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1.
Theranostics ; 11(3): 1249-1268, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33391533

RESUMO

Rationale: Maladaptive cardiac remodeling is a critical step in the progression of heart failure. Low-density lipoprotein receptor-related protein 6 (LRP6), a co-receptor of Wnt, has been implicated in cardiac protection. We aimed to study the role of cardiomyocyte-expressed LRP6 in cardiac remodeling under chronic pressure overload. Methods: Cardiac parameters were analyzed in inducible cardiac-specific LRP6 overexpressing and control mice subjected to transverse aortic constriction (TAC). Results: Cardiac LRP6 was increased at an early phase after TAC. Cardiomyocyte-specific LRP6 overexpression improved cardiac function and inhibited cardiac hypertrophy and fibrosis four weeks after TAC. The overexpression significantly inhibited ß-catenin activation, likely contributing to the inhibitory effect on cardiac hypertrophy after TAC. LRP6 overexpression reduced the expression and secretion of Wnt5a and Wnt11 by cardiomyocytes, and knockdown of Wnt5a and Wnt11 greatly inhibited cardiac fibrosis and dysfunction under pressure overload in vitro and in vivo. Cardiomyocyte-expressed LRP6 interacted with cathepsin D (CTSD, a protease) and promoted the degradation of Wnt5a and Wnt11, inhibiting cardiac fibrosis and dysfunction induced by TAC. The protease inhibitor leupeptin attenuated the interaction between LRP6 and CTSD, enhanced the expression of Wnt5a and Wnt11, and deteriorated cardiac function and fibrosis in cardiomyocyte-specific LRP6-overexpressing mice under pressure overload. Mutants from human patients, P1427Q of LRP6 and G316R of CTSD significantly inhibited the interaction between LRP6 and CTSD and increased Wnt5a and Wnt11 expression. Conclusion: Cardiomyocyte-expressed LRP6 promoted the degradation of Wnt5a and Wnt11 by regulating CTSD and inhibited cardiac fibrosis under pressure overload. Our study demonstrated a novel role of LRP6 as an anti-fibrosis regulator.

2.
Cell Death Dis ; 12(1): 78, 2021 Jan 12.
Artigo em Inglês | MEDLINE | ID: mdl-33436548

RESUMO

Coronary microembolization (CME), a common reason for periprocedural myocardial infarction (PMI), bears very important prognostic implications. However, the molecular mechanisms related to CME remain largely elusive. Statins have been shown to prevent PMI, but the underlying mechanism has not been identified. Here, we examine whether the NLRP3 inflammasome contributes to CME-induced cardiac injury and investigate the effects of statin therapy on CME. In vivo study, mice with CME were treated with 40 mg/kg/d rosuvastatin (RVS) orally or a selective NLRP3 inflammasome inhibitor MCC950 intraperitoneally (20 mg/kg/d). Mice treated with MCC950 and RVS showed improved cardiac contractile function and morphological changes, diminished fibrosis and microinfarct size, and reduced serum lactate dehydrogenase (LDH) level. Mechanistically, RVS decreased the expression of NLRP3, caspase-1, interleukin-1ß, and Gasdermin D N-terminal domains. Proteomics analysis revealed that RVS restored the energy metabolism and oxidative phosphorylation in CME. Furthermore, reduced reactive oxygen species (ROS) level and alleviated mitochondrial damage were observed in RVS-treated mice. In vitro study, RVS inhibited the activation of NLRP3 inflammasome induced by tumor necrosis factor α plus hypoxia in H9c2 cells. Meanwhile, the pyroptosis was also suppressed by RVS, indicated by the increased cell viability, decreased LDH and propidium iodide uptake in H9c2 cells. RVS also reduced the level of mitochondrial ROS generation in vitro. Our results indicate the NLRP3 inflammasome-dependent cardiac pyroptosis plays an important role in CME-induced cardiac injury and its inhibitor exerts cardioprotective effect following CME. We also uncover the anti-pyroptosis role of RVS in CME, which is associated with regulating mitochondrial ROS.

