Académique Documents
Professionnel Documents
Culture Documents
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 Resuls. Eighty-three arteriograms were carefuly 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 cardiomyop-
athy, 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 ±O.6 mm or less (SD) and coefficient of variation of <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
Downloaded from http://ahajournals.org by on September 16, 2019
(p<O.Ol) and for the left circumflex, between 3.4±0.5 and 4.2±0.6 mm (p<0.01). Women had smaller
epicardial arterial diameter than men (-9%o; p<0.001), even after normalization for body surface area
(p<O.Ol). 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<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<O.001) or dilated cardiomyopathy (+12%; p<O.OOl).
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.
(Circulation 1992;86:232-246)
KEY WoRDs * coronary anatomy * vessels, coronary, size * computer graphics * arteriography,
quantitative
In humans, certain pathological and physiological and high-flow coronary fistulae12 are processes that may
processes influence coronary artery lumen caliber. increase lumen caliber. These processes may occur in
Diffuse arteriosclerotic intimal thickening is said the absence of focal narrowing and/or luminal irregu-
to reduce lumen diameter at pathological examina- larity, so we cannot be certain that normal-appearing
tion,1-3 although a compensatory enlargement occurs.4 arterial segments are truly normal. This presents a
Reduced flow demand contracts vessel size by an endo- problem for the traditional radiographic estimate of
thelium-dependent process.5 Aging,6'7 ectasia,8-'0 Ka- arterial disease severity, the "percent stenosis," which is
wasaki syndrome," increased myocardial flow demands, based on the ratio of a focal minimum to a nearby
"normal" diameter. Percent stenosis is, experimentally,
From the Cardiovascular Research and Training Center, Car-
a uniquely effective correlate of the physiological impact
diology Division, Department of Medicine, University of Wash- of focal coronary narrowing,13-'6 but unfortunately, to
ington, Seattle. the extent that we cannot accurately assess normal
Supported in part by US Public Health Service grants HL- lumen diameter in humans, the clinical utility of this
13517, HL-19451, HL-18805, and HL-30086, in part by an Estab- estimate is diminished.2
lished Investigator Award (B.G.B.) from the American Heart One solution to this problem is to find methods
Association, and in part by a grant from the John L. Locke Jr. whereby we may predict normal lumen diameter at a
Charitable Trust. given point in the coronary anatomy and to use this
Address for correspondence: B. Greg Brown, MD, PhD, Cardi-
ology Division, RG-22, University of Washington School of Med- diameter as a normal reference for the percent stenosis.
icine, Seattle, WA 98195. At present, data on the "true" normal diameter of
Received December 4, 1990; revision accepted April 8, 1992. human coronary arteries are not available in a system-
Dodge et al Normal Lumen Diameter 233
fraction, and end-diastolic LV chamber volume were coronary artery (LCA)-dominant distribution. Not shown is
within normal limits (20.52; 50-120 ml/m2). Five pa- the "small-RCA" distribution, in which the RCA branches
tients had mild mitral insufficiency resulting from pro- into the posterior descending branch (RD) and the inferior
lapse without evidence of a dilated ventricle. None of wall branch (RI), and the posterior wall branch (CP) arises
these normal patients had structural cardiac abnormal- from the left circumflex artery. Artery segment abbreviations
ities. Indications for catheterization were the evaluation are fully detailed in Table 5.
of chest pain in 53 patients, history of ventricular
arrhythmia (premature contraction, tachycardia, fibril-
lation) in eight, Wolff-Parkinson-White disease in four, segments that corresponded approximately to these
abnormal exercise tolerance test in three, and being standard ones. In most cases, these segments were easy
potential participants in a drug trial in two. Six other to locate, and in no case was a major branch ignored in
patients had concentric LVH caused by aortic stenosis, this process. We have described this coronary artery
with or without aortic insufficiency, with aortic valve segment and branch nomenclature18 and have applied it
area of <1.2 cm2 and/or aortic valve gradient >60 in this report with minor alterations including a "small"
mm Hg, evidence of LVH on ECG, and/or wall thick- right coronary artery (RCA) anatomic distribution and
ening > 13 mm on echocardiogram. Another seven anterior (OA) and posterior (OP) branches of the
patients had DCM with global ejection fraction <0.25 obtuse marginal (OM) branch. A complete description
(six patients)- and increased end-diastolic LV chamber of coronary artery segment and branch nomenclature is
volume (six patients; .160 ml/m2). included in the "Appendix."
