] vs 84 [70-120] min, P < 0.001). However, among patients with STEMI, MACE was similar in both time periods (18.3% vs 25.7%, p = 0.168). On multivariable analysis, COVID was not independently associated with MACE; the history of diabetes, left main disease and age>65 years were the strongest predictors of MACE in the overall population. CONCLUSIONS: The COVID pandemic was not independently associated with MACE; suggesting that active primary PCI treatment preserved high-quality standards even when challenged by a severe epidemic. CLINICAL TRIAL REGISTRATION: URL: https://ClinicalTrials.gov Unique identifier: NCT04427735.

Deficiency of tenascin-C attenuated cardiac injury by inactivating TLR4/NLRP3/caspase-1 pathway after myocardial infarction.

Inflammation and pyroptosis play a deleterious role in cardiac dysfunction after myocardial infarction (MI). NLRP3/caspase-1 is a well-established axis in pyroptosis and inflammation. In this study, we examined the effects of TN-C on pyroptosis through NLRP3 is unclear. We constructed 18 TN-C-knockout and 38 WT male mice model and divided into WT sham (n = 16), WT MI (n = 22), TNKO sham (n = 6), TNKO MI (n = 12). Elisa, immunostaining, TTC, qPCR, CCK8, flow cytometry, and western blot, echocardiographic, TUNEL staining technologies were applied. Here, we found a positive correlation between TN-C and NLRP3 in heart tissue via the GEPIA database (r = 0.52, p < 0.05). The findings indicate that TN-C was elevated and peaked on the fifth day after MI. TN-C deficiency alleviated cardiac dysfunction (LVEF, FS, LVIDd, and LVIDs) and cardiomyocyte death. Though the intracellular levels of pyroptosis-related cytokine caspase-1, cleaved caspase-1, NLRP3, IL-18, IL-1ß were upregulated both in MI and H2O2 stimulation, knockout of TN-C resisted such injury and alleviated cardiac pyroptosis, which further decreased IL-6, TNF-α, MCP-1 expression. TN-C knockdown inhibited TLR4 expression, reduces the release of downstream factors by inactivating the TLR4/NF-kB pathway, while protects the cardiomyocytes. And TLR4 inhibitor TAK-242 significantly reduced NLRP3 expression levels after MI. We demonstrated for the first time a direct link between MI-induced TN-C upregulation and caspase-1-dependent cardiomyocyte pyroptosis, a process mediated, at least in part, by TLR4/NF-kB/NLRP3 and IL-18, IL-1ß signaling pathways. These findings provide new insights into the role of TN-C in post-MI cardiomyocytes' pyroptosis and inflammation.

The impact of successful chronic total occlusion percutaneous coronary intervention on long-term clinical outcomes in real world.

BACKGROUND: Coronary chronic total occlusions (CTOs) are related to increased risk of adverse clinical outcomes. The optimal treatment strategy for CTO has not been well established. We sought to examine the impact of CTO percutaneous coronary intervention (PCI) on long-term clinical outcome in the real world. METHODS: A total of 592 patients with CTO were enrolled. 29 patients were excluded due to coronary artery bypass grafting (CABG). After exclusion, 563 patients were divided into the no-revascularized group (CTO-NR group, n = 263) and successful revascularized group (CTO-R group, n = 300). The primary endpoint was cardiac death; secondary endpoint was major adverse cardiac and cerebrovascular events (MACCE), a composite of all-cause death, cardiac death, recurrent myocardial infarction, target lesion revascularization, re-hospitalization, heart failure, and stroke. RESULTS: Percent of Diabetes mellitus (53.2% vs 39.7), Chronic kidney disease (8.7% vs 3.7%), CABG history (7.6% vs 1%), three vessel disease (96.2% vs 90%) and left main coronary artery disease (25.1% vs 13.7%) was significantly higher in the CTO-NR group than in success PCI group (all P < 0.05). Moreover, the CTO-NR group has the lower ejection fraction (EF) (0.58 ± 0.11 vs 0.61 ± 0.1, p = 0.001) and fraction shortening (FS) (0.31 ± 0.07 vs 0.33 ± 0.07, p = 0.002). At a median follow-up of 12 months, CTO revascularization was superior to CTO no-revascularization in terms of cardiac death (adjusted hazard ratio [HR]: 0.27, 95% conference interval [CI] 0.11-0.64). The superiority of CTO revascularization was consistent for MACCE (HR: 0.55, 95% CI 0.35-0.79). At multivariable Cox hazards regression analysis, CTO revascularization remains one of the independent predictors of lower risk of cardiac death and MACCE. CONCLUSIONS: Successful revascularization by PCI may bring more clinical benefits. The presence of low left ventricular ejection fraction (LVEF) and LM-disease was associated with an incidence of cardiac death; CTO revascularization was a protected predictor of cardiac death. Successful revascularization by PCI offered CTO patients more clinical benefits, manifested by lower incidence of cardiac death during follow-up. The presence of LVEF < 0.5 and left main coronary artery disease (LM disease) was associated with an incidence of cardiac death; CTO revascularised was a protected predictor of cardiac death.