4.
Angiology ; 72(1): 44-49, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-32799665

RESUMO

Coronary chronic total occlusions (CTOs) are characterized by a high incidence of severe plaque calcifications, which are associated with a high use of the retrograde approach and a low success rate of percutaneous coronary intervention (PCI). However, the feasibility of rotational atherectomy (RA) in retrograde CTO-PCI remains unknown. The aim of the present study is to examine the safety and efficacy of RA in retrograde CTO-PCI. Consecutive patients (n = 129) who underwent RA during CTO-PCI were categorized into anterograde and retrograde groups according to the CTO crossing approach. The distributions of the baseline characteristics were similar in the 2 groups, but the lesion type was more complex (P = .001), and the starting burr size was smaller (P = .003) in the retrograde group than in the anterograde group. There was a trend of a higher incidence of procedural complications in the retrograde group than in the anterograde group (P = .054). Technical and procedural success and in-hospital outcomes were not significantly different between the 2 groups. In conclusion, RA was feasible in retrograde CTO PCI, but some specific precautions are required before and during the procedure. In addition, further investigation of the long-term outcomes of RA in retrograde CTO PCI is necessary.


Assuntos
Aterectomia Coronária/métodos , Oclusão Coronária/terapia , Aterectomia Coronária/efeitos adversos , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Intervenção Coronária Percutânea , Complicações Pós-Operatórias , Estudos Retrospectivos , Stents
5.
J Cell Physiol ; 236(1): 495-506, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-32542822

RESUMO

Cardiac fibrosis is a reparative process after myocardial infarction (MI), which leads to cardiac remodeling and finally heart failure. Endothelial-to-mesenchymal transition (EndMT) is induced after MI and contributes to cardiac fibrosis after MI. Orphan nuclear receptor Nur77 is a key regulator of inflammation, angiogenesis, proliferation, and apoptosis in vascular endothelial cells. Here, we investigated the role of orphan nuclear receptor Nur77 in EndMT and cardiac fibrosis after MI. Cardiac fibrosis was induced through MI by ligation of the left anterior descending coronary artery. We demonstrated that Nur77 knockout aggravated cardiac dysfunction and cardiac fibrosis 30 days after MI. Moreover, Nur77 deficiency resulted in enhanced EndMT as shown by increased expression of FSP-1, SM22α, Snail, and decreased expression of PECAM-1 and eNOS compared with wild-type mice after MI. Then, we found overexpression Nur77 in human coronary artery endothelial cells significantly inhibited interleukin 1ß and transforming growth factor ß2-induced EndMT, as shown by a reduced transition to a fibroblast-like phenotype and preserved angiogenesis potential. Mechanistically, we demonstrated that Nur77 downregulated EndMT by inhibiting the nuclear factor-κB-dependent pathway. In conclusion, Nur77 is involved in cardiac fibrosis by inhibiting EndMT and may be a promising target for therapy of cardiac fibrosis after MI.

6.
Int J Cardiol ; 322: 1-8, 2021 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-32810548

RESUMO

BACKGROUND: Endothelial progenitor cells (EPCs) participate in angiogenesis and neocollateralization. This study assessed if circulating EPCs can predict long-term improvement of global left ventricular systolic function in patients with coronary chronic total occlusions (CTOs) underwent successful percutaneous coronary intervention (PCI). METHODS: In this single-center, prospective, observational study, 115 consecutive patients with CTOs were evaluated by standard transthoracic echocardiography (ECHO) before and 9-12 months after PCI. Numbers of circulating putative EPCs were determined by flow cytometry analysis of mononuclear cells isolated from peripheral blood samples drawn before and 72 h after PCI. RESULTS: At mean 11.3 ± 2.5 months post vs. before PCI (all P < .05): by SAQ-7 summary scores, angina frequency, physical limitation and quality of life scores were greater; by ECHO, LVEDd decreased and LVEF increased, which were more significant in patients with Rentrop grades 2/3 vs. 0/1. At 72 h post vs. before PCI, CD34+VEGFR-2+CD133- (0.82 ± 0.32 × 106/L vs. 1.00 ± 0.39 × 106/L, P = .003), CD34+VEGFR-2+CD133+ (0.24 ± 0.12 × 106/L vs. 0.27 ± 0.14 × 106/L, P = .028), and CD14+Tie2+VEGFR-2+ (6.60 ± 3.32 × 106/L vs. 7.82 ± 3.91 × 106/L, P = .006) cell numbers were lower. The baseline levels of CD34+VEGFR-2+cells (P = .001) and CD14+Tie2+VEGFR-2+cells (P < .001) were association with the grade of collateralization. In addition, the baseline and peri-procedural decrease of circulating CD34+VEGFR-2+ cells correlated with the increase of LVEF (P < .001, P < .001, respectively) and the decrease of LVEDd (P = .022, P = .029, respectively) at follow-up. CONCLUSIONS: In this small study, the baseline levels of circulating CD34+VEGFR-2+ EPCs and its reduction after successful revascularization of CTOs correlated with long-term improvement in global LV systolic function.

