Aims: This study aimed to compare the diagnostic accuracy of stress myocardial perfusion imaging between cardiac magnetic resonance (CMR) and nuclear medical imaging, including single-photon emission computed tomography (SPECT) and positron emission tomography (PET), for the diagnosis of hemodynamically significant coronary artery disease (CAD) with fractional flow reserve (FFR) as the reference standard. Methods and results: We searched PubMed and Embase for all published studies that evaluated the diagnostic accuracy of stress myocardial perfusion imaging modalities, including CMR, SPECT, and PET, to diagnose hemodynamically significant CAD with FFR as the reference standard. A total of 28 articles met the inclusion criteria and were included in the meta-analysis: 14 CMR, 13 SPECT, and 5 PET articles. The results demonstrated a pooled sensitivity of 0.88 (95% confidence interval [CI]: 0.80-0.93), 0.69 (95% CI: 0.56-0.79), and 0.83 (95% CI: 0.70-0.91), and a pooled specificity of 0.89 (95% CI: 0.85-0.93), 0.85 (95% CI, 0.80-0.89), and 0.89 (95% CI, 0.86-0.91) for CMR, SPECT, and PET, respectively. The area under the curve (AUC) of CMR, PET, and SPECT was 0.94 (95% CI, 0.92-0.96), 0.92 (95% CI, 0.89-0.94), and 0.87 (95% CI, 0.83-0.89), respectively. Conclusions: CMR and PET both have high accuracy and SPECT has moderate accuracy to detect hemodynamically significant CAD with FFR as the reference standard. Furthermore, the diagnostic accuracy of CMR at 3.0 T is superior to 1.5 T. (C) 2019 Elsevier B.V. All rights reserved.
Plaque progression prediction is of fundamental significance to cardiovascular research and disease diagnosis, prevention, and treatment. Magnetic resonance image (MRI) data of carotid atherosclerotic plaques were acquired from 20 patients with consent obtained. 3D thin-layer models were constructed to calculate plaque stress and strain. Data for ten morphological and biomechanical risk factors were extracted for analysis. Wall thickness increase (WTI), plaque burden increase (PBI) and plaque area increase (PAI) were chosen as three measures for plaque progression. Generalized linear mixed models (GLMM) with 5-fold cross-validation strategy were used to calculate prediction accuracy and identify optimal predictor. The optimal predictor for PBI was the combination of lumen area (LA), plaque area (PA), lipid percent (LP), wall thickness (WT), maximum plaque wall stress (MPWS) and maximum plaque wall strain (MPWSn) with prediction accuracy = 1.4146 (area under the receiver operating characteristic curve (AUC) value is 0.7158), while PA, plaque burden (PB), WT, LP, minimum cap thickness, MPWS and MPWSn was the best for WTI (accuracy = 1.3140, AUC = 0.6552), and a combination of PA, PB, WT, MPWS, MPWSn and average plaque wall strain (APWSn) was the best for PAI with prediction accuracy = 1.3025 (AUC = 0.6657). The combinational predictors improved prediction accuracy by 9.95%, 4.01% and 1.96% over the best single predictors for PAI, PBI and WTI (AUC values improved by 9.78%, 9.45%, and 2.14%), respectively. This suggests that combining both morphological and biomechanical risk factors could lead to better patient screening strategies. (C) 2019 Elsevier B.V. All rights reserved.
