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Distal coronary embolization following acute myocardial infarction increases early infarct size and late left ventricular wall thinning in a porcine model.

Thomas RM, Lim SY, Qiang B, Osherov AB, Ghugre NR, Noyan H, Qi X, Wolff R, Ladouceur-Wodzak M, Berk TA, Butany J, Husain M, Wright GA, Strauss BH - J Cardiovasc Magn Reson (2015)

Bottom Line: Animals were sacrificed at 3 h (n = 5), 3 days (n = 20) or 6 weeks (n = 20) post-AMI.Cardiovascular magnetic resonance (CMR), serum troponin-I, and cardiac gelatinase (MMP) and survival kinase (Akt) activities were assessed.The significance of the later remodelling changes (ventricular thinning and transmurality) following DCE, possibly due to changes in MMP-2 activity and Akt activation, merits further study.

View Article: PubMed Central - PubMed

Affiliation: Schulich Heart Centre, Sunnybrook Health Sciences Center, 2075 Bayview Avenue, Room D-406, Toronto, ON, M4N 3M5, Canada. reuben.thomas@mail.utoronto.ca.

ABSTRACT

Background: Distal coronary embolization (DCE) of thrombotic material occurs frequently during percutaneous interventions for acute myocardial infarction and can alter coronary flow grades. The significance of DCE on infarct size and myocardial function remains unsettled. The aims of this study were to evaluate the effects of DCE sufficient to cause no-reflow on infarct size, cardiac function and ventricular remodeling in a porcine acute myocardial infarction model.

Methods and results: Female Yorkshire pigs underwent 60 min balloon occlusion of the left anterior descending coronary artery followed by reperfusion and injection of either microthrombi (prepared from autologous porcine blood) sufficient to cause no-reflow (DCE), or saline (control). Animals were sacrificed at 3 h (n = 5), 3 days (n = 20) or 6 weeks (n = 20) post-AMI. Cardiovascular magnetic resonance (CMR), serum troponin-I, and cardiac gelatinase (MMP) and survival kinase (Akt) activities were assessed. At 3d, DCE increased infarct size (CMR: 18.8% vs. 14.5%, p = 0.04; serum troponin-I: 13.3 vs. 6.9 ng/uL, p < 0.05) and MMP-2 activity levels (0.81 vs. 0.49, p = 0.002), with reduced activation of Akt (0.06 versus 0.26, p = 0.02). At 6 weeks, there were no differences in infarct size, ventricular volume or ejection fraction between the two groups, although infarct transmurality (70% vs. 57%, p< 0.04) and ventricular thinning (percent change in mid anteroseptal wall thickness:-25.6% vs. 0.7%, p = 0.03) were significantly increased in the DCE group.

Conclusions: DCE increased early infarct size, but without affecting later infarct size, cardiac function or ventricular volumes. The significance of the later remodelling changes (ventricular thinning and transmurality) following DCE, possibly due to changes in MMP-2 activity and Akt activation, merits further study.

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Related in: MedlinePlus

Infarct characterization 6 weeks post-AMI. a Top panel: Representative LGE images showing differences in infarct transmurality (infarct indicated by arrows). Lower panel: Average infarct transmurality was increased in DCE group compared to controls (*p = 0.04) (Control n = 11; DCE n = 9). b Top panel: Representative short axis images showing the mid-anteroseptal segment (arrows). Bottom panel: Percent change in mid anteroseptal wall thickness at 6 weeks compared to baseline in control and DCE animals. Negative values represent wall thinning. DCE treated pigs had increased wall thinning compared to controls (**p = 0.03) (Control n = 11; DCE n = 9)
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Fig5: Infarct characterization 6 weeks post-AMI. a Top panel: Representative LGE images showing differences in infarct transmurality (infarct indicated by arrows). Lower panel: Average infarct transmurality was increased in DCE group compared to controls (*p = 0.04) (Control n = 11; DCE n = 9). b Top panel: Representative short axis images showing the mid-anteroseptal segment (arrows). Bottom panel: Percent change in mid anteroseptal wall thickness at 6 weeks compared to baseline in control and DCE animals. Negative values represent wall thinning. DCE treated pigs had increased wall thinning compared to controls (**p = 0.03) (Control n = 11; DCE n = 9)

Mentions: At 6 weeks, infarct size in both groups had significant decreased by 50 %. There were no significant differences in infarct size (measured in grams or percent of LV mass) between the DCE group and controls (Percent of LV mass: 7.7 ± 2.4 % versus 6.0 ± 2.1 %, respectively, p = NS) or infarct. The average transmurality across all infarcted myocardial slices was significantly elevated in the DCE group compared with controls (70 ± 10 % versus 57 ± 15 %, p < 0.04, Fig. 5).Fig. 5


Distal coronary embolization following acute myocardial infarction increases early infarct size and late left ventricular wall thinning in a porcine model.