A sex-stratified long-term clinical outcome analysis in coronary chronic total occlusion patients.

BACKGROUND: Differences in outcomes for women and men after percutaneous coronary intervention (PCI) in chronic total occlusion (CTO) patients remain controversial. Herein, we compared the clinical outcomes by sex in CTO patients undergoing PCI. METHODS: A total of 563 consecutive patients (19% women) who were diagnosed with CTO at a single center in China from June 2017 to December 2019 were included in this study. Three hundred patients were revascularized by PCI, and 263 were not revascularized. The clinical outcomes of these patients stratified by sex were examined. The primary endpoints included the risk of major adverse cardiovascular and cerebrovascular events (MACCE); the secondary endpoint was cardiac death; hazard ratios were generated using multivariable Cox regression. RESULTS: Women represented 19% of the cohort (107/563 patients). Women have lower mean body mass index (BMI) and abdominal circumference compared with men; however, the proportion of hypertension, diabetes, and previous coronary heart disease is higher in female patients. At 2-year follow-up, there were no differences between men and women for MACCE (15.8% vs 20.6%, p = 0.234) and cardiac death (3.1% vs 5.6%, p = 0.202). Predictors of CTO recanalization revealed that age < 65 years, absence of prior CABG, no history of DM, and non-triple vessel were predictors of CTO recanalization. Sex did not predict recanalization in this regression model. Successful CTO PCI was associated with reduced MACCE. CONCLUSION: Our study suggests an equal benefit of CTO recanalization with a marked reduction in MACCE in women and men alike. Further dedicated studies are needed to confirm these findings.

Human umbilical cord mesenchymal stem cells derived exosomes exert antiapoptosis effect via activating PI3K/Akt/mTOR pathway on H9C2 cells.

BACKGROUND/OBJECTIVES: In recent years, as an alternative to stem cell therapy for cardiovascular diseases (CVD), exsomes have attracted wide attention among researchers. The present study aimed to investigate the role of human umbilical cord mesenchymal stem cells (UC-MSCs) derived exosomes play on H9C2 cells apoptosis and possible mechanisms. METHODS: Exosomes were isolated from normal UC-MSCs culture media and hypoxic preconditioning culture media. Transmission electron microscopy was used to observe the morphology of exosomes. Nanoparticle tracking analysis was used to detect the size distribution and concentration of exosomes. Western blot analysis was used to analyzed the surface marker CD63 of exosomes. H9C2 cells were induced apoptosis by hypoxia and serum deprivation (H/SD) and then were treated respectively by group. Cell Counting Kit-8 assay was used to detect viability of H9C2 cells. Apoptosis was detected by Hochest staining and annexin V-FITC/PI. The expression levels of related proteins of apoptosis, autophagy, and PI3K/Akt/mTOR pathway were analyzed by Western blot analysis. Immunofluorescence was used to analyze LC3B expression. RESULTS: Hypoxic preconditioning increased the exosomes secretion of UC-MSCs. UC-MSCs derived exosomes could inhibit H/SD-induced H9C2 cells apoptosis. Hypoxic preconditioning strengthened this antiapoptosis effect of UC-MSCs. Hypoxic preconditioning UC-MSCs derived exosomes (H-Exo) downregulated LC3B-II/I and beclin-1 and upregulated P62, p-Akt/Akt and p-mTOR/mTOR. The antiapoptotic effect of H-Exo could be attenuated by treatment with LY294002 and rapamycin. CONCLUSION: UC-MSCs derived exosomes could inhibit H9C2 cells apoptosis induced by H/SD through regulating autophagy via PI3K/Akt/mTOR pathway. Hypoxia preconditioning could enhance above effects through increasing exosomes secretion of UC-MSCs.