8.
BMC Cardiovasc Disord ; 20(1): 497, 2020 Nov 25.
Artigo em Inglês | MEDLINE | ID: mdl-33238890

RESUMO

BACKGROUND: Systematic investigation and analysis of cardiovascular health status (CVHS) of Chinese women is rare. This study aimed to assess CVHS and atherosclerotic cardiovascular disease (ASCVD) burden in the Chinese women physicians (CWP) and community-based non-physician cohort (NPC). METHODS: In this prospective, multicenter, observational study, CVHS using the American Heart Association (AHA) defined 7 metrics (such as smoking and fasting glucose) and ASCVD risk factors including hypertension, hyperlipidemia and type-2 diabetes were evaluated in CWP compared with NPC. RESULTS: Of 5832 CWP with a mean age of 44 ± 7 years, only 1.2% achieved the ideal CVHS and 90.1% showed at least 1 of the 7 AHA CVHS metrics at a poor level. Total CVHS score was significantly decreased and ASCVD risk burden was increased in postmenopausal subjects in CWP although ideal CVHS was not significantly influenced by menopause. Compared to 2596 NPC, fewer CWP had ≥ 2 risk factors (8% vs. 27%, P < 0.001); CWP scored significantly higher on healthy factors, a composite of total cholesterol, blood pressure, fasting glucose (P < 0.001), but, poorly on healthy behaviors (P < 0.001), specifically in the physical activity component; CWP also showed significantly higher levels of awareness and rates of treatment for hypertension and hyperlipidemia, but, not for type-2 diabetes. CONCLUSION: Chinese women's cardiovascular health is far from ideal and risk intervention is sub-optimal. Women physicians had lower ASCVD burden, scored higher in healthy factors, but, took part in less physical activity than the non-physician cohort. These results call for population-specific early and improved risk intervention.

9.
Ann Transl Med ; 8(18): 1162, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-33241011

RESUMO

Background: We aimed to report the 5-year outcomes of XINSORB bioresorbable sirolimus-eluting scaffolds in the treatment of single de novo coronary lesions in a first-in-human (FIM) study. This is the final report of the long-term clinical outcomes of the study. Recent studies have shown that bioresorbable scaffolds (BRSs) increase the risks of late target lesion failure (TLF) and thrombosis. Methods: In this prospective, single-arm study, eligible patients with single de novo coronary lesions were enrolled and treated with XINSORB scaffolds. The scaffolds measured 3.0 mm in diameter and 12, 15, and 18 mm in length. The clinical endpoints included TLF [cardiac death, target vessel-related myocardial infarction (TV-MI), or ischaemia-driven target lesion revascularization (ID-TLR)], its components, major adverse cardiac events (MACE), and scaffold thrombosis. Results: From September 2013 to January 2014, 30 patients were enrolled and treated with XINSORB scaffolds. The procedure had a 100% success rate. None of the patients died during the 5 years of follow-up. The primary endpoint of TLF occurred in 4 patients (13.3%). Six patients were recanalized by intervention, including 4 by ID-TLR. The rate of MACE was 16.7% (5/30). One very late case of scaffold thrombosis was recorded, which led to TV-MI. No more cases of thrombosis were recorded beyond 2 years of follow-up. The rates of clinical endpoints remained steady with no changes after 3 years of follow-up. Conclusions: Considering that this FIM study was launched at an early stage of the BRS era and without optimal implantation techniques, the clinical outcomes of TLF during the 5-year follow-up were acceptable. The rate of thrombosis was relatively low.

