Fibroblast growth factor 21 inhibits vascular calcification by ameliorating oxidative stress of vascular smooth muscle cells.

Vascular calcification is very common in clinical. Severe vascular calcification is related to the occurrence of adverse events. Oxidative stress (OS) plays a pathophysiological role in the formation of vascular calcification. Previous studies have demonstrated that fibroblast growth factor 21(FGF21) could inhibit vascular calcification both in vivo and in vitro. FGF21 has also been proved to promote the recovery of superoxide dismutase (SOD) and thereby alleviate OS. Thus, our assumption was that FGF21 inhibit vascular calcification partly by restoring the level of antioxidant SOD and reducing OS. In this study, we established the vascular calcification by 5/6 nephrectomy plus high phosphate diet chronic kidney disease (CKD) model. The results showed the receptor of FGF21, fibroblast growth factor receptor 1 (FGFR1) and ßKlotho in the aorta increased in CKD group, and mainly located in the media of the artery. Ulteriorly, immunofluorescence (IF) and IHC staining showed that FGFR1 and ßKlotho mainly existed in arterial vascular smooth muscle cells (VSMCs). When FGF21 was knock out, the calcification was more severe in FGF21 KO + CKD mice, compared to wild type (WT)+ CKD mice. The transcriptional level of vascular calcification-related genes was significantly higher in FGF21 KO mice than control group. The dihydroethidium (DHE) staining reactive oxygen species (ROS) level in the CKD group was higher compared to the control group, but lower in FGF21 KO + CKD group, and the transcriptional level of SOD1 and SOD2 in FGF21 KO + CKD group was significantly higher than that in CKD group. In conclusion, FGF21 could inhibit vascular calcification, partly by restoring the level of antioxidant SOD and reducing vascular oxidative stress. This study provides further evidence for FGF21 as a candidate drug for cardiovascular protective agents.

Procedural Characteristics and Clinical Outcomes Associated with Chronic Total Occlusion Percutaneous Coronary Intervention in Patients with a History of Prior Coronary Artery Bypass Graft: A Meta-Analysis.

Background: Owing to advances in procedural techniques and the training of interventional staff in catheterization labs, recent work has demonstrated the safety of percutaneous coronary intervention (PCI) as a treatment for patients suffering from chronic total occlusion (CTO). However, there has been little research focused on systematic comparisons of PCI outcomes in CTO patients that did or did not exhibit a history of previous coronary artery bypass grafting (CABG). Methods: Electronic databases were systematically searched for all studies comparing CTO-PCI outcomes for patients with and without a history of CABG, with event rates subsequently being compared via random-effects models with forest plots and odds ratios with 95% confidence intervals (CI), owing to the assumption of between-studies heterogeneity. Results: In total, 8 observational studies enrolling 13,509 CTO patients were identified, including 3389 and 10,120 patients with and without a history of prior CABG, respectively. Patients were enrolled in these studies from 1999-2018. Pooled analyses indicated that CABG history was not linked to a lower proportion of radial access 24 (95% CI 0.52-1.03, p = 0.08), and a prior CABG history was linked to a greater contrast volume (95% CI 0.12-0.44, p < 0.001), higher radiation dose (95% CI 0.27-0.40, p < 0.001), longer fluoroscopy time (95% CI 0.42-0.61, p < 0.001), longer procedural time (95% CI 0.38-0.64, p < 0.001), a higher number of implanted stents (95% CI 0.41-0.60, p < 0.001), longer total stent length (95% CI 0.21-0.60, p < 0.001), higher technical failure rates (95% CI 1.46-1.85, p < 0.001), and higher rates of procedural failure (95% CI 1.42-1.79, p < 0.001). The in-hospital mortality (95% CI 1.50-4.03, p < 0.001) and periprocedural mortality (95% CI 1.63-3.73, p < 0.001) of patients with a history of CABG were also higher. While stroke incidence was comparable in both groups (95% CI 0.80-4.47, p = 0.15), periprocedural major adverse cardiovascular and cerebrovascular events (MACCE) rates were significantly higher among patients exhibiting a history of CABG (95% CI 1.66-2.94, p < 0.001). Conclusions: These results suggest that CTO-PCI procedures may be more challenging and associated with lower rates of success in CABG patients relative to procedures performed in patients without any history of CABG. Moreover, in-hospital outcomes including MACCE and mortality were worse for patients that had undergone prior CABG.

