Significant Improvement in Severely Stunned Left Ventricle after Percutaneous Coronary Intervention [PDF]
Journal of Tehran University Heart Center, 2008 This is a case of severely stunned left ventricle which occurred after a non-ST elevation myocardial infarction in a 76-year-old woman who was a known case of three-vessel disease. Her symptoms and cardiac function responded well to revascularization.
Gholamreza Davoodi +5 more
doaj +2 more sources
Non-invasive imaging in detecting myocardial viability: Myocardial function versus perfusion
International Journal of Cardiology: Heart & Vasculature, 2014 Coronary artery disease (CAD) is the most prevalent and single most common cause of morbidity and mortality [1] with the resulting left ventricular (LV) dysfunction an important complication.
Iqbal A. Elfigih, Michael Y. Henein
doaj +1 more source
Glucagon-like peptide-1 derived cardioprotection does not utilize a KATP-channel dependent pathway: mechanistic insights from human supply and demand ischemia studies. [PDF]
, 2016 BACKGROUND: Glucagon-like peptide-1 (7-36) amide (GLP-1) protects against stunning and cumulative left ventricular dysfunction in humans. The mechanism remains uncertain but GLP-1 may act by opening mitochondrial K-ATP channels in a similar fashion to ...
Axell, Richard G +11 more
core +4 more sources
Contrast echocardiography in the diagnosis of myocardial stunning [PDF]
Clinical Cardiology, 1999 AbstractThe identification of viable myocardium within dysfunctional myocardium has important clinical implications. By using a microvascular tracer, myocardial contrast echocardiography may have the potential for prediction of myocardial viability in the acute and subacute phases of myocardial infarction.
Nagy A +6 more
openaire +5 more sources
Advanced Nanoparticle Therapeutics for Targeting Neutrophils in Inflammatory Diseases
Advanced Healthcare Materials, EarlyView.This review highlights recent advances in nanoparticle‐based strategies to modulate neutrophil activity in inflammatory diseases. By targeting inflammatory neutrophils, NET formation, and neutrophil apoptosis or recruitment, these approaches aim to improve therapeutic precision.
Min Ji Byun +9 more
wiley +1 more source
Myocardial dysfunction after out-of-hospital cardiac arrest: predictors and prognostic implications. [PDF]
, 2018 We aim to determine the incidence of early myocardial dysfunction after out-of-hospital cardiac arrest, risk factors associated with its development, and association with outcome.
Gaieski, David Foster +5 more
core +1 more source
The heartbreak of depression: 'Psycho-cardiac' coupling in myocardial infarction [PDF]
, 2017 Ample evidence identifies strong links between major depressive disorder (MDD) and both risk of ischemic or coronary heart disease (CHD) and resultant morbidity and mortality. The molecular mechanistic bases of these linkages are poorly defined. Systemic
Budiono, Boris P +5 more
core +1 more source
Engineering Aging: Approaches to Model and Deconstruct Biological Complexity
Advanced Materials, EarlyView.The macro‐experiences of aging are the result of an accumulation of micro‐changes that occur over time. Abstract The disparity between the global increase in life expectancy and the steady decline in health outcomes with age has been a major driver for developing new ways to research aging.
Habib Joukhdar +7 more
wiley +1 more source
Bridging the Gap in a Rare Cause of Angina
European Cardiology Review, 2021 Myocardial bridging occurs when coronary arteries run intramurally. Episodes of tachycardia can cause a dynamic obstruction that extends into diastole, compromising coronary filling time, and subsequently leading to ischaemia. Myocardial ischaemia, acute
Sumanth Khadke +2 more
doaj +1 more source
Acute cardiac inflammatory responses to postischemic reperfusion during cardiopulmonary bypass [PDF]
, 1999 Objectives: The investigation centers on whether there is a reperfusion-induced specific cardiac inflammatory reaction after bypass surgery. Background: Cardiopulmonary bypass (CPB) leads to systemic inflammation.
Becker, Bernhard F. +5 more
core +1 more source