Arteriography Measurements: Data Entry
Coronary arteries were cannulated by the Judkins The coronary angiographic films were projected with
technique with catheters of known dimension (5F to magnification to 4.4 times life-size. Frames with clear
8F). Selective coronary injections of Renografin 76 were images were selected. All segments and branches of the
filmed in standard projections with a General Electric coronary artery tree were identified, and the anatomy
Fluoricon 300 radiographic system (Milwaukee, Wis.) was reduced to a set of up to 96 defined subsegments in
with a resolution of 2.4 line pairs per millimeter. the following manner. With the exception of Al, A2,
and A3, each segment shown in Figure 1 was trisected,
Anatomic Representation and the midpoint of each third of each segment was
The anatomic segments shown in Figure 1 were identified as shown in Figure 2. For each artery, we
located in each coronary arteriogram. Although coro- digitized the two-point diameter of the catheter into a
nary anatomy tends to be somewhat more variable than Digital Equipment Corporation VAX-11/750 (May-
Figure 1 suggests, it was possible in every case to specify nard, Mass.). We then digitized the lumen diameters of
234 Circulation Vol 86, No 1 July 1992
Y-AxIS (CEPHALAD)
X-AXIS
(LATERAL)
branching from the main arteries, the lumen diameters at the distance between its origin and the apex of the heart in
point oforigin (c), proximal midpoints, and middle midpoints a view perpendicular to the long axis of the heart, as
(.) were digitized, as illustrated here for the middle left illustrated in Figure 3. If the visible length of the branch
anterior descending coronary artery (L2), the first septal (Si), was less than 25% of this distance, then it was neglected
and the second diagonal (D2). r is the radial distance from the ("absent"). When the visible length of the vessel was
coronary ostium to the artery segment. 0 is the azimuth angle
between 25% and 50%, or 50% and 75%, or >75% of
between the projection of r onto the transverse plane (X-Z this distance, then it was classified as short, medium, or
plane) and the anterior-posterior (AP) axis. (D is the angle long, respectively. Branches that could not be clearly
between r and the transverse plane (X-Z plane). '8 visualized were classified as unseen. Occasionally, a
vessel branched extensively and thus supplied a larger
myocardial mass than would otherwise be predicted by
the midpoint of each subsegment in the left main (LM), its length; it was accordingly given a longer classifica-
left anterior descending (LAD) (L1, L2, L3, IA), left tion. The three largest septal branches were classified; a
circumflex (LCx) (Ci, C2, C3, C4), and right coronary septal was long if it had at least three branches and
arteries (RCA) (R1, R2, R3, R4) that was present. For extended >65% of the distance from its origin to the
the three septal (S1, S2, S3), diagonal (D1, D2, D3), base of the septum, medium if it had two branches and
marginal (M1, M2, M3), and inferior wall branches extended approximately 50% of this distance, and oth-
(from RD, RI, RP, CP, CI, CD) and for the median erwise was short. If a single branch of the LCx was
ramus, we digitized the lumen diameter at the branch much larger than its neighbors, it was considered to be
origin and the proximal and middle midpoints. For an an OM, although a first marginal (M1) or third marginal
OM, the length of artery between its origin and its (M3) was also permitted if present. OM, OA, and OP
bifurcation was divided into three equal parts, and the length were classified according to the same reference
lumen diameters were measured at the midpoint of each length: the OM origin-to-apex distance. The posterior
of these subsegments. Diameters of the two longest descending artery, RD, and CD were required to reach
branches continuing beyond the bifurcation, OA and the apex to be long.
OP, were measured as described above for the The L4 segment was categorized to investigate
branches. whether the length of apical LAD wrap-around affects
Terminal branches (diagonal, marginal, septal, etc.) LAD lumen diameter. L4 was short if the LAD barely
were classified by size into one of five groups: long, passed the apex, medium if the LAD rounded the apex
medium, short, absent, or unseen. This branch size and made a small ramification on the inferior apical
rating refers to the vessel's length of distribution, not its region, and long if the L4 provided inferior septal
width per se; where these vessels branched, their longest branches. When the LAD did not reach the cardiac
extension was used. This classification was made by apex, L4 was absent.
Dodge et al Normal Lumen Diameter 235
FIGURE 4. Representative photographs of the left anterior descending artery with four different degrees of tortuosity:
nontortuous, slightly tortuous, moderately tortuous, and very tortuous (from left to right). This figure was present for reference
when tortuosity was classified.
The continuous spectrum of LAD tortuosity was caused by divergence of the x-ray beam was also cor-
classified into four groups: nontortuous, slightly tortu- rected in the scaling process.'8'19 Pincushion distortion
ous, moderately tortuous, and very tortuous. Examples is a small source of selective image magnification with
of each degree of tortuosity for the LAD are displayed our modern equipment and small (5-6-in.) image fields
in Figure 4. Figure 4 was present for reference when and was neglected in this analysis for all arterial sub-
tortuosity was graded. segments. However, the diameter of the scaling cathe-
Our primary goal was to provide a reference data set ter, usually found in the periphery of the image, was
Downloaded from http://ahajournals.org by on September 16, 2019
of normal men with right dominant anatomy; a second- adjusted for pincushion effects.'9
ary goal was to highlight differences between this group
and other groups with normal coronary arteries. We Validation of Vessel, Dominance, and
sought to completely measure 20 normal RCA-domi- Tortuosity Classification Methods
nant men and 10 patients from each of the other six We determined the repeatability of our classification
groups (small-RCA-dominant men, balanced men, of anatomic dominance, tortuosity, branch artery iden-
LCA-dominant men, RCA-dominant women, men with tity, and length after an interval of more than 3 months.
LVH, and men with DCM) and .5 measurements from All 73 completely measured arteriograms were ran-
each branch-length group from among the normal men. domly ordered, and the anatomic dominance of each
Though we drew from a pool of 9,160 patients, it was was consecutively reclassified. Tortuosity was consecu-
difficult to meet these goals. The occurrence of men tively reclassified in a random subset of 36 normal male
with LVH with RCA-dominant anatomy and normal patients. Each branch artery in 15 consecutive, ran-
coronary arteries was approximately 1 in 1,500. As the domly selected patients was reidentified with our no-
study progressed, it became clear that the low preva- menclature system (Figure 1 and "Appendix"), and the
lence of some rarely occurring branch arteries (e.g., long length of each was reclassified with the above origin-to-
CI) would result in counts too low for a reliable apex system. These reclassifications were then com-
population average. In 73 patients (50 normal men, 10 pared with the original set.