10.
Ann Transl Med ; 8(18): 1185, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-33241034

RESUMO

Background: Despite prompt revascularization following acute myocardial infarction, poor myocardial perfusion commonly occurs due to impaired microvascular circulation and is an independent predictor of adverse outcomes. The current trial sought to examine the effects of salvianolate on myocardial perfusion in patients with ST-segment-elevation myocardial infarction (STEMI) who were undergoing primary percutaneous coronary intervention (PCI). Methods: This randomized, double-blind, placebo-controlled, multicenter study evaluated the effects of intravenous salvianolate on the achievement of complete epicardial and myocardial reperfusion after PCI, defined as thrombolysis in myocardial infarction flow grade 3 and thrombolysis in myocardial infarction myocardial perfusion grade 3. We also measured plasma total creatine kinase-mass band fraction (CK-MB)-estimated infarct size and echocardiography-derived left ventricular ejection fraction and recorded the 30-day clinical and safety outcomes. A total of 536 patients presenting with acute STEMI were randomized to receive either an i.v. infusion of salvianolate (n=265) or placebo (n=271). Results: Salvianolate administration exerted beneficial effects on coronary microcirculation. There was a trend of reduced myocardial infarct size in the salvianolate group compared to the placebo group (P=0.070), although no significant difference in left ventricular ejection fraction was found between the two groups. Conclusions: Salvianolate administration is associated with improved myocardial perfusion in patients with STEMI undergoing PCI. A larger study is required to assess the impact of this therapy on clinical cardiac outcomes.

11.
Artigo em Inglês | MEDLINE | ID: mdl-33029742

RESUMO

We aimed to investigate whether red cell distribution width (RDW) was associated with periprocedural myocardial infarction (PMI) in patients undergoing elective percutaneous coronary intervention (PCI). Among 1723 consecutive patients undergoing elective PCI, a total of 230 (13.3%) met the diagnostic criteria of PMI. The high RDW (≥ 12.6%) group tended to have PMI (15.4% vs. 11.2%, P = 0.010). RDW was an independent predictor of PMI whether as a categorical variable (adjusted odds ratio = 1.442, 95% confidence interval = 1.088 to 1.911, P = 0.011) or a continuous variable (adjusted odds ratio = 1.236, 95% confidence interval = 1.079 to 1.415, P = 0.002). High RDW was also significantly associated with increased risk of major adverse cardiovascular events (MACE) during follow-up. However, anemia was not independently associated with PMI or MACE in the current study. In conclusion, RDW showed strong and independent association with PMI in patients undergoing elective PCI.

12.
Theranostics ; 10(21): 9663-9673, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32863952

RESUMO

Introduction: To explore the involvement of the cardiovascular system in coronavirus disease 2019 (COVID-19), we investigated whether myocardial injury occurred in COVID-19 patients and assessed the performance of serum high-sensitivity cardiac Troponin I (hs-cTnI) levels in predicting disease severity and 30-day in-hospital fatality. Methods: We included 244 COVID-19 patients, who were admitted to Renmin Hospital of Wuhan University with no preexisting cardiovascular disease or renal dysfunction. We analyzed the data including patients' clinical characteristics, cardiac biomarkers, severity of medical conditions, and 30-day in-hospital fatality. We performed multivariable Cox regressions and the receiver operating characteristic analysis to assess the association of cardiac biomarkers on admission with disease severity and prognosis. Results: In this retrospective observational study, 11% of COVID-19 patients had increased hs-cTnI levels (>40 ng/L) on admission. Of note, serum hs-cTnI levels were positively associated with the severity of medical conditions (median [interquartile range (IQR)]: 6.00 [6.00-6.00] ng/L in 91 patients with moderate conditions, 6.00 [6.00-18.00] ng/L in 107 patients with severe conditions, and 11.00 [6.00-56.75] ng/L in 46 patients with critical conditions, P for trend=0.001). Moreover, compared with those with normal cTnI levels, patients with increased hs-cTnI levels had higher in-hospital fatality (adjusted hazard ratio [95% CI]: 4.79 [1.46-15.69]). The receiver-operating characteristic curve analysis suggested that the inclusion of hs-cTnI levels into a panel of empirical prognostic factors substantially improved the prediction performance for severe or critical conditions (area under the curve (AUC): 0.71 (95% CI: 0.65-0.78) vs. 0.65 (0.58-0.72), P=0.01), as well as for 30-day fatality (AUC: 0.91 (0.85-0.96) vs. 0.77 (0.62-0.91), P=0.04). A cutoff value of 20 ng/L of hs-cTnI level led to the best prediction to 30-day fatality. Conclusions: In COVID-19 patients with no preexisting cardiovascular disease, 11% had increased hs-cTnI levels. Besides empirical prognostic factors, serum hs-cTnI levels upon admission provided independent prediction to both the severity of the medical condition and 30-day in-hospital fatality. These findings may shed important light on the clinical management of COVID-19.