Exosomes derived from SDF1-overexpressing mesenchymal stem cells inhibit ischemic myocardial cell apoptosis and promote cardiac endothelial microvascular regeneration in mice with myocardial infarction.

Exosomes extracted from mesenchymal stem cells (MSCs) was reported to reduce myocardial ischemia/reperfusion damage. Besides, stromal-derived factor 1 (SDF1a) functions as cardiac repair after myocardial infarction (MI). Therefore, the present study aims to identify whether exosomes (Exo) released from SDF1-overexpressing MSCs display a beneficial effect on ischemic myocardial infarction. Initially, a gain-of-function study was performed to investigate the function of SDF1 in ischemic myocardial cells and cardiac endothelial cells. Coculture experiments were performed to measure potential exosomic transfer of SDF1 from MSCs to ischemic myocardial cells and cardiac endothelial cells. During the coculture experiments, exosome secretion was disrupted by neutral sphingomyelinase inhibitor GW4869 and upregulated exosomal SDF1 using SDF1 plasmid. Effects of Exo-SDF1 on cardiac function in MI mice were investigated in vivo. MSCs suppressed myocardial cell apoptosis and promoted microvascular regeneration of endothelial cells through secretion of exosomes. The addition of GW4869 led to increased apoptotic capacity of myocardial cells, decreased microvascular formation ability of endothelial cells, enhanced autophagy ability, and elevated Beclin-1 level as well as ratio of LC3II/LC3I. Overexpression of SDF1 and Exo-SDF1 inhibited apoptosis and autophagy of myocardial cells, but promoted tube formation of endothelial cells. The interference of PI3K signaling pathway promoted apoptosis and autophagy of myocardial cells, but inhibited tube formation of endothelial cells. SDF1 activated the PI3K signaling pathway. Exo-SDF1 protected cardiac function of MI mice and inhibited myocardial tissue damage. This study provided evidence that SDF1 overexpression in MSCs-derived exosomes inhibited autophagy of ischemic myocardial cells and promoted microvascular production of endothelial cells.

Real-world use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers/ß-blocks in Chinese patients before acute myocardial infarction occurs: patient characteristics and hospital follow-up.

BACKGROUND: Current guidelines recommend angiotensin-converting-enzyme inhibitors (ACEI) or angiotensin-receptor blockers (ARB) or ß-blockers (ß-B) for secondary prevention in patients after an acute myocardial infarction (AMI). However, there is limited data to evaluate ACEI/ARB/ß-B (AAß) used before AMI on major adverse cardiovascular events (MACE), in China patients. OBJECTIVES: This study sought to investigate whether AAß treatment prior to AMI is associated with better hospital outcomes at the onset of AMI. METHODS: A total of 2705 patients were selected from the Cardiovascular Center Beijing Friendship Hospital Database Bank, and divided into two groups on the basis of admission prescription: AAß (n = 872) or no-AAß (n = 1833). The study was also designed using propensity-score matching (226 AAß treated patients vs 452 no-AAß treated patients). The primary outcome was a composite of cardiac death and heart function and infarct size during hospitalization follow-up. RESULTS: The mean follow-up period was about 8 days in MACE. The Cox model showed the two groups had similar risk of cardiac death. The in-hospital mortality was 3.36% (3.33% of AAß users and 3.38% of nonusers, p = 0.94). In adjusted analysis, there was still no difference in in-hospital mortality between the two groups (3.54% vs 2.88%, p = 0.64). However, the AAß treated patients were associated with better heart function and smaller infarct size than the no-AAß treated patients. CONCLUSIONS: The in-hospital MACE was similar between AAß treated patients and no-AAß treated patients. However, treatment with AAß before AMI was associated with improved heart function and smaller infarct size.

