[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.

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 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.

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.