Intracardiac measurement of pre-ejection myocardial velocities estimates the transmural extent of viable myocardium early after reperfusion in acute myocardial infarction
Cristina Pislaru, MD*,*,
Charles J. Bruce, MD ,
Marek Belohlavek, MD, PhD, FACC,
James B. Seward, MD, FACC and
James F. Greenleaf, PhD*
* Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota, USA
Division of Cardiovascular Diseases Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota, USA
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Figure 1 Schematic representation of the placement of the epicardial markers and intracardiac ultrasound interrogation plane. A and B = epicardial markers; AO = aorta; bc = percutaneous transluminal coronary angioplasty balloon catheter; ICE = intracardiac ultrasound catheter; LA = left atrium; LV = left ventricle; RV = right ventricle.
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Figure 2 Cardiac specimen image and corresponding gray-scale and color Doppler myocardial imaging (DMI) images of the anterior wall from intracardiac echocardiography. (a) The cardiac specimen was sliced through the plane that included both epicardial markers (arrows) and double-stained with Evans blue and 2,3,5-triphenyltetrazolium chloride. Nonischemic myocardium is stained in blue, ischemic, but viable, myocardium in red and infarcted myocardium in yellow-white. The apex of the heart is toward the left, base of the heart toward right. The white lines correspond with the location of M-mode lines (or gate in pulsed DMI). The yellow polygon indicates the region of interest selected for analysis of the transmural extent of necrosis in the region (transmural extent of necrosis = 100 · number of white pixels / total number of pixels). (b) The corresponding gray scale image shows the location of the epicardial markers, helping in the registration of the gross pathology images with the DMI images. (c) Color DMI frame during ischemia shows tissue velocities during the isovolumic contraction (IVC) period. Note the high-positive velocities in the nonischemic myocardium and negative velocities in the ischemic myocardium. (d) Selected color DMI frame displaying tissue velocities during the ejection phase (at the time of the peak values). Note that the difference in tissue velocities between the normal and ischemic regions is less obvious than it is for IVC tissue velocities.
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Figure 3 Data from one animal with a small anterior infarct. (a) A color Doppler myocardial imaging (DMI) frame during isovolumic contraction phase and showing the location of sample in pulsed DMI mode; epicardial markers are located at the tip of the arrows. (b) Shows a corresponding stained cardiac specimen image. The transmural extent of necrosis measured at the location of the sample gate was 6%. (c) Pulsed and color M-mode DMI at baseline, at the end of the occlusion (60 min) and after reperfusion (30 min). Note the reduced systolic (S) velocities during the ejection phase but the presence of high positive isovolumic contraction (IVC) velocity (red arrows), identifying ischemic, but viable, myocardium. The dashed vertical lines indicate the time of the aortic valve opening and closure.
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Figure 4 Data from one animal with anterior transmural infarction. (a) Shows the color Doppler myocardial imaging (DMI) frame during the isovolumic contraction phase and the location of sample in pulsed DMI mode; epicardial markers are located at the tip of the arrows. (b) Corresponding 2,3,5-triphenyltetrazolium chloride and Evans blue-stained cardiac specimen image. (c) Pulsed and color M-mode DMI at baseline, at the end of the occlusion (120 min) and after reperfusion (30 min) in the ischemic and nonischemic regions (pulsed DMI). Note in the ischemic region the reduced, but present, velocities during the ejection (S) (suggesting tethering effect) but different patterns of isovolumic contraction (IVC) velocities (red arrows), which clearly identify ischemic myocardium. No change occurred in the nonischemic region. The dashed vertical lines indicate the time of the aortic valve opening and closure. E = myocardial velocity due to early left ventricular filling; PSC = tissue velocities due to postsystolic contraction.
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Figure 5 Positive isovolumic contraction (IVC) velocity in the ischemic region throughout the experiment and its correlation with the transmural extent of necrosis (TEN). (a) Different positive IVC velocity values were found in walls with small and large transmural infarcts during ischemia and reperfusion. (b) To compensate for the large variation in positive IVC velocity between animals, the values at reperfusion were normalized to baseline. Normalized positive IVC velocity highly correlated with TEN. The line of regression is indicated.
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Figure 6 Differential isovolumic contraction (IVC) velocity versus transmural extent of necrosis (TEN). Differential IVC during ischemia (open square) and reperfusion (solid triangle) was normalized by subtracting the baseline value. A good correlation was found between differential IVC and TEN. The lines of regression are indicated for both ischemia (broken line) and reperfusion (solid line).
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