No abstract

BACKGROUND Precise knowledge of the expected "normal" lumen diameter at a given coronary anatomic location is a first step toward developing a quantitative estimate of coronary disease severity that could be more useful than the traditional "percent stenosis." METHODS AND RESULTS Eighty-three arteriograms were carefully selected from among 9,160 consecutive studies for their smooth lumen borders indicating freedom from atherosclerotic disease. Of these, 60 men and 10 women had no abnormalities of cardiac function, seven men had idiopathic dilated cardiomyopathy, and six men had left ventricular hypertrophy associated with significant aortic stenosis. Lumen diameter was measured at 96 points in 32 defined coronary segments or major branches. Measurements were scaled to the catheter, corrected for imaging distortion, and had a mean repeat measurement error of 0.12 mm. When sex, anatomic dominance, and branch length were accounted for, normal lumen diameter at each of the standard anatomic points could usually be specified with a population variance of +/- 0.6 mm or less (SD) and coefficient of variation of less than 0.25 (SD/mean). For example, the left main artery measured 4.5 +/- 0.5 mm, the proximal left anterior descending coronary artery (LAD) 3.7 +/- 0.4 mm, and the distal LAD 1.9 +/- 0.4 mm. For the LAD, lumen diameter was not affected by anatomic dominance (right versus left), but for the right coronary artery, proximal diameter varied between 3.9 +/- 0.6 and 2.8 +/- 0.5 mm (p less than 0.01) and for the left circumflex, between 3.4 +/- 0.5 and 4.2 +/- 0.6 mm (p less than 0.01). Women had smaller epicardial arterial diameter than men (-9%; p less than 0.001), even after normalization for body surface area (p less than 0.01). Branch artery caliber was unaffected by the anatomic dominance but increased with branch length, expressed as a fraction of the origin-to-apex distance (p less than 0.001). Lumen diameter was not affected by age or by vessel tortuosity but was significantly increased among men with left ventricular hypertrophy (+ 17%; p less than 0.001) or dilated cardiomyopathy (+ 12%; p less than 0.001). CONCLUSIONS This is a reference normal data set against which to compare lumen dimensions in various pathological states. It should be of particular value in the investigation of diffuse atherosclerotic disease.

No abstract

The clinically important coronary segmental anatomy has been described in a format useful for quantitative analysis and standardized display. We have determined the intrathoracic location and course of each of the 23 coronary artery segments and branches commonly used for clinical description of disease. Measurements were averaged from perpendicular angiographic viewpairs in 37 patients with normal-sized hearts. Each segment or branch is described by several points along its course; each point is specified in polar coordinates as the radial distance from the principal coronary ostium and by angles about the patient, corresponding to those describing rotation in c-arm radiographic systems. This computer-assisted measurement method is accurate to within ±0.2 cm (SD) and ±20 in phantom studies. Coronary segment location among a group of normal-sized hearts can be specified to within ± 1.0 cm (SD). For example, the left anterior descending coronary artery segment at the apex of the heart is 12.2 ± 1.0 cm from the left coronary ostium, 32 ± 40 to the left of the anterioposterior axis, and at 46 ± 70 of caudal angulation. There are several clinically important applications of this new knowledge. First, this anatomic format provides the basis for estimating regional myocardial contraction and the relative size of the myocardial region at risk from a given arterial occlusion. Second, precise knowledge of "normal" segment location greatly simplifies the computation of dimensional correction factors for quantitative arteriography. Third, viewing angles most appropriate for videodensitometric assessment of lesion lumen area may be computed from these data. The theoretical basis and numerical values needed for most of the above estimates are provided. Finally, a computer program has been written to generate a three-dimensional tree-branch vascular model from these anatomic locations. This easily used interactive program aids in teaching coronary angiographic anatomy and, of importance, permits selection of viewing angles that "best" visualize the traditionally difficult parts of the coronary tree. (Circulation 1988;78:1167-1180 Knowledge of the intrathoracic spatial locations of specified coronary segments may prove useful for several reasons. First, this knowledge could facilitate the generation of three-

Summary. The effect of peroxidative stress on tissue was studied by exposure of red blood cells (RBC) from patients with abetalipoproteinemia to minute amounts of H202 in vitro. Red blood cells from untreated patients showed a marked sensitivity to H202, as evidenced by hemolysis and lipid peroxidation (peroxidative hemolysis).The appearance of lipid peroxidation products in sensitive cells after exposure to H202 was indicated by 1) increases in the 2-thiobarbituric acid (TBA) reaction of trichloroacetic acid extracts, 2) increases in ultraviolet light absorbency of lipid extracts, and 3) decreases in polyunsaturated fatty acids. These changes were accompanied by a decrease in phosphatidyl ethanolamine and phosphatidyl serine in the RBC lipid extract. Similar lipid changes on exposure to H202 were observed in the RBC from vitamin E-deficient rats.Treatment of the patients with d-a-tocopherol polyethylene glycol succinate by mouth, or addition of dl-a-tocopherol to the incubation medium protected the RBC from peroxidative hemolysis. Tocopherol appears to provide a primary biologic defense against peroxidative hemolysis.The presence of nitrite or carbon monoxide, which produced methemoglobin and carboxyhemoglobin, respectively, inhibited peroxidative changes, suggesting a catalytic role for oxy-or deoxyhemoglobin.