AI Article Synopsis
Article Abstract
Objectives: Considering the recent discovery of postconditioning, we investigated whether intermittent dyssynchrony immediately upon reperfusion induces cardioprotection as well.
Background: Intermittent dyssynchrony, induced by ventricular pacing, preconditions myocardium.
Methods: Isolated ejecting rabbit hearts were subjected to 30-min coronary occlusion and 2-h reperfusion. Control, left ventricular (LV) pacing preconditioning (LVPpreC) (3 x 5-min LV pacing), and LV pacing postconditioning (LVPpostC) (10 x 30-s LV pacing during early reperfusion) groups were studied. Mechanical effects of LV pacing were determined using local pressure-length loops (sonomicrometry), whereas effects on myocardial lactate release and coronary flow were assessed from coronary effluent and fluorescent microspheres, respectively. Anesthetized pigs underwent 60-min coronary occlusion and 3-h reperfusion in control and right ventricular (RV) pacing postconditioning groups (RVPpostC) (10 x 30-s RV pacing during early reperfusion). In all hearts, area at risk and infarct size were determined with blue dye and triphenyltetrazolium chloride staining, respectively.
Results: Infarct size, normalized to area at risk, was 47.0 +/- 12.3% in control rabbit hearts, but significantly smaller in LVPpreC (17.8 +/- 6.4%) and LVPpostC hearts (17.9 +/- 4.4%). Left ventricular pacing significantly altered regional mechanical work, but did not affect coronary flow or lactate release. In pigs, infarct size was significantly smaller in RVPpostC (9.8 +/- 3.0%) than in control (20.6 +/- 2.2%) animals.
Conclusions: Intermittent dyssynchrony during early reperfusion reduces infarct size in 2 different animal models. Dyssynchrony-induced postconditioning cannot be attributed to graded reperfusion but may be induced by modulation of local myocardial workload. Dyssynchrony-induced postconditioning opens new possibilities for cardioprotection in the clinical setting.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jacc.2007.01.070 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Lipoprotein(a) and the risk of type I cardiorenal syndrome in patients with coronary artery disease: A retrospective clinical study.
Int J Cardiol Heart Vasc
February 2025
Shaoxing Central Hospital, No. 1 Huayu Road, Keqiao District, Shaoxing Province, 312030, China.
Objective: The present study aimed to investigate the correlation between lipoprotein(a) (Lp-a) and coronary artery disease (CAD) complicated by type I cardiorenal syndrome (CRS).
Methods: We conducted a retrospective analysis of patients diagnosed with CAD admitted to the Department of Cardiovascular Medicine at Shaoxing Central Hospital from January 2021 to December 2022, with chief complaints of "chest distress and dyspnea." Patient demographic data, biochemical indicators (including blood lipid levels and serum creatinine), cardiac function markers (such as pro-brain natriuretic peptide, pro-BNP), echocardiography, and coronary angiography results were collected.
Enhancing cardiac regeneration: direct reprogramming of fibroblasts into myocardial-like cells using extracellular vesicles secreted by cardiomyocytes.
Mol Cell Biochem
December 2024
Henan Key Laboratory of Medical Tissue Regeneration, Xinxiang Medical University, Henan Xinxiang, 453003, People's Republic of China.
To investigate the promoting effect of extracellular vesicles derived from myocardial cells (CM-EVs) on the reprogramming of cardiac fibroblasts (CFs) into cardiomyocyte-like cells (iCMs) and their therapeutic effect on myocardial infarction (MI) in rats. Cell experiments: The differential adhesion method was used to obtain Sprague Dawley (SD) suckling rat CFs and cardiomyocytes (CMs), while the ultracentrifugation method was used to obtain CM-EVs. Transmission electron microscopy and nanoparticle tracking technology were used to analyze and determine the morphology and particle size of CM-EVs.
View Article and Find Full Text PDFBRD4 inhibition rewires cardiac macrophages toward a protective phenotype marked by low MHC class II expression.
Am J Physiol Heart Circ Physiol
December 2024
Department of Medicine, Division of Cardiology, University of Colorado Anschutz Medical Campus; Aurora, CO, USA.
Bromodomain and extra-terminal domain (BET) proteins, including BRD4, bind acetylated chromatin and co-activate gene transcription. A BET inhibitor, JQ1, prevents and reverses pathological cardiac remodeling in preclinical models of heart failure. However, the underlying cellular mechanisms by which JQ1 improves cardiac structure and function remain poorly defined.
View Article and Find Full Text PDFBackground: Loss of stromal interaction molecule 1 (STIM1) expression in smooth muscle cells protects against ischemia-reperfusion (I/R) injury. Whether and how decreased STIM1 expression in cardiomyocytes (CM) impacts cardiac remodeling in response to I/R injury remains unknown.
Objective: To examine mechanisms by which decreased CM-STIM1 expression in the adult heart modulates cardiac function before and after I/R injury.
Metabolomics study of APETx2 post-conditioning on myocardial ischemia-reperfusion injury.
Front Pharmacol
December 2024
Department of Anesthesiology, The Affiliated Baiyun Hospital of Guizhou Medical University, Guiyang, Guizhou Province, China.
Background: Acid-sensing ion channels are activated during myocardial ischemia and are implicated in the mechanism of myocardial ischemia-reperfusion injury (MIRI). Acid-sensing ion channel 3 (ASIC3), the most pH-sensitive member of the ASIC family, is highly expressed in myocardial tissues. However, the role of ASIC3 in MIRI and its precise effects on the myocardial metabolome remain unclear.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!