Objective: To evaluate the role of YKL-40 as a biomarker of disease activity in patients with Takayasu arteritis (TA). Methods: The study included 40 patients diagnosed with TA between January 2017 and January 2018. 40 age and sex matched healthy controls were included. Serum levels of YKL-40, as well as IL-6, IL-8, IL-17, sCD163, VEGF, MMP-2, MMP-9, OPN, PTX-3 and IFN-gamma, were detected at the base line and end of the 6-month follow-up. Modified Kerr criteria, in which MRA was performed instead of traditional angiography, was used a standard measure of disease activity. The association of the measured biomarkers with disease activity was analysed. Results: The serum levels of YKL-40, IL-6, IL-8, IFN-gamma, MMP-2, MMP-9, PTX-3 and OPN were significantly higher in active disease than in inactive disease. Significant differences in the serum levels of YKL-40, IL-6 and PTX-3 were also observed according to the disease activity degree. Logistic analysis demonstrated that high YKL-40 levels and high IL-6 levels were independent risk factors for active disease. When YKL-40 was combined with IL-6, the specificity and sensitivity for detecting active disease were increased (87.6% and 70.4% respectively); similar findings were obtained when YKL-40 was combined with CRP (72.3% and 84.6% respectively). A predictive model of active disease using ESR, CRP, IL-6, PTX-3 and MMP-9 showed significantly improved diagnostic efficiency when YKL-40 was added to the model (sensitivity: 85.1%; specificity: 94.3%; NRI value: 12.4%; IDI value: 4.6%, p < 0.05). Conclusions: Serum YKL-40 concentrations may be a useful biomarker of disease activity in TA. (C) 2019 Elsevier B.V. All rights reserved.
Objective: The aim of this study is to identify the mutation spectrum of FBN1 in patients with Marfan syndrome (MFS) or Marfan-Like Phenotypes and to analyze the genotype-phenotype correlations of existing literature. Methods and results: A total of 21 unrelated patients with a definite or suspected clinical diagnosis of MFS were recruited for research. Eleven FBN1 mutations were identified in 12 patients who strictly fulfilled the Ghent criteria for MFS, and 1 FBN1 mutations were detected in 9 patients with suspected MFS by screening the mutations of FBN1. These FBN1 mutations include 10 novel mutations (c. 357 C>A, c. 493 C>T, c. 1374 T>A, c. 4143 delG, c. 6987 C>G, c. 7238 G>A, c. 7765 A>G, c. 8200 A>G, c. 8431 G>A, c. 8547 T>G,) and 2 previously reported mutations (c. 4567 C>T, c. 4615 C>T). By searching PubMed and Embase (from 1990 up to December 2018), twenty nine studies (including the present study) with 890 subjects with MFS or Marfan-like phenotypes were included to analyze the genotype-phenotype correlations. Several genotype-phenotype correlations were founded. Firstly, mutations of premature termination codons (PTC) were associated with an increased risk of major cardiovascular involvements. Secondly, the frequency of patients with major cardiovascular involvement in exons 43-65 group was as high as that in exons 24-32 group (71.4% vs. 77.0%; p = 0.238). Finally, cysteine missense mutations might be associated with major cardiovascular involvements. Conclusions: These results extended the FBN1 mutation spectrum of this rare disease and revealed the genotype-phenotype correlations in MFS by analyzing existing literature. (C) 2019 Elsevier B.V. All rights reserved.
Objectives: Concerns about safety make physicians reluctant to prescribe neprilysin-renin-angiotensin system (RAS) inhibitors. This meta-analysis was performed to assess the efficacy and safety of combined neprilysin and RAS inhibition in heart failure. Background: Combined inhibitors of neprilysin and RAS reduced heart failure hospitalization and cardiovascular death. While adverse events of neprilysin-RAS inhibitors in clinical trials are still controversial. Methods: Medline, the Cochrane Library and Clinicaltrials.gov were searched for randomized controlled trials (RCTs). Twelve studies covering 21,212 patients were eligible for inclusion. Results: Compared with RAS inhibition, neprilysin-RAS inhibition had a significant decrease in the mortality of heart failure [Odds Ratio (OR) 0.84; 95% Confidence Interval (CI) 0.78-0.91; P < 0.05], cardiovascular death (OR 0.78; 95% CI 0.69-0.88; P < 0.05), all-cause death (OR 0.86; 95% CI 0.79-0.93; P < 0.05) and the occurrence of renal dysfunction (OR 0.78; 95% CI 0.63-0.96; P < 0.05). The incidence of hypotension (OR 1.44; 95% CI 1.15-1.80; P < 0.05) and dizziness (OR 1.46; 95% CI 1.32-1.62; P < 0.05) was obviously increased in neprilysin-RAS inhibition compared with RAS inhibition. There were no significant differences in any adverse events, serious adverse events, myocardial ischemia, angioedema, hyperkalemia, fatigure, cough, gastrointestinal disorders and infections compared neprilysin-RAS inhibition with RAS inhibition alone. Conclusions: The available evidence are supportive of the use of combined neprilysin and RAS inhibition in heart failure with close observation of blood pressure. (C) 2019 Elsevier B.V. All rights reserved.
