Objective This study aimed to determine whether STE could help detect subclinical myocardial dysfunction in patients with CSFP. Methods Sixty patients with CSFP confirmed by CAG and 51 controls with normal coronary flow were prospectively enrolled. Coronary angiographic data and conventional and speckle tracking echocardiographic parameters of the LV and RV were obtained for every subject. Results Compared with controls, CSFP patients presented with higher BMI and TG levels, but lower HDL‐C levels. Conventional echocardiographic parameters of biventricular systolic and diastolic function did not differ between the two groups (all P > 0.05). The GLS of the LV and RV was significantly impaired in CSFP patients compared with that in controls (−19.03% vs −21.42%, P < 0.001 and −19.72% vs −22.96%, P = 0.001, respectively). The myocardial impairment pattern of CSFP patients was homogenous in the RV and heterogeneous in the LV, where only endo‐ and mid‐myocardial layers were affected. LV‐GLS and RV‐GLS were found to be well correlated with mTFC and HDL‐C in CSFP groups (r = 0.463 vs r = 0.439; r = −0.569 vs r = −0.552, all P < 0.05). ROC curve analysis demonstrated that LV‐GLS‐endo had the highest AUC (0.867, P < 0.001) for predicting subclinical myocardial impairment in CSFP patients. Conclusions Subclinical myocardial systolic dysfunction occurs in both ventricles, and GLS could be an effective method to detect early‐stage myocardial impairment in patients with CSFP.
Previous studies reported a controversial left ventricular (LV) function impairment and pathophysiology in patients with coronary slow flow (CSF). Greater arterial load has been shown to increase aortic impedance and endothelial shear stress, potentially affecting coronary anatomy and function. We investigated LV systolic function by a new layer-specific strain technology and assessed the association between pulsatile arterial load and contractility. A total of 70 patients with CSF and 50 controls with normal coronary angiography were included in the study. Layer-specific longitudinal and circumferential strains were assessed from endocardium, midmyocardium, and epicardium (global longitudinal strain (GLS)-endo, GLS-mid, GLS-epi and GCS-endo, GCSmid, GCS-epi) by two-dimensional speckle tracking imaging (2D-STI). Pulsatile arterial load was estimated by indexed arterial compliance (ACI). Layer-specific GLS showed a decreasing gradient from the endocardium to the epicardium in both the controls and CSF group. GLS-endo and GLS-mid in the CSF group were significantly lower than the control group (all P < 0.05). Layer-specific longitudinal strain showed a good correlation with the number of affected coronary arteries (all P < 0.05) and the mean thrombolysis in the myocardial infarction frame count (TFC) (all P < 0.05). ACI was lower in patients with CSF (P = 0.005), and ACI was correlated negatively with layer-specific GLS (all P < 0.05). Layer-specific evaluation of the LV provides an understanding of the layer-specific properties of the LV wall and the possible process of the LV impairment in patients with CSF. Greater pulsatile arterial load, as manifested by a lower ACI, is coupled with worse LV longitudinal function in patients with CSF.
The specific recognition of cancer cells by the body's immune system is an essential step in initiating antitumor immunity. However, the decreased expression of major histocompatibility complex class I (MHC-1) and overexpression of programmed death ligand 1 (PD-L1) causes insufficient tumor-associated antigens presentation and inactivation of T cells, which accounts for poor immunogenicity. To remodel tumor immunogenicity, herein, a dual-activatable binary CRISPR nanomedicine (DBCN) that can efficiently deliver a CRISPR system into tumor tissues and specifically control its activation is reported. This DBCN is made of a thioketal-cross-linked polyplex core and an acid-detachable polymer shell, which can maintain stability during blood circulation, while detaching a polymer shell to facilitate the cellular internalization of the CRISPR system after entering tumor tissues and ultimately activating gene editing under exogenous laser irradiation, thereby maximizing the therapeutic benefits and reducing potential safety concerns. With the collaborative application of multiple CRISPR systems, DBCN efficiently corrects both dysregulation of MHC-1 and PD-L1 expression in tumors, thus initiating robust T celldependent antitumor immune responses to inhibit malignant tumor growth, metastasis, and recurrence. Given the increasing abundance of CRISPR toolkits, this research provides an appealing therapeutic strategy and a universal delivery platform to develop more advanced CRISPR-based cancer treatments.
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