Low Expression of FFAR2 in Peripheral White Blood Cells May Be a Genetic Marker for Early Diagnosis of Acute Myocardial InfarctionRead the full article
Cardiology Research and Practice publishes original research articles, review articles, and clinical studies focusing on the diagnosis and treatment of cardiovascular diseases, including hypertension, arrhythmia, heart failure, and vascular disease.
Dr. Terrence Ruddy is Director of Nuclear Cardiology at the University of Ottawa Heart Institute, and Professor of Medicine and Radiology at the University of Ottawa. His research is in SPECT and PET imaging techniques in cardiovascular disease.
Latest ArticlesMore articles
Plasma Choline as a Diagnostic Biomarker in Slow Coronary Flow
Aim. The slow coronary flow (SCF) phenomenon was characterized by delayed perfusion of epicardial arteries, and no obvious coronary artery lesion in coronary angiography. The prognosis of patients with slow coronary flow was poor. However, there is lack of rapid, simple, and accurate method for SCF diagnosis. This study aimed to explore the utility of plasma choline as a diagnostic biomarker for SCF. Methods. Patients with coronary artery stenosis <40% evaluated by the coronary angiogram method were recruited in this study and were grouped into normal coronary flow (NCF) and SCF by thrombolysis in myocardial infarction frame count (TFC). Plasma choline concentrations of patients with NCF and SCF were quantified by Ultra Performance Liquid Chromatography Tandem Mass Spectrometry. Correlation analysis was performed between plasma choline concentration and TFC. Receiver operating characteristic (ROC) curve analysis with or without confounding factor adjustment was applied to predict the diagnostic power of plasma choline in SCF. Results. Forty-four patients with SCF and 21 patients with NCF were included in this study. TFC in LAD, LCX, and RCA and mean TFC were significantly higher in patients with SCF in comparison with patients with NCF (32.67 ± 8.37 vs. 20.66 ± 3.41, ). Plasma choline level was obviously higher in patients with SCF when compared with patients with NCF (754.65 ± 238.18 vs. 635.79 ± 108.25, ). Plasma choline level had significantly positive correlation with Mean TFC (r = 0.364, ). Receiver operating characteristic (ROC) analysis showed that choline with or without confounding factor adjustment had an AUC score of 0.65 and 0.77, respectively. Conclusions. TFC were closely related with plasma choline level, and plasma choline can be a suitable and stable diagnostic biomarker for SCF.
Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance
Background. Individuals at a prediabetic stage have had an augmented cardiovascular disease (CVD) risk and CVD-related mortality compared to normal glucose tolerance (NGT) individuals, which may be attributed to the impaired vascular endothelial repair capacity. In this study, circulating endothelial progenitor cells’ (EPCs) number and activity were evaluated, and the underlying mechanisms in premenopausal women with impaired glucose regulation were explored. Methods. Circulating EPCs’ number and activity and flow-mediated dilation (FMD) were compared in premenopausal women with NGT, isolated impaired fasting glucose (i-IFG), or isolated impaired glucose tolerance (i-IGT). Plasma nitric oxide (NO), EPCs-secreted NO, and intracellular BH4 levels were also measured. The key proteins (Tie2, Akt, eNOS, and GTPCH I) in the guanosine triphosphate cyclohydrolase/tetrahydrobiopterin (GTPCH/BH4) pathway and Tie2/Akt/eNOS signaling pathway were evaluated in these women. Results. It was observed that the i-IGT premenopausal women not i-IFG premenopausal women had a significant reduction in circulating EPCs’ number and activity as well as reduced FMD when compared to NGT subjects. Plasma NO levels or EPCs-secreted NO also decreased only in i-IGT women. The expression of GTCPH I as well as intracellular BH4 levels declined in i-IGT women; however, the alternations of key proteins’ expression in the Tie2/Akt/eNOS signaling pathway were not observed in either i-IGT or i-IFG women. Conclusions. The endothelial repair capacity was impaired in i-IGT premenopausal women but was preserved in i-IFG counterparts. The underlying mechanism may be associated with the downregulated GTCPH I pathway and reduced NO productions.
