Abstract

Currently, the coronary angiogram remains the “gold standard” for the detection and quantification of coronary arterial disease. Clinical assessment of the arteriogram is usually based simply on the relative percent narrowing of the column of angiographic dye. However, such analysis oversimplifies and is not accurate for evaluating the extent and severity of coronary artery atherosclerosis. Recently a new generation of ultrasonic devices has become available for intraoperative evaluation of coronary arterial anatomy. These high frequency echocardiography transducers use 12 MHz probes. The transducer is placed directly over the epicardium during open heart surgery to evaluate the coronary artery. With this technique, demonstration of coronary artery anatomy, including wall and cross-sectional lumen, is available in vivo. We have undertaken numerous validation studies in vitro and in vivo of animal and postmortem human heart preparations to show that this technique can be used to accurately measure luminal area, luminal diameter, and wall thickness. Subsequently in patients intraoperatively the extent of atherosclerosis using luminal diameter to wall thickness (LD/WT) ratios was compared with the routine angiographic evaluation of coronary arterial disease using percent stenosis measurements. LD/WT ratios from arterial segments with no visible angiographic disease but with angiographic lesions elsewhere in the same coronary artery showed marked variability. The majority were in the range of LD/WT ratios of those segments where high frequency echocardiography recording was made at the site of “angiographic” disease. This indicates that in vivo atherosclerosis is more widespread than the angiogram predicts and underlies the difficulties of using percent stenosis angiographically to determine the extent and severity of coronary arterial disease. In a second study we have demonstrated that there is marked variability and eccentricity in coronary plaque geometry, luminal morphology, and placement of the residual lumen with respect to the atherosclerotic plaque. This eccentricity results in some relatively “normal” coronary wall at the site of maximum atherosclerosis, theoretically preserving the ability to vasodilate and vasoconstrict. Studies with high frequency echocardiography are underway to study the capability of arteries with atherosclerosis to vasodilate. We have evaluated atherosclerotic remodeling of coronary arteries and found that remodeling occurs in an attempt by the artery to preserve its residual luminal size during encroachment on the lumen by the atherosclerotic plaque. This is the first in vivo demonstration of this process in human coronary arteries. Coronary arterial bypass grafts have been evaluated in animal models and at the time of intraoperative coronary anastomoses to evaluate the adequacy of graft anastomoses and compare vein grafts with internal mammary grafts. This dynamic in vivo technique supports and extends information obtainable from pathologic studies. It contributes to our understanding of the pathologic anatomy of coronary arterial disease.

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