Cathepsin S inhibition in dendritic cells prevents Th17 cell differentiation in perivascular adipose tissues following vascular injury in diabetic rats.

In the context of diabetes mellitus (DM), the circulating cathepsin S (CTSS) level is significantly higher in the cardiovascular disease group. Therefore, this study was designed to investigate the role of CTSS in restenosis following carotid injury in diabetic rats. To induce DM, 60 mg/kg of streptozotocin (STZ) in citrate buffer was injected intraperitoneally into Sprague-Dawley rats. After successful modeling of DM, wire injury of the rat carotid artery was performed, followed by adenovirus transduction. Levels of blood glucose and Th17 cell surface antigens including ROR-γt, IL-17A, IL-17F, IL-22, and IL-23 in perivascular adipose tissues (PVAT) were evaluated. For in vitro analysis, human dendritic cells (DCs) were treated with 5.6-25 mM glucose for 24 h. The morphology of DCs was observed using an optical microscope. CD4+ T cells derived from human peripheral blood mononuclear cells were cocultured with DCs for 5 days. Levels of IL-6, CTSS, ROR-γt, IL-17A, IL-17F, IL-22 and IL-23 were measured. Flow cytometry was conducted to detect DC surface biomarkers (CD1a, CD83, and CD86) and Th17 cell differentiation. The collected DCs presented a treelike shape and were positive for CD1a, CD83, and CD86. Glucose impaired DC viability at the dose of 35 mM. Glucose treatment led to an increase in CTSS and IL-6 expression in DCs. Glucose-treated DCs promoted the differentiation of Th17 cells. CTSS depletion downregulated IL-6 expression and inhibited Th17 cell differentiation in vitro and in vivo. CTSS inhibition in DCs inhibits Th17 cell differentiation in PVAT tissues from diabetic rats following vascular injury.

The predictive value of the triglyceride-glucose index for cardiovascular events in patients with coronary chronic total occlusion.

BACKGROUND: Chronic total occlusion (CTO) of the coronary artery is a difficult problem in clinical practice. The triglyceride-glucose (TyG) index is an effective risk predictor of cardiovascular risk. However, the relationship between the TyG index and the prognosis of CTO patients remains unstudied. Thus, the present study aimed to investigate the relationship between the TyG index and cardiovascular risk in CTO patients. METHODS: This was a single-centre, retrospective cohort study. We retrospectively enrolled 652 patients with CTO lesions diagnosed by angiography and who underwent revascularization through PCI. Patients were routinely followed up for 24 months unless meeting the endpoint. The primary endpoint was the composite of all-cause death, nonfatal myocardial infarction, unplanned revascularization, and nonfatal ischaemic stroke. To test the association of the TyG index with cardiovascular risk, the categorized TyG index and Cox proportional hazards regression models were utilized. RESULTS: A total of 652 patients were enrolled in the final analysis (male: 83.7%, age: 58.2 ± 10.49 years). The average TyG index was 8.8 ± 0.57. CTO PCIs were procedurally successfully completed in 503 (77.15%) patients. During the follow-up period of 22.8 ± 3.84 months, 73 (11.19%) major adverse cardiovascular and cerebral events (MACCEs) occurred. When fully adjusted, there was a 2.09-fold risk for MACCEs among patients with the highest TyG index compared with those with the lowest TyG index [T2 vs. T1: hazard ratio (HR) 1.24, 95% confidence interval (CI) 0.65-2.38, P = 0.057; T3 vs. T1: HR 2.09, 95% CI 1.14-3.86, P = 0.018; P for trend = 0.036]. The restricted cubic spline (RCS) analysis showed that the HR for MACCEs increased as the TyG index increased over 8.71 [HR per standard deviation (SD) 1.740, 95% CI 1.23-2.46, P = 0.002]. The risk of MACCEs increased with increasing tertiles of TyG index in successful CTO PCI patients and nondiabetes mellitus (DM) patients (P < 0.05) but not in patients with failed CTO PCI and DM patients. CONCLUSION: The study revealed that the TyG index had significant relevance to cardiovascular risk in CTO patients and suggests that the TyG index is feasible for predicting cardiovascular risk in CTO patients.