normal women, six men with LVH, and seven men with
DCM), all artery subsegments present were measured. Validation of Measurement Methods
The counts for some branches were then augmented by
making measurements at selected artery sites in 10 We determined the accuracy and variability of this
additional normal male patients, accounting for some of method by measuring known diameters from films of a
the apparent discrepancies in patient numbers in the roughly heart-sized styrofoam block in multiple viewing
tables. For groups in which patients could be found angles with the General Electric Fluoricon 300 radio-
more frequently, data were collected only until the graphic equipment. This block contained a household
target sample was obtained. pin, the head representing the location of a coronary
ostium, and two brass tubes positioned to represent the
Measurements: Theoretical catheter and a subsegment with 3.25-mm lumen diam-
To reduce an angiographic image to true scale, opti- eter. The spatial relations between these locations were
cal and uniform x-ray magnifications were compensated determined.'8 At the selected site, opposite sides of the
directly by use of the catheter, which was of known tube were digitized in a fashion identical to that de-
diameter, as a scale factor. Out-of-plane magnification scribed for the arteries. The widths at these locations
236 Circulation Vol 86, No 1 July 1992
were computed and compared with the known been taking chronic nitrates, lumen diameters were not
diameters. different from patients not on nitrates. Similarly, lumen
The measurement variability was determined by re- caliber was unaffected in three patients receiving cal-
tracing and analyzing arterial subsegments in the coro- cium channel blockers; we know that these do not
nary arteriograms of six normal RCA-dominant men. acutely affect epicardial lumen caliber.23
The first and second sets of measurements were then
compared. Error Calculations on Brass Tube Phantom Model
A comparison between computed and actual mea-
Statistics surements of the brass tube showed a high degree of
Population variation of arterial lumen diameter has accuracy. In five views, from 480 RAO to 480 LAO with
been expressed in terms of the SD and the coefficient of 200 caudal to 300 cranial angulation, errors between
variation (SD/mean) of a group of measurements at a -0.13 and 0.10 mm were observed. The mean error
specified point for a given sex, anatomic variation, and (+SD) was <0.03 mm (±0.12), and the mean absolute
pathological state. Comparisons of mean lumen caliber error was 0.10 mm (+0.03), suggesting that the complex
among those groups used pooled Student's t tests. scaling logic was correctly implemented for these
Comparisons of body surface area (BSA)-normalized measurements.
lumen area for 12 main artery segments from normal Repeatability of Lumen Diameter Measurement
men, women, and men with LVH or DCM were made
Downloaded from http://ahajournals.org by on September 16, 2019
by Sign test,20 as was a comparison between long, A high degree of repeatability was observed when
medium-length, and short terminal branch arteries at 19 arteriograms were reanalyzed. In six angiograms, the
segments, each with three subsegments. The influence lumen diameters of a total of 213 subsegments were
of age on arterial lumen diameter was tested by remeasured, 132 by the original tracer and 81 by a
ANOVA. A difference was considered statistically sig- second tracer. For all vessels, the mean difference
nificant if the two-sided probability of the observed between first and second measurements (error) was
result, under the null hypothesis, was p<0.05. 0.12+0.34 mm, independent of vessel size over the
diameter range of 0.5-5.0 mm. The mean intraobserver
Results and interobserver errors were similar: 0.13±0.30 and
Baseline Patient Characteristics 0.10+0.40 mm, respectively.
The 83 patients (Table 1) were of mean age 45+± 13 Repeatability in Classification of Dominance, Vessel
years and had normal blood pressure (systolic, 118+15 Identity, Branch Length, and Tortuosity
mm Hg; diastolic, 71+9 mm Hg) and normal lipids (TC, Comparisons between the original and second classi-
187±36 mg/dl; LDL, 120±32 mg/dl; HDL, 44±12 mg/ fication sets reveal a high degree of precision. Anatomic
dl; apo B, 101±25 mg/dl). Of 50 normal men in whom dominance was exactly reidentified in 92% of 73 angio-
all artery segments were measured, diastolic blood grams; 8% had one-step differences involving large-
pressure exceeded 85 mm Hg (maximum 95 mm Hg) in RCA versus small-RCA dominance. Of the 161 branch
six. Those with normal blood pressure had a mean arteries present on first reading, 95% were correctly
proximal subsegment (Llp, Rlp, and Clp) lumen diam- reidentified. Among these, branch length (long, me-
eter of 3.56 mm, and those with 285 mm Hg measured dium, short) was correctly reclassified in 77%; one
3.66 mm (p=NS). Among 50 normal men, the TC, septal branch had more than a one-step difference.
LDL/HDL ratio, and apo B were measured in 48 and Tortuosity classification was exactly repeated in 83% of
were normal in 46, 46, and 44, respectively (<90th 36 angiograms; the remainder had one-step differences.
population percentile for age21.22). Abnormal lipid levels
had no effect on lumen diameter in this group with Diameter of the Main Arteries in
normal arteries. For example, 44 patients with normal Normal Right-Dominant Men
apo B had a mean proximal subsegment lumen diameter The main coronary arteries are the conduit vessel
of 3.57 mm; four with an elevated level measured 3.52 skeleton from which the branches ramify. They include
mm (p=NS). We were able to obtain medication infor- the LM, the interventricular course of the LAD, and the
mation for 73 of these 83 patients. By the exclusion atrioventricular groove courses of the RCA and LCx.
criterion, none of these patients continued chronic Each patient has 12 such segments; because of varying
nitrates at the time of catheterization; for three who had anatomic dominance, there are 13 main artery segments
Dodge et al Normal Lumen Diameter 237
in this description (a patient may have either R4 or C4). Differences Among Main Arteries Caused by
As shown in Table 2 and Figure 5, lumen caliber at the Variations in Anatomic Distribution
midpoint of each segment varied from 4.5 -mm diameter As shown in Table 2, the diameters of the LM artery
in the LM artery to 1.6 mm in the terminal LCx (C3). and segments of the LAD were unaffected by anatomic
The coefficient of variation (SD/mean) of lumen diam- distribution. The LCx, however, was usually significantly
eter at these selected points is <0.25 in 75% of locations larger when measured in a left-dominant distribution
and <0.20 in 58%. (A complete tabulation of the 12 than in a right. Conversely, the RCA was significantly
main artery segments in RCA-dominant men, each with larger when measured in a right-dominant than in a
three subsegments, is presented in Table 6.) left-dominant or a balanced distribution. The normal
Rlp a
a
Rlm a 10 1
Downloaded from http://ahajournals.org by on September 16, 2019
Rid m71arlwr~lm,m,Zgp~
R2p 1 --------
RCA m a
p 25
R3M
=4p
R4m 0 9
a a,
a
PAd X5XXXt 0 .1
1 0 0 A
LMp a
LM I-
Mm_
JLMM 02 ^4
Lbm 1 1
9 9 a
a! !