Assuntos
Cardiomiopatias/etiologia , Infecções por Coronavirus/complicações , Pneumonia Viral/complicações , Troponina I/sangue , Idoso , Cardiomiopatias/sangue , China , Estudos de Coortes , Infecções por Coronavirus/sangue , Infecções por Coronavirus/mortalidade , Feminino , Hospitalização , Humanos , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/sangue , Pneumonia Viral/mortalidade , Valor Preditivo dos Testes , Prognóstico , Estudos Retrospectivos
13.
Circulation ; 2020 Sep 29.
Artigo em Inglês | MEDLINE | ID: mdl-32988222

RESUMO

Background: Proprotein convertase subtilisin/kexin 9 (PCSK9), mainly secreted by the liver and released into the blood, elevates plasma low-density lipoprotein (LDL) cholesterol by degrading LDL receptor. Pleiotropic effects of PCSK9 beyond lipid-metabolism have been shown. However, the direct effects of PCSK9 on platelet activation and thrombosis, as well as the underlying mechanisms, still remain unclear. Methods: We detected the direct effects of PCSK9 on agonists-induced platelet aggregation, dense granule ATP release, integrin αIIbß3 activation, α granule release, spreading, and clot retraction. These studies were complemented by in vivo analysis of FeCl3-injured mouse mesenteric arteriole thrombosis. We also investigated the underlying mechanisms. Using myocardial infarct (MI) model, we explored the effects of PCSK9 on microvascular obstruction and infarct expansion post-MI. Results: PCSK9 directly enhances agonists-induced platelet aggregation, dense granule ATP release, integrin αIIbß3 activation, P-selection release from α granules, spreading, and clot retraction. In line, PCSK9 enhances in vivo thrombosis in a FeCl3-injured mesenteric arteriole thrombosis mouse model, while PCSK9 inhibitor evolocumab ameliorates its enhancing effects. Mechanism studies revealed that PCSK9 binds to platelet CD36 and thus activates Src kinase and mitogen-activated protein kinase (MAPK)- extracellular signal-regulated kinase 5 and c-Jun N-terminal kinase, increases the generation of reactive oxygen species, as well as activates the p38MAPK/cytosolic phospholipase A2/cyclooxygenase-1/thromboxane A2 signaling pathways downstream of CD36 to enhance platelet activation. Using CD36 knockout mice, we showed the enhancing effects of PCSK9 on platelet activation are CD36 dependent. Consistently and importantly, aspirin abolishes the enhancing effects of PCSK9 on platelet activation and in vivo thrombosis. Finally, we showed that PCSK9 activating platelet CD36 aggravates microvascular obstruction and promotes MI expansion post-MI. Conclusions: PCSK9 in plasma directly enhances platelet activation and in vivo thrombosis, as well as MI expansion post-MI, by binding to platelet CD36 and thus activating the downstream signaling pathways. PCSK9 inhibitors or aspirin abolish the enhancing effects of PCSK9, supporting the use of aspirin in patients with high plasma PCSK9 levels in addition to PCSK9 inhibitors to prevent thrombotic complications.

