Literature DB >> 2033197

Acute effects of delayed reperfusion on myocardial infarct shape and left ventricular volume: a potential mechanism of additional benefits from thrombolytic therapy.

E J Brown1, R D Swinford, P Gadde, O Lillis.   

Abstract

The purpose of this study was to characterize the effects of late reperfusion on myocardial infarct shape and to quantitate associated changes in left ventricular volume. Reperfusion was delayed until there was no salvage of ischemic myocardium. Dogs underwent 6.5 h of left anterior descending coronary artery occlusion (n = 5) or 5.5 h of occlusion and 1 h of reperfusion (n = 5). Infarct shape was measured with pairs of ultrasonic crystals implanted circumferentially in the mid myocardium. Infarct stiffness was determined from end-diastolic pressure-segment length curves produced by aortic clamping. Left ventricular volume was measured with three pairs of endocardial ultrasonic crystals and the effect of infarct shape change on left ventricular volume was determined. Infarct size, expressed as a percent of the area at risk, was similar in reperfused (97 +/- 1%) and nonreperfused (98 +/- 1%) hearts. After coronary artery occlusion, infarct segments became akinetic and functional dilation, measured as end-diastolic ultrasonic crystal separation, increased to a similar extent in reperfused (24 +/- 7%) and nonreperfused (19 +/- 3%) hearts. In 13 additional dogs that underwent reperfusion and instrumentation with endocardial ultrasonic crystals for volume measurement, left ventricular volume increased 42 +/- 6% over the preocclusion level (p less than 0.001). Within minutes of reperfusion, the infarct stiffened, infarct dilation decreased to 1 +/- 4% over the baseline preocclusion level (p less than 0.05 vs. prereperfusion) and left ventricular volume decreased to 16 +/- 11% over the baseline level (p less than 0.01 vs. postocclusion). Thus, coronary artery reperfusion reverses initial infarct dilation. Changes in infarct dilation occur immediately after reperfusion and are accompanied by infarct stiffening and a decrease in left ventricular volume. Reperfusion can affect infarct shape and stiffness at a point in time when myocardial salvage is no longer possible.

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Year:  1991        PMID: 2033197     DOI: 10.1016/0735-1097(91)90660-2

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


  6 in total

1.  Coronary Artery Patency and Survival in Clinical Trials.

Authors: 
Journal:  J Thromb Thrombolysis       Date:  1997       Impact factor: 2.300

2.  The Open-Artery Hypothesis: An Overview.

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Journal:  J Thromb Thrombolysis       Date:  1997       Impact factor: 2.300

Review 3.  Why Is Infarct Expansion Such an Elusive Therapeutic Target?

Authors:  William J Richardson; Jeffrey W Holmes
Journal:  J Cardiovasc Transl Res       Date:  2015-09-21       Impact factor: 4.132

Review 4.  Physiological Implications of Myocardial Scar Structure.

Authors:  William J Richardson; Samantha A Clarke; T Alexander Quinn; Jeffrey W Holmes
Journal:  Compr Physiol       Date:  2015-09-20       Impact factor: 9.090

5.  Effects of Late Coronary Artery Reperfusion on Left Ventricular Remodeling Persist for 10 Weeks After Experimental Rat Myocardial Infarction and Are Associated with Improved Survival.

Authors: 
Journal:  J Thromb Thrombolysis       Date:  1994       Impact factor: 2.300

6.  Significance of perfusion of the infarct related coronary artery for susceptibility to ventricular tachyarrhythmias in patients with previous myocardial infarction.

Authors:  H V Huikuri; M J Koistinen; K E Airaksinen; M J Ikäheimo
Journal:  Heart       Date:  1996-01       Impact factor: 5.994

  6 in total

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