Establishment of a Risk Scoring Model for Perioperative Unex-Plained Shock during Percutaneous Coronary Intervention for the Treatment of Chronic Total Occlusion.

Background: Several complications can contribute to the risk of shock during the chronic total occlusion (CTO) percutaneous coronary intervention (PCI) procedure. However, some patients that develop shock do not exhibit any apparent complications, and few studies to date have discussed the risk of unexplained perioperative shock in patients undergoing CTO PCI. Accordingly, this study was designed with the goal of defining perioperative risk factors linked to the odds of unexplained shock during CTO PCI. Methods: In total, this study analyzed data from 924 patients that underwent CTO PCI without any in-hospital complications from January 2016-August 2021. Cardiologists collected data pertaining to patient clinical characteristics, laboratory findings, angiographic findings, and procedural characteristics. Patients were separated into two groups based upon whether or not they experienced perioperative shock. The relationship between specific variables and perioperative shock incidence was assessed via a multivariable stepwise logistic regression approach. A risk-scoring nomogram was then designed for use as a tool to guide patient risk assessment efforts during PCI procedural planning. Results: Overall, 4.8% of these patients (44/924) experienced unexplained perioperative shock. Independent predictors associated with unexplained shock during CTO PCI included baseline systolic pressure (odds ratio (OR) 0.968, 95% confidence interval (CI): 0.945-0.991), baseline heart rate (OR 1.055, 95% CI: 1.020-1.091), baseline hemoglobin (OR 0.970, 95% CI: 0.947-0.994), procedure duration (OR 1.008, 95% CI: 1.002-1.015), J-CTO score (OR 1.521, 95% CI: 1.021-2.267), and use of a retrograde approach (OR 3.252, 95% CI: 1.426-7.415). The unbiased C-index estimate was 0.859, and this model exhibited excellent calibration. Conclusions: The risk of unexplained shock is an important consideration for clinicians performing the CTO PCI procedure. These analyses revealed unexplained shock risk to be independently related to lower baseline systolic pressure, higher baseline heart rate, lower baseline hemoglobin, more procedure time, higher J-CTO score, and more use of a retrograde approach.

Possible effects of fibroblast growth factor 21 on vascular calcification via suppressing activating transcription factor 4 mediated apoptosis and osteogenic transformation in rats.

Vascular calcification (VC), a significant risk factor of many cardio-cerebral vascular diseases, is a perplexing issue with no effective treatment in clinical work up to now. Endoplasmic reticulum stress (ERS) mediated apoptosis has been proved to be a significant mechanism for initiating VC process. Activating transcription factor 4 (ATF4), a key transcription factor of ERS, is most closely associated with VC. Fibroblast growth factor 21 (FGF21), an atypical member of the FGFs family, has a protective biological function in various metabolic diseases by ERS pathways. However, the possible effects of FGF21 on VC by regulating ERS, especially through the ATF4 pathway, is still unclear. Our research provides the first evidence that exogenous FGF21 treatment can alleviate the vitamin D3 plus nicotine-induced VC at least in part via suppressing ATF4 mediated apoptosis and osteogenic transformation in rats.

[Fibroblast growth factor 21 plays a protective role in cardiovascular diseases by inducing autophagy].

Fibroblast growth factor 21 (FGF21) is a growth factor with endocrine function in the fibroblast growth factor family. Previous reports have shown that FGF21 is involved in the regulation of energy metabolism and plays a protective role in cardiovascular diseases such as coronary heart disease, diabetes, non-alcoholic fatty liver disease and so on. Recent studies have found that FGF21 can induce autophagy in a variety of tissues and organs, and autophagy is involved in many pathological processes of cardiovascular diseases, including vascular calcification, atherosclerosis, and myocardial ischemia-reperfusion injury. Therefore, FGF21 may play a protective role in a variety of cardiovascular diseases by regulating autophagy. This article reviews the research progress on the protective role of FGF21 in cardiovascular diseases by inducing autophagy.