Combination of Left Ventricular End-Diastolic Diameter and QRS Duration Strongly Predicts Good Response to and Prognosis of Cardiac Resynchronization Therapy
Background. Approximately 20–40% of recipients of cardiac resynchronization therapy (CRT) do not respond to it based on the current patient selection criteria. The purpose of this study was to identify baseline parameters that can predict CRT response and to evaluate the effect of those predictive parameters on long-term prognosis. Methods. This was a retrospective, nonrandomized, noncontrolled cohort study. Patients who received CRT in our centre were divided into responders and nonresponders by the definition of CRT response (an increase in left ventricular ejection fraction (LVEF) of ≥5% and improvement of ≥1 New York Heart Association (NYHA) class from baseline to the 6-month follow-up). Results. Of the 101 patients, 68 were responders and 33 were nonresponders. Left ventricular end-diastolic diameter (LVEDD; OR: 0.88, 95% CI: 0.81–0.95, ) and QRS duration (OR: 1.07, 95% CI: 1.04–1.10, ) were independent predictors of CRT response. The combination of LVEDD and QRS duration was more valuable for predicting CRT response (AUC 0.836; 95% CI: 0.76–0.91; ). Moreover, the combination of LVEDD ≤ 71 mm and QRS duration ≥ 170 ms had a low incidence of all-cause mortality, HF hospitalisation, and the composite endpoint. In addition, baseline LVEDD had a positive correlation with QRS duration (, ). Responders to CRT had better LV reverse remodeling. Conclusion. The combination of LVEDD and QRS duration provided more robust prediction of CRT response. Moreover, the combination of LVEDD ≤ 71 mm and QRS duration ≥ 170 ms was associated with a low incidence of all-cause mortality, HF hospitalisation, and the composite endpoint. Our results may be useful to provide individualized patient selection for CRT.
The Impact of Statins before High-Risk CABG on Postoperative Multiple Organ Function
Background. The purpose of this cohort study was to investigate the independent relationship between preoperative statin therapy (PST) and postoperative severe multiorgan failure, measured by the Sequential Organ Failure Assessment (SOFA) maximum greater than 11, in high-risk patients undergoing isolated coronary artery bypass grafting (CABG). Methods. The present study is a perspective, single-center, cohort analysis enrolling high-risk patients undergoing CABG from Jan 1, 2018, to Dec 31, 2018, in Beijing Anzhen hospital. Results. Among a total of 880 high-risk patients undergoing isolated CABG included in this study, 503 (57.2%) experienced statin therapy before CABG. The SOFA maximum was significantly lower in the PST group compared with the control group (7.8 ± 3.0 v 9.2 ± 3.4, ). Multivariate logistic regression analysis demonstrated the incidence of the severe multiorgan dysfunction, measured by SOFA maximum ≥11, was dramatically reduced in the PST group (OR, 0.68, 95% CI 0.50–0.92, ). Furthermore, preoperative statin therapy (PST) might be associated with a decreased risk of postoperative major adverse cardiovascular and cerebral events and acute kidney injury, but an increased risk of postoperative hepatic inadequacy. Conclusion. SOFA maximum was significantly lower in the PST group compared with the control group and the incidence of the severe multiorgan dysfunction was dramatically reduced in the PST group. The findings of this study might shed new light on questions of positive or negative effects of PST on multiple organ function after high-risk CABG, so as to ultimately improve high-risk patient in-hospital outcomes from CABG.
Serum VEGF: Diagnostic Value of Acute Coronary Syndrome from Stable Angina Pectoris and Prognostic Value of Coronary Artery Disease
Background. Although the level of serum vascular endothelial growth factor (VEGF) is elevated in coronary artery disease (CAD) patients, its potential role in acute coronary syndrome (ACS) or stable angina pectoris (SAP) patients remains unclear. Objectives. To evaluate diagnostic accuracy of serum VEGF in determining ACS patients from SAP and analyze the association of serum VEGF with coronary artery lesions in SAP or the GRACE score in ACS, which is involved in the poor prognosis of low serum VEGF. Methods. 248 CAD patients and 48 healthy subjects were enrolled in this study. Serum VEGF levels were detected by using ELISA. The Gensini score or GRACE score was calculated among SAP or ACS patients. All the patients were followed up for a period of 12 months (mean: 10.77 months). Results. VEGF serum concentrations were higher in the ACS subgroup than in the SAP subgroup () with diagnostic accuracy of ACS from SAP (AUC: 0.667, sensitivity: 68.5%, specificity: 60.1%, ). Patients with high risk of Gensini score showed reduced VEGF levels () accompanied by a negative correlation (r = −0.396, ). Patients with a higher GRACE score indicated lower VEGF levels (). Low serum VEGF was one of the potential risk factors with adjusted HR of 0.531 (). Conclusion. Serum VEGF exhibits efficient diagnostic value for detection of ACS from SAP with a cutoff value of 648.75 pg/mL. Low serum VEGF indicates severe coronary artery lesions and a higher GRACE score, which suggests poor clinical outcomes.
Urine-Derived Induced Pluripotent Stem Cells in Cardiovascular Disease
Recent studies have demonstrated that stem cells are equipped with the potential to differentiate into various types of cells, including cardiomyocytes. Meanwhile, stem cells are highly promising in curing cardiovascular diseases. However, owing to the ethical challenges posed in stem cell acquisition and the complexity and invasive nature of the method, large-scale expansions and clinical applications in the laboratory have been limited. The current generation of cardiomyocytes is available from diverse sources; urine is one of the promising sources among them. Although advanced research was established in the generation of human urine cells as cardiomyocytes, the reprogramming of urine cells to cardiomyocytes remains unclear. In this context, it is necessary to develop a minimally invasive method to create induced pluripotent stem cells (iPSCs). This review focuses on the latest advances in research on urine-derived iPSCs and their application mechanisms in cardiovascular diseases.