Myocardial ischemia and reperfusion are associated with an increased stiffness of remote nonischemic myocardium.

Anesth Analg

Nullfield Department of Anesthetics, University of Oxford, Radcliffe Infirmary, United Kingdom.

Published: April 1996

During and after an ischemic injury, maintenance and recovery of cardiac function may critically depend on remote nonischemic myocardium. Graded myocardial ischemia is associated with an approximately 50% increase in stiffness of nonischemic myocardium. We determined whether this increase in stiffness is unique to the ischemic period or persists during reperfusion. Ten anesthetized (isoflurane 1.0% vol/vol) open-chest dogs were instrumented to measure left ventricular pressure and dimensions (sonomicrometry) in ischemic and nonischemic myocardium. Regional chamber stiffness and myocardial stiffness were assessed using the end-diastolic pressure-length relationship which was modified by stepwise infusion and withdrawal of 200 mL of the animals' own blood during baseline, 45 min low flow ischemia (systolic bulge), and 60 min after the onset of reperfusion. In remote nonischemic myocardium, regional myocardial ischemia was associated with a significant (P < 0.05) increase in chamber stiffness (+44%) and myocardial stiffness (+48%). Sixty minutes after the onset of reperfusion, chamber stiffness (+54%, P < 0.05 versus baseline) and myocardial stiffness (+55%, P < 0.05 versus baseline) remained increased. Thus, the ischemia-induced increase in stiffness of remote nonischemic myocardium persists for at least 60 min after reperfusion.

Download full-text PDF

Source
http://dx.doi.org/10.1097/00000539-199604000-00004DOI Listing

Publication Analysis

Top Keywords

nonischemic myocardium
24
remote nonischemic
16
myocardial ischemia
12
increase stiffness
12
chamber stiffness
12
myocardial stiffness
12
stiffness
10
stiffness remote
8
ischemia associated
8
myocardium regional
8

Similar Publications

Background/objectives: This study aimed to evaluate layer-specific strain according to etiology and assess whether subtle changes in longitudinal and circumferential layer strain are involved in predicting cardiac mortality during a two-year follow-up in patients with dilated cardiomyopathy admitted with heart failure decompensation.

Methods: 97 patients with dilated cardiomyopathy and a left ventricle ejection fraction ≤ 40% were recruited, 51 with ischemic and 46 with nonischemic etiologies. Conventional and two-dimensional speckle-tracking echocardiography (2D-STE) were conducted in dilated cardiomyopathy patients with a compensated phase of heart failure before discharge.

View Article and Find Full Text PDF

Fibroblasts play a pivotal role in key processes within the heart, particularly in cardiac remodeling that follows both ischemic and non-ischemic injury. During remodeling, fibroblasts drive fibrosis and inflammation by reorganizing the extracellular matrix and modulating the immune response, including toll-like receptor (TLR) activation, to promote tissue stabilization. Building on findings from our prior research on heart tissue from patients with advanced coronary artery disease and aortic valve disease, this study sought to explore specific effects of TLR1, TLR3, and TLR7 activation on NF-κB signaling, proinflammatory cytokine production, and γ-protocadherin expression in cardiac fibroblasts.

View Article and Find Full Text PDF

Background: Better risk stratification is needed to evaluate patients with non-ischemic cardiomyopathy (NICM) for prophylactic implantable cardioverter-defibrillators (ICD). Growing evidence suggests cardiac magnetic resonance imaging (CMR) may be useful in this regard.

Objective: We aimed to determine if late-gadolinium enhancement (LGE) seen on CMR (dichotomized as none/minimal <2% vs significant ≥2%) predicts appropriate ICD therapies (primary endpoint) and/or all-cause mortality/transplant/left-ventricular assist device (LVAD) implantation (secondary endpoint) in NICM patients.

View Article and Find Full Text PDF

The heart is a dynamic pump whose function is influenced by its mechanical properties. The viscoelastic properties of the heart, i.e.

View Article and Find Full Text PDF

DSG2, encoding desmoglein-2, is one of the causative genes of arrhythmogenic cardiomyopathy. We previously identified a homozygous DSG2 p.Arg119Ter stop-gain variant in a patient with juvenile-onset cardiomyopathy and advanced biventricular heart failure.

View Article and Find Full Text PDF

Want 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!