14.
Adv Ther ; 37(10): 4220-4232, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32770531

RESUMO

INTRODUCTION: The pharmacodynamics (PD) and pharmacokinetics (PK) study of ticagrelor loading dose (LD) in Chinese patients with acute coronary syndrome (ACS) without opioid administration has never been investigated. Therefore, the aim of this study was to evaluate the antiplatelet effects and the PK parameters of ticagrelor in Chinese patients with ACS without opioid administration. METHODS: A sample size of 30 eligible patients with ACS were enrolled in this study. Blood samples were obtained predose and 1, 2, 4, 8, and 12 h after 180 mg LD of ticagrelor. P2Y12 reactivity units (PRU) and plasma concentrations of ticagrelor and its two metabolites were measured. RESULTS: In total, 15 patients were admitted to ST segment elevation myocardial infarction (STEMI) and non-ST segment elevation myocardial infarction (NSTEMI) groups, respectively. For patients with NSTEMI, PRU declined significantly during the first 4 h and maintained a relatively stable antiplatelet effect from 4 to 12 h after LD. A similar trend was found in the STEMI group without significant differences of PRU in each designed time compared with patients with NSTEMI (P > 0.05). Tmax of metabolite AR-C124910XX was 4 h after LD for both groups. There were no significant differences for drug concentration, Cmax, or AUC of ticagrelor and AR-C124910XX between patients with STEMI and NSTEMI (P > 0.05). CONCLUSIONS: For Chinese patients with ACS, at least 4 h was needed to achieve an adequate antiplatelet effect for ticagrelor LD. There were no differences in PK or PD between Chinese patients with STEMI and NSTEMI. CLINICAL TRIAL REGISTRATION: ChiCTR1800014764.

15.
J Nucl Cardiol ; 2020 Aug 07.
Artigo em Inglês | MEDLINE | ID: mdl-32770319

RESUMO

BACKGROUND: The aim of this study was to investigate the correlation of coronary flow reserve (CFR) assessed by rest/stress myocardial perfusion imaging with dynamic single-photon emission computed tomography (SPECT) with intracoronary pressure-derived fractional flow reserve (FFR) in patients with single-vessel coronary artery disease (CAD). METHODS: Patients with suspected or known stable CAD who were referred for invasive coronary angiography were prospectively enrolled. Both invasive FFR and SPECT were performed in subjects with single-vessel intermediate coronary stenosis. A cutoff value of < 0.8 was used to define abnormal FFR. RESULTS: A total of 34 patients were enrolled. The mean age of the subjects was 62.1 ± 6.7 years, and 79.4% were male. SPECT-derived CFR showed a significantly moderate correlation with FFR (r = 0.505, P = .003). The diagnostic performance for the identification of abnormal FFR in terms of sensitivity, specificity, and accuracy was 88.9%, 83.3%, and 87.9%, respectively, for CFR, with an optimized cutoff value of 1.73. CONCLUSION: In patients with single-vessel CAD, SPECT CFR was useful for the detection of functionally significant stenosis. Our data support the use of this technique as an optional method for hemodynamic assessment, especially when FFR results are in normal range.