Thomas RM, Lim SY, Qiang B, Osherov AB, Ghugre NR, Noyan H, Qi X, Wolff R, Ladouceur-Wodzak M, Berk TA, Butany J, Husain M, Wright GA, Strauss BH - J Cardiovasc Magn Reson (2015)

Infarct characterization 6 weeks post-AMI. a Top panel: Representative LGE images showing differences in infarct transmurality (infarct indicated by arrows). Lower panel: Average infarct transmurality was increased in DCE group compared to controls (*p = 0.04) (Control n = 11; DCE n = 9). b Top panel: Representative short axis images showing the mid-anteroseptal segment (arrows). Bottom panel: Percent change in mid anteroseptal wall thickness at 6 weeks compared to baseline in control and DCE animals. Negative values represent wall thinning. DCE treated pigs had increased wall thinning compared to controls (**p = 0.03) (Control n = 11; DCE n = 9)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4666124&req=5

Fig5: Infarct characterization 6 weeks post-AMI. a Top panel: Representative LGE images showing differences in infarct transmurality (infarct indicated by arrows). Lower panel: Average infarct transmurality was increased in DCE group compared to controls (*p = 0.04) (Control n = 11; DCE n = 9). b Top panel: Representative short axis images showing the mid-anteroseptal segment (arrows). Bottom panel: Percent change in mid anteroseptal wall thickness at 6 weeks compared to baseline in control and DCE animals. Negative values represent wall thinning. DCE treated pigs had increased wall thinning compared to controls (**p = 0.03) (Control n = 11; DCE n = 9)
Mentions: At 6 weeks, infarct size in both groups had significant decreased by 50 %. There were no significant differences in infarct size (measured in grams or percent of LV mass) between the DCE group and controls (Percent of LV mass: 7.7 ± 2.4 % versus 6.0 ± 2.1 %, respectively, p = NS) or infarct. The average transmurality across all infarcted myocardial slices was significantly elevated in the DCE group compared with controls (70 ± 10 % versus 57 ± 15 %, p < 0.04, Fig. 5).Fig. 5

Bottom Line: Animals were sacrificed at 3 h (n = 5), 3 days (n = 20) or 6 weeks (n = 20) post-AMI.Cardiovascular magnetic resonance (CMR), serum troponin-I, and cardiac gelatinase (MMP) and survival kinase (Akt) activities were assessed.The significance of the later remodelling changes (ventricular thinning and transmurality) following DCE, possibly due to changes in MMP-2 activity and Akt activation, merits further study.

View Article: PubMed Central - PubMed

Affiliation: Schulich Heart Centre, Sunnybrook Health Sciences Center, 2075 Bayview Avenue, Room D-406, Toronto, ON, M4N 3M5, Canada. reuben.thomas@mail.utoronto.ca.

ABSTRACT

Background: Distal coronary embolization (DCE) of thrombotic material occurs frequently during percutaneous interventions for acute myocardial infarction and can alter coronary flow grades. The significance of DCE on infarct size and myocardial function remains unsettled. The aims of this study were to evaluate the effects of DCE sufficient to cause no-reflow on infarct size, cardiac function and ventricular remodeling in a porcine acute myocardial infarction model.

Methods and results: Female Yorkshire pigs underwent 60 min balloon occlusion of the left anterior descending coronary artery followed by reperfusion and injection of either microthrombi (prepared from autologous porcine blood) sufficient to cause no-reflow (DCE), or saline (control). Animals were sacrificed at 3 h (n = 5), 3 days (n = 20) or 6 weeks (n = 20) post-AMI. Cardiovascular magnetic resonance (CMR), serum troponin-I, and cardiac gelatinase (MMP) and survival kinase (Akt) activities were assessed. At 3d, DCE increased infarct size (CMR: 18.8% vs. 14.5%, p = 0.04; serum troponin-I: 13.3 vs. 6.9 ng/uL, p < 0.05) and MMP-2 activity levels (0.81 vs. 0.49, p = 0.002), with reduced activation of Akt (0.06 versus 0.26, p = 0.02). At 6 weeks, there were no differences in infarct size, ventricular volume or ejection fraction between the two groups, although infarct transmurality (70% vs. 57%, p< 0.04) and ventricular thinning (percent change in mid anteroseptal wall thickness:-25.6% vs. 0.7%, p = 0.03) were significantly increased in the DCE group.

Conclusions: DCE increased early infarct size, but without affecting later infarct size, cardiac function or ventricular volumes. The significance of the later remodelling changes (ventricular thinning and transmurality) following DCE, possibly due to changes in MMP-2 activity and Akt activation, merits further study.

Show MeSH
Related in: MedlinePlus