Human umbilical cord blood derived mesenchymal stem cells improve cardiac function in cTnT(R141W) transgenic mouse of dilated cardiomyopathy.

Cell transplantation is a promising strategy in regenerative medicine. Beneficial effects of bone marrow mesenchymal stem cells (BM-MSCs) on heart disease have been widely reported. However, the MSCs in these studies have been mainly derived from autologous animals, and data on MSCs from human umbilical cord blood (UCB-MSCs) are still scarce. We investigated whether intramyocardial xenogeneic administration of UCB-MSCs is beneficial for preserving heart function in a cTnT(R141W) transgenic mouse of dilated cardiomyopathy (DCM). Cultured UCB-MSCs, which were identified by there morphology, differentiation and cell surface markers, were transplanted into cTnT(R141W) transgenic mice to examine apoptosis, fibrosis, vasculogenesis and the associated Akt pathway. Moreover, we measured the expression levels of VEGF and IGF-1, which are growth factors required for differentiation into cardiomyocytes, and are also involved in cardiac regeneration and improving heart function. One month after transplantation, MSCs significantly decreased chamber dilation and contractile dysfunction in the cTnT(R141W) mice. MSCs transplanted hearts showed a significant decrease in cardiac apoptosis and its regulation by the Akt pathway. Cardiac fibrosis and cytoplasmic vacuolisation were significantly attenuated in the MSCs group. Importantly, the levels of VEGF and IGF-1 were increased in the MSCs transplanted hearts. In vitro, the MSC-conditioned medium displayed anti-apoptotic activity in h9c2 cardiomyocytes subjected to hypoxia. These results further confirm the paracrine effects of MSCs. In conclusion, UCB-MSCs preserve cardiac function after intramyocardial transplantation in a DCM mouse, and this effect may be associated with reductions in cellular apoptosis, inflammation, hypertrophy and myocardial fibrosis; in addition to; up-regulation of Akt, VEGF and IGF-1; and enhanced angiogenesis.

Trimetazidine protects umbilical cord mesenchymal stem cells against hypoxia and serum deprivation induced apoptosis by activation of Akt.

BACKGROUND: Mesenchymal stem cell (MSC) transplantation is a promising therapy for cardiac repair. However, the efficacy is limited by the poor viability of MSCs in the infarcted heart. Recent findings have implicated that trimetazidine (TMZ) enhanced the survival of the stem cells under various conditions. However, as the stem cells in these studies were animal-derived, little information is available about the effects of TMZ on human MSCs. Herein, we propose that TMZ may protect human MSCs against apoptosis induced by Hypoxia/Serum deprivation (H/SD). METHODS: Human umbilical cord MSCs (UC-MSCs) from Wharton's jelly were pretreated with 10µM TMZ of H/SD with or without the Akt inhibitor LY294002. The morphological changes were assessed using Hoechst 33342. Apoptosis was evaluated via Annexin V/PI staining; and apoptosis-related proteins were detected using Western-blot. Protein chip technology was used to screen for differences between the cell supernatants. RESULTS: TMZ had a significant protective effect against H/SD-induced apoptosis, accompanied by an increase in Bcl-2 and p-Akt. The TMZ-mediated anti-apoptotic effect on MSCs could be attenuated by treatment with LY294002. Moreover, protein chip assays showed that TMZ treatment increased the paracrine functions of MSCs. CONCLUSION: Trimetazidine protects human UC-MSCs from H/SD-induced apoptosis via the Akt pathway and may therefore be a potentially useful therapeutic adjunct for transplanting MSCs into damaged heart after myocardial infarction.