16.
BMC Cardiovasc Disord ; 20(1): 325, 2020 07 07.
Artigo em Inglês | MEDLINE | ID: mdl-32635890

RESUMO

BACKGROUND: Provisional 1-stent technique is currently regarded as the default approach for the majority of bifurcation lesions. Nonetheless, 2-stent techniques may be required for complex bifurcations with high compromise risk or fatal consequences of side branch (SB) occlusion. Limitations exist in current approaches, as stents gap, multiple metal layers and stent malapposition caused by imprecise placement with fluoroscopic guide and intrinsic technical defects. This study was designed to investigate the effectiveness of the novel Szabo 2-stent technique for coronary bifurcation lesions. METHODS: In the Szabo 2-stent technique, one stent is precisely implanted at the SB ostium with Szabo technique resulting in a single strut protruding into the main vessel (MV). After MV rewiring and SB guidewire withdrawal, another stent is implanted in MV followed by proximal optimization technique, SB rewiring, and final kissing inflation (FKI). RESULTS: The technique tested successfully in silicone tubes (n = 9) with: procedure duration, 31.2 ± 6.8 min; MV and SB rewiring time, 26.8 ± 11.2 s and 33.3 ± 15 s; easy FKI; and 2.3 ± 0.5 balloons/procedure. Bifurcation lesions (n = 22) were treated with angiographic success in MV and SB, respectively: increased minimal lumen diameter (0.63 ± 0.32 mm to 3.20 ± 0.35 mm; 0.49 ± 0.37 mm to 2.67 ± 0.25 mm); low residual stenosis (12.4 ± 2.4%; 12.4 ± 2.3%); and intravascular ultrasound confirmed (n = 19) full coverage; minimal overlap and malapposition; minimal lumen area (2.4 ± 1.2 mm2; 2.1 ± 1.0 mm2); plaque burden (78.1 ± 11.3%; 71.6 ± 15.5%); and minimal stent area (9.1 ± 1.6 mm2; 6.1 ± 1.3 mm2). Periprocedural cardiac troponin increased in 1 asymptomatic patient without electrocardiographic change. There was no target lesion failure (cardiac death, myocardial infarction, target lesion revascularization) at 6-month follow-up. CONCLUSIONS: The Szabo 2-stent technique for bifurcation lesions provided acceptable safety and efficacy at short-term follow-up.

17.
Heart Lung Circ ; 29(12): 1758-1765, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32622915

RESUMO

BACKGROUND: This study evaluated whether the Controlling Nutritional Status (CONUT) score could predict clinical outcomes in ST elevation myocardial infarction (STEMI) patients. METHODS: We performed a retrospective cohort study of STEMI patients after primary percutaneous coronary intervention (pPCI). The endpoint was major adverse cardiac event (MACE). Information was obtained from medical records and via telephone calls. Patients were divided into three groups: normal (CONUT score 0-1; n=278), mild-moderate (score 2-4; n=418), and severe (score ≥5; n=55) groups. RESULTS: During the 24.6±12 months follow-up, MACEs were observed in 65 (8.7%) patients. The incidence of MACEs was 6.1%, 5.5%, and 45.5% in the normal, mild-moderate, and severe group, respectively (p<0.001). Kaplan-Meier curves revealed that patients with a CONUT score ≥5 had the significantly highest rate of MACE, myocardial re-infarction, and vessel revascularisation. In three Cox proportional hazard models, the CONUT scores were unexceptionally associated with MACE, even after adjusting all other variables (hazard ratio, 12.09; 95% confidence interval [CI], 5.09-28.7; p<0.001). The C-statistic of the CONUT score for the prediction of MACE was 0.692 (95% CI, 0.613-0.771; p<0.001), which is close to that of Global Registry of Acute Coronary Events. CONCLUSIONS: The nutritional status evaluated by the CONUT score can independently predict clinical outcomes in STEMI patients, which suggests that active nutritional management is meaningful for these patients after PCI.

18.
Stem Cell Res Ther ; 11(1): 224, 2020 06 08.
Artigo em Inglês | MEDLINE | ID: mdl-32513270

RESUMO

BACKGROUND: Myocardial infarction (MI) is a major cause of death worldwide. Although percutaneous coronary intervention and coronary artery bypass grafting can prolong life, cardiac damage persists. In particular, cardiomyocytes have no regenerative capacity. Mesenchymal stem cells (MSCs) are attractive candidates for the treatment of MI. The manner by which MSCs exert a beneficial effect upon injured cells is a source of continued study. METHODS: After the isolation and identification of exosomes from MSCs, the expression of miR-210 was determined by microarray chip. Subsequently, gain- and loss-function approaches were conducted to detect the role of exosomes and exosomal-miR-210 in cell proliferation and apoptosis of cardiomyocytes, as well as the MI in vivo. Dual-Luciferase Report Gene System was used to demonstrate the target gene of miR-210. RESULTS: We tested the hypothesis that MSC-derived exosomes transfer specific miRNA to protect cardiomyocytes from apoptotic cell death. Interestingly, direct cardiac injection of MSC exosomes reduced infarct size and improved heart function after coronary ligation. In vitro, the MSC exosomes enhanced cardiomyocyte survival to hypoxia. Confirmation of exosome uptake in myocytes was confirmed. Dual-luciferase reporter assay implicated miR-210 as a mediator of the therapeutic effect and AIFM3 as a downstream target. Treatment with miR-210 overexpressing MSC exosomes improved myocyte protection to both in vitro and in vivo stress. Furthermore, the endogenous and exogenous miR-210 had the same therapeutic effects. CONCLUSION: These results demonstrated that the beneficial effects offered by MSC-exosomes transplantation after MI are at least partially because of excreted exosome containing mainly miR-210.

