Regional Myocyte Hypertrophy Parallels Regional Myocardial Dysfunction During Post-infarct Remodeling

Kramer, Christopher M.; Rogers, W. Todd; Park, C S; Seibel, P.S.; Shaffer, Amy; Theobald, Therese M.; Reichek, Nathaniel; Onodera, Tatsuyuki; Gerdes, A. Martin

doi:10.1006/jmcc.1998.0741

Cited by 55 publications

(45 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…4,8,11,20,21 Sixty-two sheep completed the protocol (5 sheep died of ventricular arrhythmia on the day of infarction). All procedures followed were in accordance with the "Position of the American Heart Association on Research Animal Use," adopted by the Association in November 1984, and the Institutional Animal Care and Use Committee at Allegheny General Hospital.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…For analysis of regional intramyocardial function, breath-hold-tagged short-axis images were obtained spanning the LV from apex to base as previously described. 4,21 Imaging parameters included 7-mm slice thickness, 7-mm tag stripe separation, TR 70 ms (with view-sharing, yielding a 35-ms temporal resolution), TE 4 ms, 128ϫ56 matrix, 25-cm field of view, final interpolated pixel size 0.95 mm 2 , and 2 signal averages. The ventilator was held at end expiration during all breath-hold sequences.…”

Section: Magnetic Resonance Imagingmentioning

confidence: 99%

“…4,21 LVM, ESV, and EDV were then indexed to body weight in kilograms (LVMI, ESVI, and EDVI). Infarct size at 8 weeks was measured as the mass of thinned infarcted tissue from interleaved end-diastolic short-axis images and was expressed as a percentage of myocardial mass by previously published techniques that have been demonstrated to correlate highly with a pathological "gold standard" in this model.…”

Section: Mr Image Analysismentioning

confidence: 99%

“…L eft ventricular (LV) remodeling after myocardial infarction is characterized by infarct expansion, 1,2 myocyte hypertrophy, 3,4 myocyte slippage, 5 lengthening of noninfarcted segments, 6 -8 global ventricular dilatation, 7 and dysfunction in noninfarcted regions adjacent to the infarct. 8 ACE inhibition (ACEI) attenuates postinfarction LV remodeling in experimental models 9 -11 and improves survival in humans.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Combined Angiotensin II Receptor Antagonism and Angiotensin-Converting Enzyme Inhibition Further Attenuates Postinfarction Left Ventricular Remodeling

et al. 2001

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Experimental Protocolmentioning

confidence: 99%

Section: Magnetic Resonance Imagingmentioning

confidence: 99%

Section: Mr Image Analysismentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Combined Angiotensin II Receptor Antagonism and Angiotensin-Converting Enzyme Inhibition Further Attenuates Postinfarction Left Ventricular Remodeling

et al. 2001

Self Cite

View full text Add to dashboard Cite

show abstract

“…Myocardium surrounding the infarct becomes hypertrophied, and histological studies have shown early cellular changes remote from the infarct site within the first 24 hours. 15 Cardiac remodelling begins early after myocardial infarction even though the clinical consequences, especially cardiac failure and arrhythmia, may not be apparent until many years later.…”

Section: Cardiac Remodellingmentioning

confidence: 99%

Early initiation of ACE inhibitor treatment after acute myocardial infarction - a missed therapeutic opportunity?

Waring

2000

J Renin Angiotensin Aldosterone Syst

View full text Add to dashboard Cite

MR tagging early after myocardial infarction in mice demonstrates contractile dysfunction in adjacent and remote regions

Epstein

Yang

Gilson

et al. 2002

Magnetic Resonance in Med

Self Cite

132

101

View full text Add to dashboard Cite

The purpose of this study was to use MR myocardial tagging to assess regional cardiac function after myocardial infarction (MI) in mice. Eight mice were imaged before and 1 day after MI. MRI included cine imaging, myocardial tagging, and contrast-enhanced imaging. Regional percent circumferential shortening (%CS) was measured from the tagged images, and the region of hyperenhancement on the contrast-enhanced images was used to determine the infarcted, adjacent, and remote zones. Ejection fraction (EF) fell from 59% ؎ 6% at baseline to 32% ؎ 6% after MI (P < 0.01). At baseline, %CS was 14.5% ؎ 3.4%. After MI, %CS was 0.7% ؎ 4.4% in the infarcted zone, 7.4% ؎ 4.4% in the adjacent zone, and 11.8% ؎ 4.2% in the remote zone. %CS was statistically different for all comparisons between the infarcted, adjacent, remote, and baseline groups (P < 0.01 Transgenic and knockout mice can be used to study the genes and basic mechanisms involved in cardiovascular disease, and have therefore assumed a central role in modern cardiovascular research. Over the past 3 years, MRI has emerged as an accurate, noninvasive imaging modality for measuring murine cardiac structure and function in vivo (1-3). Examples demonstrating cardiac MRI in transgenic mouse research include studies of myocardial infarction (MI) (4) and left ventricular (LV) remodeling (5). To date, such studies have used MRI to measure myocardial mass, end-diastolic volume (EDV), end-systolic volume (ESV), and ejection fraction (EF). While such measures of global cardiac function are very useful, in the setting of coronary heart disease (where contractile dysfunction is generally localized to specific coronary territories) it is critically important to evaluate myocardial function on a regional basis. In the current study, we sought to demonstrate that myocardial tagging (6,7) could be used to measure regional contractile function in a mouse model of reperfused MI. METHODS Animal PreparationNine C57BL/6 mice were used in this study, which was approved by the University of Virginia Animal Care and Use Committee. MI was surgically induced as described previously (8). Briefly, mice were anesthetized, the upper portion of the trachea was exposed, and an endotracheal tube was inserted orally. Artificial respiration was maintained with an SAR-830/P ventilator (FiO2 of 0.80, rate of 100 strokes/min, stroke volume 2.0 -2.5 ml). After intubation, an incision was made to open the left pleural cavity. A piece of 7-0 silk suture was passed underneath the left anterior descending coronary artery (LAD) at the level of the lower left atrium and myocardial ischemia was induced by tying down the suture over PE-10 tubing. After 60 min of LAD occlusion, reperfusion was achieved by loosening the suture. Significant ECG changes (widening of the QRS wave and ST segment elevation as monitored with a PowerLab data recorder) and blanching within the region at risk were used to confirm coronary occlusion. A volume of 1-1.5 ml 5% dextrose was given intraperitoneally (i.p.) to replace fluids. Body...

show abstract

Regional Myocyte Hypertrophy Parallels Regional Myocardial Dysfunction During Post-infarct Remodeling

Cited by 55 publications

References 0 publications

Combined Angiotensin II Receptor Antagonism and Angiotensin-Converting Enzyme Inhibition Further Attenuates Postinfarction Left Ventricular Remodeling

Combined Angiotensin II Receptor Antagonism and Angiotensin-Converting Enzyme Inhibition Further Attenuates Postinfarction Left Ventricular Remodeling

Early initiation of ACE inhibitor treatment after acute myocardial infarction - a missed therapeutic opportunity?

MR tagging early after myocardial infarction in mice demonstrates contractile dysfunction in adjacent and remote regions

Contact Info

Product

Resources

About