Clinical prediction factors of nonchronic total occlusion lesion progression in patients with unstable angina receiving percutaneous coronary intervention for chronic total occlusion lesions.

Background: In this study, we investigated clinical prediction factors of nonchronic total occlusion lesion (NCTOL) progression in patients who underwent percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) lesions. Methods: In total, 450 patients with unstable angina (mean age = 57.1 ± 9.2 years) who underwent PCI for CTO lesions between January 2016 and December 2018 at Beijing Anzhen Hospital were enrolled in this study. A clinical and angiographic follow-up examination was performed 12 months postoperatively. The patients were divided into NCTOL progression (145 cases) and control (305 cases) groups based on the outcome of the 12-month angiographic follow-up. The clinical and angiographic features of the participants were analyzed. Results: The adenosine diphosphate-induced platelet aggregation (ADP-IPA) rate and levels of lipoprotein (a) (Lp(a)) in the NCTOL progression group were significantly higher than those in the control group (51.89 ± 14.81 vs. 39.63 ± 17.12, P < 0.01; 0.22 ± 0.26 vs. 0.14 ± 0.18, P < 0.05, respectively). Logistic regression showed that the ADP-IPA rate (odds ratio = 1.047, 95 % confidence interval: 1.014-1.082, P = 0.005) and Lp(a) (odds ratio = 11.972, 95 % confidence interval: 1.230-116.570, P = 0.033) were independent predictors of NCTOL progression. Partial correlation analysis demonstrated that the ADP-IPA rate was positively correlated with NCTOL progression (r = 0. 351, P < 0.001). Receiver operating characteristic curve showed that the boundary point of the ADP-IPA rate to predict NCTOL progression was 30 % (sensitivity, 86.2 %; specificity, 68.9 %). Conclusions: NCTOL progression is an important cause of recurrent PCI in patients with coronary artery disease after PCI for CTO lesions. The ADP-IPA rate is a useful predictor for NCTOL progression in patients with unstable angina who undergo PCI for CTO lesions.

Effect of dynamic platelet-to-lymphocyte ratio on the prognosis of patients with esophageal squamous cell carcinoma receiving chemoradiotherapy.

Systemic inflammatory load affects the long-term developmental outcomes in patients with malignancy. The purpose of this study was to investigate the effect of the dynamic levels of platelet-to-lymphocyte ratio (PLR) at different treatment stages on the prognosis of patients with esophageal squamous cell carcinoma (ESCC) undergoing chemoradiotherapy. This study included 168 patients who received chemoradiotherapy between 2012 and 2018. PLR levels at different treatment stages were calculated based on blood test results. The association between PLR and overall survival (OS) was determined using the Kaplan-Meier method and Cox proportional regression models. The cutoff values of PLR before and after treatment of 168 patients with ESCC were 195.7 and 403.6, respectively. The 5-year OS rates of patients in the low and high pre-PLR groups were 42.1% and 21.7%, respectively. The overall 5-year OS rate of all patients was 27.1%. Multivariate analysis results showed that patient age (hazard ratio [HR] = 1.736; 95% confidence interval (CI) = 1.129-2.669; P = .012), alcohol consumption (HR = 1.622; 95%CI = 1.050-2.508; P = .029), T stage (HR = 12.483; 95%CI = 3.719-41.896; P < .001), pre-PLR (HR = 1.716; 95%CI = 1.069-2.756; P = .025), post-PLR (HR = 1.664; 95%CI = 1.106-2.503; P = .015) were independent factors of the prognosis of patients with ESCC. PLR at different treatment stages can be used to effectively evaluate the prognosis of patients with ESCC undergoing chemoradiotherapy.

Palmdelphin Deficiency Evokes NF-κB Signaling in Valvular Endothelial Cells and Aggravates Aortic Valvular Remodeling.