19.
Clin Cardiol ; 43(7): 796-802, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32562427

RESUMO

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) could cause virulent infection leading to Corona Virus Disease 2019 (COVID-19)-related pneumonia as well as multiple organ injuries. HYPOTHESIS: COVID-19 infection may result in cardiovascular manifestations leading to worse clinical outcome. METHODS: Fifty four severe and critical patients with confirmed COVID-19 were enrolled. Risk factors predicting the severity of COVID-19 were analyzed. RESULTS: Of the 54 patients (56.1 ± 13.5 years old, 66.7% male) with COVID-19, 39 were diagnosed as severe and 15 as critical cases. The occurrence of diabetes, the level of D-dimer, inflammatory and cardiac markers in critical cases were significantly higher. Troponin I (TnI) elevation occurred in 42.6% of all the severe and critical patients. Three patients experienced hypotension at admission and were all diagnosed as critical cases consequently. Hypotension was found in one severe case and seven critical cases during hospitalization. Sinus tachycardia is the most common type of arrythmia and was observed in 23 severe patients and all the critical patients. Atrioventricular block and ventricular tachycardia were observed in critical patients at end stage while bradycardia and atrial fibrillation were less common. Mild pericardial effusion was observed in one severe case and five critical cases. Three critical cases suffered new onset of heart failure. Hypotension during treatment, severe myocardial injury and pericardial effusion were independent risk factors predicting the critical status of COVID-19 infection. CONCLUSION: This study has systemically observed the impact of COVID-19 on cardiovascular system, including myocardial injury, blood pressure, arrythmia and cardiac function in severe and critical cases. Monitoring of vital signs and cardiac function of COVID-19 patients and applying potential interventions especially for those with hypotension during treatment, severe myocardial injury or pericardial effusion, is of vital importance.


Assuntos
Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/epidemiologia , Causas de Morte , Infecções por Coronavirus/diagnóstico , Infecções por Coronavirus/epidemiologia , Pneumonia Viral/diagnóstico , Pneumonia Viral/epidemiologia , Adulto , Idoso , Doenças Cardiovasculares/terapia , China/epidemiologia , Estudos de Coortes , Comorbidade , Infecções por Coronavirus/terapia , Estado Terminal/mortalidade , Estado Terminal/terapia , Feminino , Humanos , Incidência , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Monitorização Fisiológica , Análise Multivariada , Pandemias , Pneumonia Viral/terapia , Estudos Retrospectivos , Medição de Risco , Índice de Gravidade de Doença , Análise de Sobrevida
20.
Biomaterials ; 255: 120168, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32562944

RESUMO

Stem cell-derived extracellular vesicles (EVs) have been demonstrated to be effective in heart repair and regeneration post infarction. However, the poor homing efficiency and low yields of these therapeutics remain the major obstacles before they can be used in the clinic. To improve the delivery efficiency of EVs to ischemia-injured myocardium, we modified mesenchymal stem cell (MSC)-derived EVs with monocyte mimics through the method of membrane fusion. Monocyte mimic-bioinspired MSC-EVs (Mon-Exos) exhibited enhanced targeting efficiency to injured myocardium by mimicking the recruitment feature of monocytes after MI/RI, thus contributing to these exclusive adhesive molecules on monocyte mimics, particularly the Mac1/LFA1-ICAM-1 interaction. Through this strategy, Mon-Exos were shown to promote endothelial maturation during angiogenesis and modulate macrophage subpopulations after MI/RI, consistent with MSC-Exos biofunctions, and eventually improve therapeutic outcomes in cardiac function and pathohistology changes after treatments in a mouse MI/RI model. Ultimately, this strategy might provide us with a better way to assess the effects of stem cell EVs and offer additional techniques to help clinicians better manage regenerative therapeutics for ischemic heart diseases.

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