Llm
FIGuRE5. Bargraph showingmean lumen
Lld diameters of main artery segments in normal
12p %%%%%M% ' * right-dominant men. RCA, right coronary
artery; LM, left main artery; LAD, left
LAD anterior descending coronary artery; LCx,
L3m,p left circumflex artery. Artery segment abbre-
13d_ viations are presented in Table 5.
L4p'
L4m y^XX,,,
L4d_
Clmd
LCx C2m
C2d_
C3p EM-Ar-"a
1 9
C3m
C3d I **
a c a1
1
0
5
a
1,
a
1
5
0 11 2 3 4 5
Mean Lumen Diameter ± SD (mm)
238 Circulation Vol 86, No 1 July 1992
width of most arterial subsegments in men can be shows that long branches were usually significantly
specified to within ±0.6 mm (±SD) when anatomic wider than medium-length branches [p<0.001], and
dominance is accounted for. (A complete tabulation of short vessels were usually significantly narrower than
all 13 main artery segments possible in normal men, medium length vessels [p<O.OOi].)
each with three subsegments, is presented in Table 6.) The influence of terminal LAD (L4) length upon
For these normal arteries, a round cross section was LAD lumen diameter was investigated. We found no
assumed,24'25 and the lumen cross-sectional area was effect of L4 length (long, medium, or short) on LAD
estimated to be (i7/4)(Diameter)2. The summed cross- lumen diameter when L4 was present. When L4 was
sectional area of Rlm, Llm, and Clm was calculated present, the mean lumen diameters at Llm, L2m, and
and, per MacAlpin et al,17 was called the total coronary L3m were 3.7+0.4, 2.8±0.5, and 1.9±0.4 mm, compared
area (TCA). In men with the large-RCA-dominant with 3.5±0.4 mm (p=NS), 2.3±0.6 mm (p<0.01), and
distribution, the TCA was 32.1±7.3 mm2 with the RCA 1.2±0.3 mm (p<O.01), respectively, when L4 was ab-
Downloaded from http://ahajournals.org by on September 16, 2019
contributing 38% of the total area, the LCx 29%, and sent. LA was absent in 14% of the normal men studied.
the LAD 33%. In normal men with small-right-coro-
nary, balanced, and dominant-left-coronary distribu- Influence of Sex and Pathological State
tions, the TCAs were 33.5 ±9.3, 26.8 +5.2, and 30.7 +5.5 Selected and representative lumen diameters are
mm2, respectively (p=NS). given in Table 4 for the large-right-dominant distribu-
Influence of Artery Length tion of women, normal men, and men with LVH caused
Table 3 shows considerable variation in branch diam-
by aortic valve stenosis or with idiopathic DCM. In
eter. For these branches of the three main arteries,
nearly all comparisons, lumen caliber was smaller in
diameter was unaffected by the dominance of the ana- normal women than in normal men (-9±8% [SD];
tomic distribution. For example, there was no difference p<O.OOi for group), although this difference at individ-
in diameter of descending (RD, CD) or posterior (RP, ual points was statistically significant for only the prox-
CP) branches arising from the RCA or the LCx to imal artery subsegments (R1, LM, Llp, Clp, and Clm;
supply the inferior wall. The principal determinant of each p<0.05). In men, those with LVH or with DCM
branch diameter was the extent of its epicardial distri- had wider vessels (+17±12% and +12±11%, respec-
bution, as characterized by its length relative to the tively; p<0.001 each group), but these differences for
distance from its origin to the LV apex (long, medium, individual subsegments were significant only in the RCA
short), as described above and in Figure 3. The diame- (Ri through R4; each with p<0.05) with LVH and
ter of the principal diagonal, marginal, and inferior wall portions of the RCA (Rlm through R3; each with
branches averaged 2.4-2.6 mm at their origin if classi- p<0.05) with DCM. (A complete listing of lumen diam-
fied as long, 1.8-2.2 mm if of medium extent, and eters of the main coronary arteries in women, normal
1.4-1.6 mm if short. For a given branch and size men, and men with LVH or DCM is found in Table 8.)
classification, diameters were relatively uniform; the Figure 6 compares BSA-normalized segment lumen
coefficient of population variation of the lumen diame- areas in women and in men with LVH or DCM with
ter of a given subsegment was <0.25 for 76% of the those in normal men. It contains coronary lumen area
measured points and <0.20 for 48%. The coefficient of estimates derived from 1,452 measurements of lumen
variation of lumen diameter decreased as vessel length diameter. Mean segment areas (averaged from proxi-
increased. The expected width of most normal terminal mal, median, and distal measures) of each of the 12
branches can be specified to within ±0.5 mm (SD) when main artery segments were calculated and divided by
grouped by vessel length. (A complete tabulation of the BSA to normalize for differences in body size between
19 possible branch segments, each with three subseg- groups. Within a group, a 1.0 ratio occurs when the
ments, in normal men is presented in Table 7. The BSA-normalized area at a specific segment is the same
statistical comparison from the more complete Table 7 as that found in normal men. Women tend to have
*v
Dodge et al Normal Lumen Diameter 239
TABLE 4. Effect of Sex, Left Ventricular Hypertrophy, and Dilated Cardiomyopathy on Selected Coronary Artery
Diameter Measurements in Right Coronary Artery-Dominant Patients
Normal men Normal women DCM men LVH men
Diameter Diameter Diameter Diameter
Location n (mm) n (mm) n (mm) n (mm)
Rl middle 20 3.9±0.6 10 3.3±0.6* 7 4.5±0.5* 6 4.6±0.7*
(1.0±0.2) (0.8±0.2) (1.2±0.1) (1.2±0.2)
LM middle 18* 4.5±0.5 10 3.9±0.4t 7 4.8±0.3 6 4.9±0.4
(1.0±0.1) (0.9±0.1) (1.1±0.1) (1.1±0.1)
Li middle 20 3.6±0.5 10 3.2±0.5 7 3.8±0.5 6 3.9±0.5
(1.0±0.1) (0.9±0.1) (1.1±0.1) (1.1±0.1)
Cl middle 20 3.4±0.5 10 2.9±0.6* 7 3.3±0.7 6 3.6±0.6
(1.0±0.1) (0.9±0.2) (1.0±0.2) (1.1±0.2)
DCM, dilated cardiomyopathy; LVH, left ventricular hypertrophy; R, right coronary artery; LM, left main; L, left
anterior descending artery; C, circumflex artery (refer to Figure 1 and Table 5). For each patient group/artery location,
the mean±SD in millimeters is above, and the ratio (mean±SD) in normal men is below in parentheses.