Palmd-deficient mice of advanced age manifest increased aortic valve peak velocity, thickened aortic valve leaflets, and excessive extracellular matrix deposition, which are key features of calcific aortic valve disease. PALMD is predominantly expressed in endothelial cells of aortic valves, and PALMD-silenced valvular endothelial cells are prone to oscillatory shear stress-induced endothelial-to-mesenchymal transition. Mechanistically, PALMD is associated with TNFAIP3 interaction protein 1, a binding protein of TNFAIP3 and IKBKG in NF-κB signaling. Loss of PALMD impairs TNFAIP3-dependent deubiquitinating activity and promotes the ubiquitination of IKBKG and subsequent NF-κB activation. Adeno-associated virus-mediated PALMD overexpression ameliorates aortic valvular remodeling in mice with calcific aortic valve disease, indicating protection.

Lesion characteristics and procedural complications of chronic total occlusion percutaneous coronary intervention in patients with prior bypass surgery: A meta-analysis.

Coronary artery bypass graft (CABG) accelerates the prevalence of native coronary chronic total occlusion (CTO), and this kind of CTO shows extensive challenging and complex atherosclerotic pathology. As a result, the procedural success rate of percutaneous coronary intervention (PCI) is inferior to another kind of lesions. The present meta-analysis aims to compare the lesion characteristics and procedural complications of CTO-PCI in patients with or without prior CABG. A total of 8 studies, comprising of 13439 patients, published from inception to August 2021 were included in this meta-analysis. Results were pooled using random effects model and are presented as odds ratio (OR) with 95% confidence intervals (95% CIs). From the 13439 patients enrolled, 3349 (24.9%) patients had previous CABG and 10090 (75.1%) formed the control group in our analysis. For the clinical characteristic, compared to the non-CABG patients, prior CABG patients were older (OR, 3.98; 95% CI, 3.19-4.78; p < .001; I2 = 72%), had more male (OR, 1.30; 95% CI, 1.14-1.49; p < .001; I2 = 6%), diabetes mellitus (OR, 1.54; 95% CI, 1.36-1.73; p < .001; I2 = 37%), dyslipidemia (OR, 1.89; 95% CI, 1.33-2.69; p < .001; I2 = 81%), hypertension (OR, 1.88; 95% CI, 1.46-2.41; p < .001; I2 = 71%), previous myocardial infarction (OR, 1.94; 95% CI, 1.48-2.56; p < .001; I2 = 85%), and previous PCI (OR, 1.74; 95% CI, 1.52-1.98; p < .001; I2 = 22%). Non-CABG patents had more current smoker (OR, .45; 95% CI, 0.27-0.74; p < .001; I2 = 91%). BMI (OR, -0.01; 95% CI, -0.07-0.06; p = .85; I2 = 36%) were similar in both groups. For lesions location, the right coronary artery (RCA) was predominant target vessel in both groups (50.5% vs 48.7%; p＝.49), although, the left circumflex (LCX) was more frequently CTO in the prior CABG group (27.3% vs 18.9%; p＜.01), while left anterior descending artery (LAD) in non-CABG ones (16.0% vs 29.1%; p＜0.01). For lesions characteristics, prior CABG patients had more blunt stump (OR, 1.71; 95% CI, 1.46-2.00; p < .001; I2 = 40%), proximal cap ambiguity (OR, 1.45; 95% CI, 1.28-1.64; p < .001; I2 = 0.0%), severe calcifications (OR, 2.91; 95% CI, 2.19-3.86; p < .001; I2 = 83%), more bending (OR, 3.07; 95% CI, 2.61-3.62; p < .001; I2 = 0%), lesion length > 20 mm (OR, 1.59; 95% CI, 1.10-2.29; p = .01; I2 = 83%), inadequate distal landing zone (OR, 1.95; 95% CI, 1.75-2.18; p＜.001; I2 = 0.0%), distal cap at bifurcation (OR, 1.65; 95% CI, 1.46-1.88; p < .001; I2 = 0.0%), and higher J-CTO score (SMD, 0.52; 95% CI, 0.42-0.63; p < .001; I2 = 65%). But side branch at proximal entry (OR, 0.88; 95% CI, 0.72-1.07; p = .21; I2 = 45%), in-stent CTO (OR, 0.99; 95% CI, 0.86-1.14; p = .88; I2 = 0.0%), lack of interventional collaterals (OR, 0.80; 95% CI, 0.55-1.15; p = .23; I2 = 78%), and previously failed attempt (OR, 0.73; 95% CI, 0.48-1.11; p = .14; I2 = 89%) were similar in both groups. For complication, prior CABG patients had more perforation with need for intervention (OR, 1.91; 95% CI, 1.36-2.69; p < 0.001; I2 = 34%), contrast-induced nephropathy (OR, 3.40; 95% CI, 1.31-8.78; p = .01; I2 = 0.0%). Non-CABG patents had more tamponade (OR, 0.25; 95% CI, 0.09-0.72; p = .01; I2 = 0.0%), and the major bleeding complication (OR, 1.18; 95% CI, 0.57-2.44; p = .65; I2 = 0%) were no significant difference in both groups. In conclusion, Patients with prior CABG undergoing CTO-PCI have more complex lesion characteristics, though procedural complication rates were comparable.

