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.

We sought to identify theoretical advantages and applications of the centerline method for quantitative assessment of regional ventricular function. Motion was measured along 100 chords constructed perpendicular to a centerline drawn midway between the end-diastolic and end-systolic contours, and normalized for heart size. Abnormality was expressed in units of standard deviations from the mean motion in a normal reference population to indicate both the severity and significance of the wall motion abnormality. The mean abnormality averaged over 100 chords correlated highly with the area ejection fraction (r = .97). The centerline method uses a "sliding window" to measure motion where it is abnormal, because assessment of wall motion in predefined regions of the ventricular contour underestimates abnormality. From the 100 data points, the extent (% of contour) of regional abnormalities can also be determined. The

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SUMMARY The effect of sublingual or intracoronary nitroglycerin (NTG) on luminal caliber in normal and diseased portions of epicardial coronary arteries was determined in 85 lesions from 57 typical patients with ischemic heart disease. Measurements were made from coronary angiograms, using a computer-assisted method and a carefully blinded protocol for analysis of the pre-and post-NTG angiograms. Luminal area in the "normal" portion of the diseased segment and at its maximum constriction and an estimate of flow resistance in the stenosis were computed. Luminal area increased 1.27 mm2 (p < 0.001) in the "normal" regions, an average increase of 18% over the control area. Dilation with NTG depended strongly on vessel size; area increased 35% in normal vessels of 1.6-2.3 mm luminal diameter and only 9% in vessels 4.0-5.0 mm in diameter. Lesions were grouped into four levels of severity by percent stenosis. Minimum luminal area increased 0.35 mm2 (p < 0.01) at the narrowest point in moderate lesions, a 22% area increase, and 0.14 mm2 (p < 0.001) in severe lesions, a 36% area increase. Stenosis dilation resulted in an average 25% reduction (p < 0.01) in estimated stenosis flow resistance in moderate lesions and a 38% reduction (p < 0.001) in severe lesions. A statistically significant resistance reduction of greater than 20% occurred in 15 of 20 severe stenoses; only two of 20 showed no measurable dilation. We reviewed recent literature on hemodynamic responses to NTG and determined that changes of this magnitude are among the largest reported. We conclude that vasodilation of epicardial coronary stenoses is usually a major component of the beneficial response to NTG.We support that conclusion by demonstrating a striking improvement in ischemic left ventricular compliance abnormalities after low-dose intracoronary NTG. NITROGLYCERIN (NTG) affords dramatic relief of angina pectoris in patients with coronary artery disease; yet its mechanisms of action are complex and, in certain respects, controversial. NTG is said to reduce the myocardial oxygen requirement by diminishing systolic wall tension through reduced systemic pressure (afterload) and reduced left ventricular (LV) diastolic pressure and cavity size (preload

To study the mechanisms of myocardial ischemia during isometric exercise, handgrip was sustained, for 4.5