tReported segment numbers vary because of absent LM.
*p<0.05, tp<0.01.
A complete tabulation may be found in Table 8.
15.3% smaller BSA-normalized segment area for main constant (15.2±3.6 mm2/m2) for men of all ages. Nor-
artery branches (p<O.O1), and men with LVH or with malized cross-sectional areas of individual main arteries
DCM have 36.8% (p<O.O1) or 30.5% (p<0.05) larger in all normal men likewise showed no trend with aging.
segment area, respectively, than normal men.
Influence of Tortuosity
Influence ofAge We found a positive correlation between age and
Figure 7 shows that there is no age-related trend in LAD tortuosity but none between LAD tortuosity and
Downloaded from http://ahajournals.org by on September 16, 2019
TCA, as defined above, in normal men when normalized lumen diameter. The four tortuosity categories were
for BSA (p=NS). Thus, BSA-normalized TCA is a numbered in increasing order of tortuousness as illus-
1.8
a 1.8
1.6 1.6
MEO
L
1.4 * l
1.4
a * a
.0i 1.2 a
m U 1.2
a o
1.0 1.0
a a
E .5 0.8' 0.8
Eo 4
0.6 0.6
0.4 0.4
0.2' p < 0.01 p < 0.01 p < 0.05 0.2
ll
0.0 . -3. --r- n
1.0 3.0 5.0 1.0 3.0 5.0 1.0 3.0 5.0
nary artery bypass graft surgery33-35; however, our velocity in arteries of various sizes'6 and can be esti-
measurements at two of the five most commonly grafted mated at QN/AN= 11.1 cm/sec for a proximal LAD of
sites (L2 and R3) were not significantly different be- area 10.2 mm2 (3.6 mm diameter; see Table 2) supplying
tween men and women. Too few of the remaining three its basal myocardial needs of 68 ml/min.46 As normal
common graft sites (M1, Dl, and RD) were measured in total flow is maintained in the face of substantial
women to allow comparisons. Other explanations for narrowing, the physiological impact of the stenosis can
this operative mortality difference have been offered.36 be approximated as AP=0.05 (AN/A,)2 using the two
With 441 lumen measurements in the main arteries of expressions above. Thus, hypothetically, a better arte-
male patients with LVH or DCM, our results compare riographic index of the hemodynamic impact of a ste-
favorably with measurements made by others during notic coronary artery lesion at any site in the coronary
life7"26 and postmortem.28'37 Resting blood flow per unit anatomy might result from the above comparison of the
myocardium is normal in patients with severe aortic measured minimum area with its expected normal area
valve disease38 and decreased in those with DCM,39 at that site. The value of this approach remains to be
whereas myocardial mass is greatly increased in tested. This report represents an important first step
both.40,4l The total blood flow is thus increased in toward investigating this hypothesis by determining
patients with aortic stenosis4243 and may be increased in whether and with what degree of confidence it is
patients with DCM.39 We found coronary area to be possible to specify the expected lumen caliber of a given
significantly increased in hypertrophied and dilated normal coronary artery segment.
hearts. As total flow equals cross-sectional area multi- These normal widths have been included in an edu-
plied by velocity, this is probably an adaptive phenom- cational Macintosh computer program'8 (see Figure 3)
enon, with coronary size increasing to satisfy myocardial permitting a two-dimensional projection of the three-
demand for an augmented blood supply37 while preserv- dimensional normal coronary artery tree from any
ing velocity by means of partially characterized autoreg- user-specified viewing angle. This may be of benefit to
ulatory pathways.5"12 first-year cardiology fellows; medicine, surgery, and
Arteries are said to dilate with age, as they diffusely radiology residents; medical students; and others trying
narrow with progressive intimal disease.46,7 Depending to develop an appreciation for the normal coronary
on the predominant effect, either greater or lesser anatomy.
lumen diameter would result. During aging, the histo- Certain limitations of our study may have increased
logical increase in diameter of the internal elastica measurement variance. These include infrequent in-
offsets increased intimal thickness, possibly as an adap- stances of retrospectively unavailable information on
tation to the advance of intimal thickening with age LV size or wall thickness, concomitant drug use (10 of
rather than a direct effect of aging on the arterial wall.4 83 patients), and lack of direct measures of scaling
Downloaded from http://ahajournals.org by on September 16, 2019
We found no evidence that lumen caliber is influenced catheter dimensions, which may introduce 1-2% addi-
by age in these adults without angiographically apparent tional variance.47 Automated quantitative angiographic
atherosclerosis, a finding in agreement with that of measurements of nonnylon catheters may systematically
others.44 underestimate true size (by micrometer) by 3.5%47;
The population variation in tortuosity of the coronary however, this does not affect dimensional accuracy with
artery tree, increasing with age, has long been noted.45 the approach we use.19 Finally, a relatively small num-
As did others,44 we found a significant positive relation ber of normal women and men with DCM or LVH were
between age and tortuosity but no significant relation studied.
