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Quantitative and Qualitative Characterization of the Acute Changes in Myocardial Structure and Function after Distal Coronary Microembolization Using MDCT

Rationale and Objectives

To determine the potential of multidetector computed tomography (MDCT) in assessing, at 72 hours, the effects of distal coronary microembolization on myocardial structure and function.

Materials and Methods

Microembolic material (total volume=16 mm 3 of 40–120 μm diameter) was selectively delivered in the left anterior descending coronary artery under x-ray fluoroscopy ( n = 6 pigs). After 72 hours, 64-slice MDCT was used to assess LV function, perfusion, and viability. For comparison between the measurements at 80 kV, 120 kV, and postmortem we used Bland-Altman and Pearson correlation. Histochemical and histopathological staining was used for quantitative and qualitative characterization of microinfarct.

Results

Cine MDCT showed the deleterious effects of microembolization on systolic wall thickening, LV volumes, and ejection fraction. Perfusion parameters, such as max upslope, peak attenuation, and time to peak, differed between microinfarct territory and remote myocardium. Inconsistency in visualizing microinfarct was observed using tube voltages of 80 kV and 120 kV. The extent of heterogeneous microinfarct was 4.5 ± 1.0 % of LV mass at 80 kV, 6.1 ± 0.9% LV at 120 kV, and 5.9 ± 1.1% LV on postmortem. There was significant difference in the extent of microinfarct measured on 80 kV MDCT compared with 120 kV and postmortem. Microscopic examination revealed the random distribution of obstructed microvessels surrounded by myocardial necrosis and inflammatory cells in all animals.

Conclusion

Both visible and nonvisible microinfarct cause perfusion deficit and LV dysfunction. MDCT is sensitive for quantifying early functional changes in LV caused by microembolization. Further improvement in spatial resolution of this technology is needed to improve visualization of microinfarct.

Distal coronary microembolization occurs during percutaneous coronary interventions (PCI) and other diseases, such as atherosclerosis plaque rupture, valvular disease, endocarditis, arrhythmias, heart-lung bypass surgery, and in-patient with congenital heart disease. It is also seen in patients with hypertension, diabetes, systemic lupus erythematosus, and sickle cell disease. Distal coronary microembolization causes microinfarct, arrhythmia, and sudden death .

Microinfarct imaging is a challenge because of the low spatial resolution of conventional diagnostic scanners and motion artifacts. Doppler ultrasound has been used for detection of coronary microembolization during PCI procedures . Porto et al found that the extent of microinfarct is related to the volume of embolic material . Choi et al described the association between microinfarct and impaired myocardial perfusion in 14 patients . Multiple clinical studies highlighted the importance of distal coronary microembolization. In the 2007 guidelines, the American College of Cardiology and European Society of Cardiology confirmed the deleterious effects of distal coronary microembolization.

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Materials and methods

Experimental Protocol

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Microemboli Volume

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MDCT Imaging

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Image Analysis

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Histochemical and Histopathological Studies

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Statistical Analysis

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Results

Selective Delivery of Microemboli

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Figure 1, (a) Electrocardiogram (ECG) tracings before ( top block ) and after ( bottom block ) delivery of 16 mm 3 volume embolic materials (40–120 μm diameter). The bottom ECG tracing shows the change in the ST-wave at 1 hour after delivery of microemboli. (b) Left anterior descending coronary artery angiography before ( left ) and after coronary microembolization ( center, arrow ). Right angiogram shows the slow filling (8 seconds) of the iodinated contrast media in the artery ( arrowhead ).

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Microinfarct

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Figure 2, The visibility of microinfarct on multidetector computed tomography images using 80 kV ( left images ) and 120 kV ( center images ) in two representative animals. Arrows show the extent of microinfarct in the territory of left anterior descending coronary artery. Note the correspondence of the microinfarct with triphenyl tetrazolium chloride stain ( right, left ventricular slices ).

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Figure 3, Bland-Altman test ( top plots ) shows the agreement in measuring the extent of microinfarct using noninvasive multidetector computed tomography imaging and postmortem histochemical triphenyl tetrazolium chloride staining. The 120 kV tube voltage provided better agreement to TTC than 80 kV. Pearson correlations ( bottom plots ) for 80 kV and 120 kV with TTC histochemical stain show the close correlation coefficient and the small standard error of the estimate.

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Perfusion and Function

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Figure 4, First-pass multidetector computed tomography showing the passage of iodinated contrast media in the left ventricular chamber ( square ), normal myocardium ( triangle ) and microinfarct subregion ( circle ). The presented values were averaged from two slices (4-mm slice thickness). Distal coronary microemboli caused regional ischemia designated by (*).

Table 1

Multidetector Computed Tomography Data Obtained 72 Hours after Selective Left Anterior Descending Artery Delivery of 16 mm 3 Volume of 40–120 μm Diameter Embolic Materials

Body weight (kg) 32 ± 1 Heart rate (beats/min) 81 ± 3 Stroke volume (mL) 27.0 ± 1.4 End diastolic volume (mL) 79.1 ± 3.5 End systolic volume (mL) 52.0 ± 4.1 Ejection fraction (%) 34.7 ± 2.5 Left ventricular mass (g) 85.7 ± 1.9

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Figure 5, Multislice multidetector computed tomography images show the lack of systolic wall thickening ( arrowheads ) from diastole ( left images ) to systole ( center images ) at the site of microembolic subregion ( arrows ) as shown in delayed enhanced ( right images ). Note the increase in systolic wall thickness in the free and posterior walls.

Figure 6, Quantitative analysis of left ventricular (LV) systolic wall thickening acquired averaged from six slices (4-mm slice thickness). The first segment is the posteroseptal junction between right ventricular and LV and the microinfarct subregion located at the anteroseptal wall. * P < .01 compared to remote myocardium (free LV wall), paired Student t -test.

Table 2

First-pass Multidetector Computed Tomography Perfusion Parameters Obtained in Remote Myocardium and Microinfarct Subregion 72 Hours after Delivery of Embolic Materials

Left Ventricular blood Remote Myocardium Microinfarct Max upslope (seconds -1 ) 82 ± 9 16 ± 2 6 ± 2 ∗ Peak attenuation (Hounsfield units) 635 ± 47 123 ± 15 83 ± 7 ∗ Time to the peak (seconds) 11.7 ± 2.1 15.7 ± 1.9 22.3 ± 2.6 ∗

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Histopathology

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Discussion

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Microinfarct

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Function and Perfusion

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Technical Considerations

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Practical Applications

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