Background: Recent studies showed bioresorbable scaffold (BRS) increased risks of late target lesion failure (TLF) and thrombosis. XINSORB scaffold is a poly-L-lactic acid based BRS. Methods: The study included randomization and registry parts. Eligible patients with one or two de novo lesions were randomly 1:1 assigned to XINSORB scaffold and sirolimus-eluting stent (SES) in randomization part. These patients were clinically and angiographically assessed. In registry part, patients were treated with XINSORB scaffold only and were clinically assessed. The primary endpoint was in-segment late luminal loss (LLL) at 12-month in randomization part. The secondary endpoint was 12-month TLF in all XINSORB-treated patients. Results: Total 395 and 798 patients were enrolled in randomization and registry part, respectively. Device success was 98.0% (1069/1091) in all XINSORB-treated and 100% (221/221) in SES-treated lesions. The primary endpoint of in-segment LLL at 12-month was 0.19 +/- 0.32 mm in XINSORB and 0.31 +/- 0.41 mm in SES (P=0.003), which met the noninferior margin of 0.195 mm (95% CI: -0.20, -0.04, P << 0.0001). No difference was found in TLF between two devices. In all XINSORB-treated patients, 12-month TLF was 0.8% (8/998), which also met the noninferior margin of 9.0% (95% CI: 0.3%, 1.4%, P << 0.0001). Only one device thrombosis was recorded in all XINSORB-treated patients while none in SES. Conclusions: In the multicenter clinical trial, XINSORB BRS was noninferior to sirolimus-eluting stent for the primary endpoint of in-segment LLL at 12-month in patients with simple and moderate complex de novo coronary lesions. TLF at 12-month was low and comparable. (C) 2019 Published by Elsevier B.V.
Background: Long axis strain (LAS) is a parameter derived from standard cardiovascular magnetic resonance imaging. However, the prognostic value of biventricular LAS in hypertrophic cardiomyopathy (HCM) is unknown. Methods: Patients with HCM (n = 384) and healthy volunteers (n = 150) were included in the study. Left ventricular (LV)-LAS was defined as the percentage change in the length measured from the epicardial border of the LV apex to the midpoint of a line connecting the mitral annulus at end-systole and end-diastole. Right ventricular (RV)-LAS represented the percentage change of length between epicardial border of the LV apex to the midpoint of a line connecting the tricuspid annulus at end-systole and end-diastole. The primary endpoint was a combination of all-cause death and sudden cardiac death aborted by appropriate implantable cardioverter-defibrillator discharge and cardiopulmonary resuscitation after syncope. The secondary endpoint was a combination of the primary endpoint and hospitalization for congestive heart failure. Results: Twenty-nine patients (7.6%) achieved the primary endpoint, and the secondary endpoint occurred in 66 (17.2%) patients. In multivariate Cox regression analysis, RV-LAS was an independent prognostic factor for the primary (hazard ratio (HR), 1.13) and secondary (HR, 1.11) endpoints. In the subgroup of patients with a normal RV ejection fraction (EF) (>45.0%, n = 345), impaired RV-LAS was associated with adverse outcomes and might add incremental prognostic value to RVEF and tricuspid annular plane systolic excursion (TAPSE) (p < 0.01). Conclusions: RV-LAS is an independent predictor of adverse prognosis in HCM in addition to RVEF and TAPSE. (C) 2019 Elsevier B.V. All rights reserved.