between tortuosity and lumen diameter. Tortuosity may With this article, an anatomic nomenclature scheme
be a normal aging phenomenon and not secondary to a has now been fully defined. It is concise, easy to
disease process. remember because of the correspondence of the loca-
The percent diameter stenosis is the most commonly tion code to the widely accepted coronary arterial
used arteriographic index of coronary disease severity, nomenclature, and repeatable. We have shown in nor-
but objections have been raised to its use in patients mal men that the combination of subsegment location,
with atherosclerosis.1-3 Chief among these is that nar- anatomic distribution pattern (RCA dominant, small-
rowed segments are frequently compared with adjacent RCA dominant, balanced, and LCA dominant), and the
less narrowed but diffusely diseased segments, and thus branch artery length categories (long, medium, short,
the actual severity of a lesion may be underestimated. and absent) permits an estimate of normal lumen
As a result, in humans, measures of percent stenosis do diameter with a relatively small population variance. We
not correlate with the physiological significance of cor- believe that this anatomic scheme18 corresponds to the
onary atherosclerotic lesions ranging from 20% to clinically relevant coronary anatomy and should be
60%.3 considered for use as a standardized description of
The physiological impact of a stenosis is related to the these vessels in future investigations.
blood pressure loss (AP) that occurs as blood flows
through it. This is reasonably well approximated by the Appendix
dynamic loss, AP=3.8 (Q/A )2, where Q is blood flow Quantitative Description of the Human Coronary
(cm3/sec), A, is minimum lumen cross-sectional area Anatomy: Nomenclature and Measurements of
(mm2) in the stenosis, and AP is in millimeters of Subsegment Spatial Location and
mercury.23 Because the arterial flow volume differs Normal Lumen Diameter
greatly at different points in the coronary anatomy, no In a coronary arteriogram, the anatomic segments shown in
single value of stenosis area, A,, can be used to estimate Figure 1 can be located (not all segments are labeled).
a lesion's severity. However, the ratio (normal flow/ Although coronary anatomy tends to be somewhat more
normal area) (QN/AN) is experimentally a fairly constant variable than Figure 1 suggests, it is usually easy to specify
242 Circulation Vol 86, No 1 July 1992
segments that correspond approximately to these standard anatomic variant arising at a trifurcation of the LM and is
ones as described in Table 5. The LM artery has a single called a branch. Because of the variable nature of the branches
segment. The LAD is separated into four segments, as illus- that originate at or very near the bifurcation of the LM, the
trated in Figure 1, defined by 1) its origin from the LM, 2) the angiographer must decide whether a given case is best classi-
first septal perforator (S1), 3) the third septal perforator (S3, fied as a first diagonal (D1), first marginal (M1), or if inter-
not labeled in Figure 1), 4) the cardiac apex, and 5) its terminal mediate between the two, as a median ramus.
point on the inferior wall. S3 commonly arises near the bend of The LCx, with a right- and small-right-dominant anatomy,
the LAD in RAO views and often is near the origin of the is divided into three parts (Cl, C2, and C3) by the first and
second diagonal. These landmarks may serve as alternative second marginal branches (Ml and M2). In this case, the
markers. If none of these are identified, the L2-L3 transition atrioventricular groove continuation of the LCx (C3) is usually
is defined as halfway from Si to the cardiac apex. Branches small. In the case of small-right-dominant anatomy, the
from the main arteries are numbered from proximal (1) to posterior wall branch (CP) originates at the distal end of C3.
distal (3). The possible branches of the LAD included the With a balanced anatomic distribution, the LCx has a fourth