Effect of high-sensitivity C-reactive protein on the relationship between haemoglobin A1c and cardiovascular events in patients with acute coronary syndrome undergoing percutaneous coronary intervention: a cohort study.

Background: There are different opinions on haemoglobin A1c (HbA1c) in predicting cardiovascular events after percutaneous coronary intervention (PCI). Some factors may affect the ability of HbA1c to predict cardiovascular events, resulting in this inconsistency. Inflammation is a direct and whole-process participant in atherosclerosis. However, no one has studied the effect of inflammation on the correlation between HbA1c and cardiovascular events. Therefore, we aimed to test the hypothesis that high-sensitivity C-reactive protein (hsCRP) modulates HbA1c-related cardiovascular events in patients with the acute coronary syndrome (ACS) undergoing PCI. Methods: This was a retrospective cohort study. We enrolled patients with ACS who were hospitalized for PCI and followed up for 24 months. The primary outcome was the composite of major adverse cardiovascular and cerebrovascular events (MACCEs), including all-cause death, nonfatal myocardial infarction, nonfatal stroke, and unplanned repeat revascularization. We stratified the overall population by HbA1c tertiles and hsCRP median. The relationship between HbA1c, hsCRP, and cardiovascular events was analysed by the Cox proportional hazard regression model. Results: A total of 2,023 patients were enrolled in this study (age: 59.7±10.03 years old, 78.1% male patients). After the 24-month follow-up, 152 (7.51%) events occurred. Patients with hsCRP >1.21 mg/L had an increased cardiovascular risk compared with patients with hsCRP ≤1.21 mg/L [hazard ratio (HR) 1.58, 95% confidence interval (CI): 1.12-2.24, P=0.010]. We did not observe a significant correlation between HbA1c and cardiovascular events. Furthermore, we stratified patients by hsCRP ≤1.21 or >1.21 mg/L and found that the correlation between HbA1c and cardiovascular events was only significant in patients with hsCRP ≤1.21 mg/L (tertile 2 vs. tertile 1: HR 1.76, 95% CI: 0.79-3.90, P=0.165, tertile 3 vs. tertile 1: HR 3.03, 95% CI: 1.50-6.12, P=0.002; P=0.008 for trend) but not in patients with hsCRP >1.21 mg/L. Conclusions: This study showed that hsCRP may affect the relationship between HbA1c and the risk of cardiovascular events in patients with ACS after PCI. This finding suggests that the risk of cardiovascular events may be underestimated when only HbA1c is used as a predictor of cardiovascular risk. HbA1c has a better predictive value in the absence or low levels of inflammation states represented by hsCRP as a predictor of cardiovascular events.

Effect of ischemic postconditioning on cell apoptosis and expression of relevant genes in non-culprit coronary arteries.

