| Objective:The purpose of the study was to use velocity vector imaging (VVI) to evaluate evolutions of left ventricular regional and global functional within 8 weeks after myocardial infarction induced by occlusion of coronary artery in New Zealand white rabbits. Characteristics of cardiac mechanics in normal rabbits were also established. Another purpose was to investigate value of VVI combing with low dose dobutamine stress in assessing myocardial viability after myocardial infarction.Methods:Forty five male New Zealand white rabbits were divided into sham operation group (SH group) and myocardial infarction group (MI group). Dynamic cardiac images of left long axis views, short axis views at mitral valve level, papillary muscle level and apex level were collected 1 day before, as well as 1 day,3 days,1 week,2 weeks,4 weeks and 8 weeks after myocardial infarction. Low dose dobutamine stress testing was performed 8 weeks after myocardial infarction and dynamic cardiac images were also collected. All of these images were analyzed off-line using VVI software. At the end of the experiment, hearts were removed from chest, with triphenyltetrazolium chloride staining (TTC), hematoxylin and eosin staining (HE), and electron microscope examinations.Results:In basic condition, longitudinal velocity decreased from basal to apical segment (p<0.05), strain and strain rate did not change (p>0.05); radial velocity in anteroseptal and anterior segment were greater than that in other segments at the same level (p<0.05), whereas greatest circumferential strain and strain rate located in anterior and lateral segment (p<0.05); rotation of the base and apex of left ventricle in opposite direction during systole and diastole were observed; rotate angle, rotate velocity and recoiling velocity at apical level were greater than that at basal level (p<0.05); twist angle of left ventricle was 10.76±2.24°Ejection fraction and fractional shortening decreased after myocardial infarction (p<0.05). WI parameters reflecting long-aixs and short-axis motion in both infarction and margin segment decreased dramatically 1 day after myocardial infarction (p<0.05), and deteriorated gradually until 4 week. In non-infarction segment, longitudinal velocity, strain, and strain rate decreased 1 day after myocardial infarction but without significance (p<0.05). Two weeks later, longitudinal parameters were statistically lower than that pre-operative (p<0.05). Radial velocity, circumferential strain and strain rate in non-infarction segment increased 1 and 3 days after myocardial infarction with significance (p<0.05), whereas decreased subsequently. Rotate angle, rotate velocity, and recoiling velocity decreased both at basal and apical level (p<0.05). Changes at apical level were greater than that at basal level. Twist angle, twist velocity, and untwisting velocity of left ventricle also decreased after myocardial infarction (p<0.05).Strain and strain rate did not change in non-viable segment after infusion of dobutamine (p>0.05). Systolic strain and strain rate in viable segment significantly increased after dobutamine infusion (p<0.05), diastolic parameters also increased but without significance (p>0.05).Myocardial infarction was confirmed by TTC and HE staining. Under electron microscope examination, myocardium was replaced by scar tissue in infarction area. Myofibril depletion and disorganization, mitochondria depletion and vacuolation were also observed in margin area.Conclusions:1. Changes of regional myocardial function occurred after myocardial infarction:①as time went, regional long-axis and short-axis motion both in infarction and margin area gradually decreased until 4 week, with parameters in infarction area lower than that in margin area.②Transient compensative enhancement of myocardial short-axis motion was observed, following with regional dysfunction.③Systolic twist and diastolic untwisting decreased after myocardial infarction, which was mainly caused by changes at apical level.2. Velocity, strain and strain rate could be used to differentiate infarct from non-infarct myocardium, with strain and strain rate better than velocity, long-axis parameters better than short-axis parameters. 3. Changes of myocardial mechanics are based on changes of ultrastructure after myocardial infarction.4. VVI combining with low dose dobutamine stress could also be used to assess myocardial viability after myocardial infarction, with short-axis parameters better than long-axis parameters.5. VVI can be used to quantitatively evaluate myocardial mechanics in rabbits. Regular patterns of heart motion were found in normal rabbits.
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