three largest septal branches (S1-S3) and the three largest segment (C4) distal to CP and gives rise to an inferior wall
diagonal branches (D1-D3). A median ramus branch is an branch (CI). With a left dominant anatomy, the LCx also gives
Dodge et al Normal Lumen Diameter 243
TABLE 6. Lumen Diameter and Spatial Location of 13 Main Artery Segments, Each With Three Subsegments, in Normal Men
Lumen diameter
RCA dominant Small RCA dominant Balanced dominant LCA dominant Spatial location'8
Subsegment Diameter (mm) n Diameter (mm) n Diameter (mm) n Diameter (mm) n r 6 4' n
Left main
LMp 4.5±0.6 18(a) 4.6+0.5 10 4.3±0.4 9(a) 4.6+0.4 10 0.3 830 70 19
m 4.5±0.5 18(a) 4.6±0.5 10 4.4±0.4 9(a) 4.6±0.4 10 0.7 800 40 19
d 4.5±0.4 18(a) 4.6+0.5 10 4.4±0.3 9(a) 4.5 ±0.4 10 1.1 790 00 19
Left anterior
descending
Llp 3.7±0.5 20 3.9+0.4 10 3.8±0.2 10 3.8+0.3 10 1.6 700 -30 19
m 3.6±0.5 20 3.8±0.4 10 3.6±0.4 10 3.7+0.2 10 2.3 630 -50 19
d 3.5±0.6 20 3.8±0.5 10 3.4±0.5 10 3.5±0.3 10 3.0 590 -80 19
L2p 2.9±0.5 20 3.5±0.6t 10 2.8±0.7 10 3.1±0.4 10 4.0 510 -90 19
m 2.5±0.5 20 2.9±0.7 10 2.5±0.4 10 2.8+0.4 10 5.3 44° -120 19
d 2.3±0.4 20 2.5±0.6 10 2.3±0.4 10 2.6±0.4* 10 6.5 390 -170 19
L3p 2.0±0.5 20 2.1±0.6 10 2.0±0.4 10 2.4±0.4* 10 8.0 330 -230 19
m 1.7±0.5 20 1.9±0.5 10 1.8±0.4 10 2.0+0.3 10 10.1 300 -320 19
d 1.4±0.5 20 1.7±0.4 10 1.6±0.3 10 1.9±0.5t 10 11.8 310 -400 19
L4p 1.4±0.5 15(b) 1.3±0.3 8(c) 1.3±0.4 8(d) 1.7±0.4 7(e) 12.2 320 -460 16
m 1.1±0.4 15(b) 1.1±0.4 8(c) 1.2±0.4 8(d) 1.5±0.2* 7(e) 11.8 330 -490 16
d 0.9±0.3 15(b) 1.0±0.3 8(c) 0.9±0.3 8(d) 1.1+0.2 7(e) 11.4 340 -520 16
Left circumflex
Clp 3.4±0.5 20 3.6±0.7 10 3.6±0.6 10 4.3±0.6t 10 1.4 860 -12° 19
m 3.4±0.5 20 3.5±0.8 10 3.4±0.5 10 4.2+0.6t 10 1.8 940 -240 19
d 3.3±0.5 20 3.5±0.8 10 3.5±0.5 10 4.1±0.6t 10 2.2 1020 -310 19
C2p 2.8±0.5 11(f) 3.0±0.8 9(g) 3.1±0.5 7(g) 3.4±0.6* 7(g) 2.6 1070 -330 18
m 2.8±0.6 11(f) 3.0±0.8 9(g) 3.2±0.4 7(g) 3.4+0.6* 7(g) 3.1 1160 -370 18
d 2.7±0.5 11(f) 2.9±0.8 9(g) 3.1±0.6 7(g) 3.3+0.7 7(g) 3.6 1200 -410 18
C3p 1.7±0.6 19(h) 2.2±0.8* 10 2.6±0.6t 10 3.3+0.6t 10 4.1 1260 -450 17
m 1.6±0.6 19(h) 2.2±0.8* 10 2.5±0.5t 10 3.2+0.5t 10 4.7 1350 -510 17
d 1.3±0.5 19(h) 2.1±0.8t 10 2.3±0.5t 10 2.9+0.5t 10 5.4 1410 -560 17
C4p 0 0 1.7±0.3 9 (i) 2.4+0.5 10 5.7 1560 -67° 6
m 0 0 1.5±0.4 9 (i) 2.2+0.5 10 5.9 1660 -710 6
Downloaded from http://ahajournals.org by on September 16, 2019
TABLE 7. Lumen Diameter and Spatial Location of Branch Artery Subsegments by Length in Normal Men
Lumen diameter
Short Medium Long Spatial location18
Subsegment Diameter (mm) n Diameter (mm) n Diameter (mm) n r 0 ( n
Septals
Slo 1.0L0.3t 6 1.4±0.2 34 1.8±0.5t 12 3.3 570 _90 19
p 1.1+0.2* 6 1.3±0.2 34 1.8±0.4t 12 3.7 500 -170 19
m 0.9+0.2* 6 1.0±0.2 34 1.1±0.3 12 4.3 350 -31° 19
S2o 0.8±0.0* 7 1.1±0.3 36 1.9±0.3t 9 5.1 440 -12° 19
p 0.8±0.1* 7 1.1±0.3 36 1.7±0.2t 9 5.3 400 -18° 19
m 0.7±0.1 7 0.9±0.2 36 1.4±0.3t 9 5.8 310 -290 19
S3o 0.9±0.2* 12 1.1±0.3 36 1.4±0.2 2 6.9 370 -190 19
p 0.8±0.2t 12 1.0+0.2 36 1.3±0.1 2 7.0 340 -230 19
m 0.7±0.2* 12 0.9±0.2 36 1.2±0.0 2 7.3 300 -310 19
Diagonals
Dlo 1.4±0.3t 10 2.1±0.5 28 2.4±0.3* 10 3.2 610 -80 19
p 1.3±0.3t 10 1.9±0.4 28 2.3±0.2* 10 4.2 610 -13° 19
m 1.1±0.2t 10 1.5±0.3 28 1.8±0.2* 10 6.2 610 -230 19
D2o 1.2±0.3t 11 1.9±0.4 22 2.6±0.3t 11 4.9 470 -120 19
p 1.2±0.2t 11 1.7±0.4 22 2.4±0.4t 11 5.9 470 -160 19
m 1.0±0.2t 11 1.4±0.2 22 1.9±0.4t 11 7.7 490 -24` 19
D3o 1.1 ±0.2t 19 1.7±0.3 13 2.4 1 6.6 410 -180 18
p 1.0±0.2t 19 1.6±0.3 13 2.3 1 7.4 410 -210 18
m 0.9±0.2t 19 1.3±0.2 13 1.7 1 9.0 430 -260 18
Marginals
MRo 1.4±0.3t 8 1.8±0.2 6 2.7±0.3t 10 1.2 850 -100 7
TABLE 8. Lumen Diameter of 12 Main Artery Segments, Each With Three Subsegments, in Normal Men, Normal Women, Men With
Left Ventricular Hypertrophy, and Men With Dilated Cardiomyopathy, All light Coronary Artery Dominant
Normal men Normal women Men with DCM Men with LVH