This study was performed to determine the effect of ischemic postconditioning on cell apoptosis and angiotensin II receptor type 1 (AT1), connexin 43 (Cx43), and ß-tubulin mRNA expression in non-culprit arteries. Non-culprit arterial tissues were isolated from a rabbit myocardial ischemia-reperfusion model and randomly divided into sham, ischemia-reperfusion, and ischemic postconditioning groups. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Expression of angiotensin II, AT1, Cx43, and ß-tubulin mRNA was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). TUNEL analysis indicated significantly higher ratios of apoptotic cells in the ischemia-reperfusion group than in the sham group. However, significantly fewer apoptotic cells were observed in the ischemic postconditioning group than in the ischemia-reperfusion group. The qRT-PCR results indicated significantly higher expression of AT1, Cx43, and ß-tubulin mRNA in the ischemia-reperfusion group than in the sham group. However, expression of AT1, Cx43, and ß-tubulin was lower in the ischemic postconditioning group than in the ischemia-reperfusion group. The ratios of apoptotic cells and mRNA expression of AT1, Cx43, and ß-tubulin in non-culprit arteries were increased after ischemia-reperfusion. Ischemic postconditioning may decrease these features and inhibit the progression of non-culprit arteries.

Clinical and angiographic characteristics of patients with spontaneous reperfusion in ST-segment elevation myocardial infarction.

This study aims to investigate the clinical and angiographic characteristics of patients with spontaneous reperfusion in ST-segment elevation myocardial infarction (STEMI).A total of 519 patients with STEMI were enrolled in this study, who underwent primary percutaneous coronary intervention (PCI) treatments at Beijing Anzhen Hospital from January 2015 to December 2018. The patients were divided into 2 groups according to the TIMI flow grade before primary PCI, the non-spontaneous reperfusion group (TIMI flow grade 0-II) and the spontaneous reperfusion group (TIMI flow grade III). The incidence rate, the clinically relevant factors, and the features of the coronary angiographic lesions of spontaneous reperfusion from the 2 groups were recorded and analyzed.There were significant differences between the 2 groups in age, CTnI peak value, high thrombus burden, and locations of lesions in the distant of left anterior descending artery (LAD) (P = .000, .000, .002, .000, and .003, respectively). However, there were no significant differences between the groups in other clinic aspects including gender, hypertension, diabetes mellitus, smoking history, hyperlipemia, angina pectoris history, culprit vessel distribution, lesion distribution in left circumflex artery (LCX) and right coronary artery (RCA), and collateral circulation (P > .05 for all).Compared to the patients without spontaneous reperfusion, patients with spontaneous reperfusion were younger in age, lower in CTnI peak value, and higher in thrombosis burden, with culprit lesions mostly located in the distant of LAD.

Effect of ramipril on progression of nonculprit lesions in patients with ST-elevation myocardial infarction after primary percutaneous coronary intervention.

OBJECTIVE: To investigate the effect of ramipril on progression of nonculprit lesions in patients with ST-elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PPCI). METHODS: A total of 200 patients (60.1 ± 11.3 years) with STEMI who underwent successful PPCI from January 2010 to December 2013 were enrolled in this study. All patients underwent PPCI as treatment for culprit lesions. Patients were divided into two groups according to the dosage of ramipril used at hospital discharge as follows: high dosage group (2.5-10 mg, q.d.) and low dosage group (1.25-2.5 mg, q.d.). Clinical and angiographic follow-up was performed for 12 months. The primary endpoint was clinically-driven percutaneous coronary intervention (PCI) for nonculprit lesions. The clinical and angiographic features were analyzed. RESULTS: Clinical and angiographic follow-up was performed with 87 patients in the high dosage group and 113 patients in the low dosage group. The numbers of patients who underwent additional PCI were six and 20 in the high and low dosage groups, respectively. The rate of having additional PCI performed was lower in the high dosage group than in the low dosage group (6.90% vs. 17.70%, P = 0.03). CONCLUSIONS: A high dosage of ramipril may prevent progression of nonculprit lesions, which could be the major cause of recurrent PCI in patients with STEMI after PPCI.