Plasma-derived extracellular vesicles transfer microRNA-130a-3p to alleviate myocardial ischemia/reperfusion injury by targeting ATG16L1.

Extracellular vesicles (EVs) are implicated in myocardial ischemia/reperfusion (I/R) injury as modulators by shuttling diverse cargoes, including microRNAs (miRNAs). The current study was initiated to unravel the potential involvement of plasma-derived EVs carrying miR-130a-3p on myocardial I/R injury. Rats were induced with moderate endoplasmic reticulum stress, followed by isolation of plasma-derived EVs. Then, an I/R rat model and hypoxia/reoxygenation (H/R) cardiomyoblast model were established to simulate a myocardial I/R injury environment where miR-130a-3p was found to be abundantly expressed. miR-130a-3p was confirmed to target and negatively regulate autophagy-related 16-like 1 (ATG16L1) in cardiomyoblasts. Based on a co-culture system, miR-130a-3p delivered by EVs derived from plasma protected H/R-exposed cardiomyoblasts against H/R-induced excessive cardiomyoblast autophagy, inflammation, and damage, improving cardiac dysfunction as well as myocardial I/R-induced cardiac dysfunction and tissue injury. The mechanism underlying the functional role of EVs-loaded miR-130a-3p was found to be dependent on its targeting relation with ATG16L1. The protective action of EV-carried miR-130a-3p was further re-produced in a rat model serving as in vivo validation as evidenced by improved cardiac function, tissue injury, myocardial fibrosis, and myocardial infarction. Collectively, miR-130a-3p shuttled by plasma-derived EVs was demonstrated to alleviate excessive cardiomyoblast autophagy and improve myocardial I/R injury.

Quantitative Evaluation of Myocardial Strain After Myocardial Infarction with Cardiovascular Magnetic Resonance Tissue-Tracking Imaging.

To investigate the value of cardiovascular magnetic resonance tissue-tracking (CMR-TT) imaging in the differentiation of subendocardial and transmural myocardial infarction (MI) and determine whether strain parameters are enable to detect adverse left ventricular (LV) remodeling.Global peak circumferential, longitudinal, and radial strains (GPCS, GPLS, GPRS) and segmental peak circumferential, longitudinal, and radial strains (PCS, PLS, PRS) in accordance with the 16-segment model were all derived. All positive segments were divided into two groups according to transmural degree. All patients were dichotomized in accordance with the existence of LV remodeling, which was defined as infarct size (IS) > 24%.Patients with MI showed significant lower GPRS, GPCS, and GPLS than the control group (16.41% ± 8.92%, -8.77%± 3.51%, -7.54% ± 2.43% versus 32.41% ± 12.99%, -14.92% ± 3.32%, -11.50% ± 2.51%). Lower PRS [3.25% (-5.57, 7.835) versus 19.94% (12.50, 30.75), P < 0.001] and PCS (-3.81 ± 4.60% versus -8.97± 4.43%, P < 0.001) can be found in transmural infarcted segments compared to subendocardial infarcted segments. PLS between transmural and subendocardial infarcted segments (-4.03% ± 4.88% versus -4.34% ± 4.98%), without however statistical significance (P = 0.523). The optimal cutoff value for PRS in the discriminate diagnosis of MI was 8.97% with a sensitivity of 81.8% and specificity of 98.0%. The optimal cutoff value for PCS was -7.56% with a sensitivity of 83.6% and specificity of 72.1%. Receiver operating characteristic (ROC) analysis revealed an optimal cutoff GPRS of 15.45%, and GPCS of -6.72% yielded high diagnostic accuracy in the identification of remodeling, which was higher than left ventricular ejection fraction (LVEF).CMR-TT can differentiate between subendocardial and transmural infarction and detect LV remodeling, and the diagnostic value was superior to conventional functional parameters.

Two Patients with Coincident Noncompacted Myocardium and Hypertrophic Cardiomyopathy.

To our knowledge, left ventricular noncompaction (LVNC) and hypertrophic cardiomyopathy (HCM) commonly occur as separate disorders in different patients; however, LVNC associated with HCM, which is called hypertrophic LVNC, is relatively rare.1) Here we report two sporadic cases of hypertrophic LVNC which were diagnosed by echocardiography and cardiac magnetic resonance (CMR).

Left ventricular myocardial strain in ventricular arrhythmia without structural heart disease using cardiac magnetic resonance.

Ventricular arrhythmia (VA) in structurally normal heart is considered as benign. However, these arrhythmias have been recently reported to induce left ventricular (LV) dysfunction. Up to now, there is no efficacious method to detect abnormal myocardial systolic function in VA patients. Therefore, in the current study, we used cardiac magnetic resonance feature tracking (CMR-FT) on balanced steady state free precision (SSFP) cine images to investigate LV myocardial strain in 42 VA patients without known heart disease as well as in 29 normal volunteers. As compared with controls, VA patients had lower peak values of radial and circumferential strain (RS, CS) in both basal and middle parts of LV and the peak value of longitudinal strain (LS) in VA patients was also decreased in middle LV. Moreover, as revealed by LV myocardial segmental peak strain, reduced RS, CS and LS peaks in VA were more significant in anterior, inferoseptal and anterolateral segments, especially for the patients with frequent premature ventricular complexes. Our results suggested that VA in normal heart is associated with abnormal segmental wall motion, which can be efficaciously detected by CMR-FT derived strain analysis. And early clinical management should be considered to prevent further significant symptoms in these patients.

Evaluation of left ventricular strain in patients with dilated cardiomyopathy.

Objective Dilated cardiomyopathy (DCM) can cause structural and functional changes in the left ventricle (LV). In this study, we evaluated whether cardiac magnetic resonance tissue-tracking (MR-TT) can be applied to the detection of LV abnormalities in patients with DCM. Methods We used MR-TT to analyze the global peak radial strain (GPRS), global peak circumferential strain (GPCS), and global peak longitudinal strain (GPLS) in every segment of the LV in 23 patients with DCM and 25 controls. The LV ejection fraction was also measured as a function indicator. Results Compared with the controls, the GPRS, GPCS, and GPLS were significantly reduced in patients with DCM, indicating global LV function impairment in all directions. We also identified a significant linear correlation between the GPRS, GPCS, and GPLS and the LV ejection fraction, indicating that LV function relies on coordinated wall motion from all directions. Moreover, we found that patients with DCM had a significantly reduced magnitude of the PRS, PCS, and PLS in most segments at different levels, indicating impaired myocardial function in most LV regions. Conclusions Our results demonstrate that LV myocardial strain in patients with DCM can be sensitively detected by MR-TT (not only the global LV function changes but also the segmental strain), which can help to identify the injured segment at an early stage and guide clinical treatment.