Subsegment Diameter (mm) n Diameter (mm) n Diameter (mm) n Diameter (mm) n
Left main
LMp 4.5±0.6 18(a) 4.0±0.5* 10 4.8±0.2 7 4.8+0.3 6
m 4.5±0.5 18(a) 3.9+0.4t 10 4.8+0.3 7 4.90.4 6
d 4.5+0.4 18(a) 3.8±0.3t 10 4.7±0.3 7 4.7+0.4 6
Left anterior descending
Llp 3.7±0.5 20 3.3±-0.4* 10 3.9±0.5 7 4.2±0.4* 6
m 3.6±0.5 20 3.2+0.5 10 3.8±0.5 7 3.90.5 6
d 3.5±0.6 20 3.1±0.5 10 3.6±0.3 7 3.6±0.7 6
L2p 2.9±0.5 20 2.8±0.5 10 3.1±0.5 7 3.2±0.4 6
m 2.5±0.5 20 2.4±0.4 10 2.8±0.5 7 3.0±0.4 6
d 2.3±0.4 20 2.2±0.5 10 2.4±0.4 7 2.8±0.4t 6
L3p 2.0±0.5 20 1.9±0.4 10 2.2±0.4 7 2.5±0.5 6
m 1.7±0.5 20 1.6±0.4 10 2.0±0.4 7 2.1±0.5 6
d 1.4±0.5 20 1.4±0.3 10 1.7±0.3 7 1.8±0.6 6
L4p 1.4+0.5 15(b) 1.1±0.5 8(c) 1.3±0.3 6(d) 1.1±0.2 3(e)
m 1.1±0.4 15(b) 0.9±0.3 8(c) 1.1±0.3 6(d) 1.1±0.4 3(e)
d 0.9±0.3 15(b) 0.7±0.2 8(c) 0.8±0.2 6(d) 1.0±0.2 3(e)
Left circumflex
Clp 3.4±0.5 20 2.9±0.5* 10 3.5±0.6 7 3.6±0.8 6
m 3.4±0.5 20 2.9±0.6* 10 3.3±0.7 7 3.6±0.6 6
d 3.3±0.5 20 2.9±0.6 10 3.1±0.7 7 3.6±0.6 6
C2p 2.8±0.5 11(f) 3.1±0.4 6(g) 3.1±0.5 4(g) 3.3±0.3* 4(g)
m 2.8±0.6 11(f) 3.1±0.4 6(g) 3.1±0.5 4(g) 3.3±0.2 4(g)
d 2.7±0.5 11(f) 3.0±0.4 6(g) 3.1±0.6 4(g) 3.1±0.3 4(g)
C3p 1.7±0.6 19 1.5±0.5 10 2.2±1.0 7 2.0±0.6 6
m 1.6±0.6 19 1.4±0.6 10 2.1±1.0 7 1.7±0.6 6
d 1.3±0.5 19 1.2±0.6 10 1.9±1.0 7 1.5±0.6 6
Right coronary
Rlp 4.0±0.6 20 3.4±0.7* 10 4.6±0.6 7 4.9±0.7t 6
m 3.9±0.6 20 3.3±0.6* 10 4.5±0.5* 7 4.6±0.7* 6
Downloaded from http://ahajournals.org by on September 16, 2019
6. Learoyd BM, Taylor MG: Alterations with age in the viscoelastic 27. Baroldi G, Scomazzoni G: Coronary Circulation in the Normal and
properties of human arterial walls. Circ Res 1966;18:278-292 the Pathologic Heart. Washington, DC, Armed Forces Institutes of
7. Bader H: Dependence of wall stress in the human thoracic aorta Pathology, 1967, pp 5-23
on age and pressure. Circ Res 1967;20:354-361 28. Harrison CV, Wood P: Hypertensive and ischemic heart disease: A
8. Markis JE, Joffe CD, Cohn PF, Feen DJ, Herman MV, Gorlin R: comparative clinical and pathological study. Br Heart J 1949;11:
Clinical significance of coronary artery ectasia. Am J Cardiol 1976; 205-229
37:217-222 29. Zamir M, Chee H: Segment analysis of human coronary arteries.
9. Swaye PS, Fisher LD, Litwin P, Vignola PA, Judkins MP, Kemp Blood Vessels 1987;24:76-84
HG, Mudd JG, Gosselin AJ: Aneurysmal coronary artery disease. 30. Koiwa Y, Bahn RC, Ritman EL: Regional myocardial volume
Circulation 1983;67:134-138 perfused by the coronary artery branch: Estimation in vivo. Circu-
10. Hartnell GG, Parnell BM, Pridie RB: Coronary artery ectasia: Its lation 1986;74:157-163
prevalence and clinical significance in 4,993 patients. Br Heart J 31. Woods JD: Relative ischaemia in the hypertrophied heart. Lancet
1985;54:392-395 1961;1:696-698
11. Takahashi M, Mason W, Lewis AB: Regression of coronary aneu- 32. Kennedy JW, Baxley WA, Figley MM, Dodge HT, Blackmon JR:
rysms in patients with Kawasaki syndrome. Circulation 1987;75: Quantitative angiocardiography: I. The normal left ventricle in
387-394 man. Circulation 1966;34:272-278
12. Jaffe RB, Glancy DL, Epstein SE, Brown BG, Morrow AG: Cor- 33. Kennedy JW, Kaiser GC, Fisher LD, Fritz JK, Meyers W, Mudd
onary arterial-right heart fistulae: Long-term observations in JG, Ryan TJ: Clinical and angiographic predictors of operative
seven patients. Circulation 1973;48:133-143 mortality from the Collaborative Study in Coronary Artery Sur-
13. Young DF, Cholvin NR, Roth AC: Pressure drop across artificially gery (CASS). Circulation 1981;63:793-802
34. Spray TL, Roberts WC: Status of the grafts and the native coro-
induced stenoses in the femoral arteries of dogs. Circ Res 1975;36: nary arteries proximal and distal to coronary anastomotic sites of
735-743 aortocoronary bypass grafts. Circulation 1977;55:741-749
14. Gould KL, Lipscomb K: Effects of coronary stenoses on coronary 35. Fisher LD, Kennedy JW, Davis KB, Maynard C, Fritz JK, Kaiser
flow reserve and resistance. Am J Cardiol 1974;34:48-55 G, Myers WO: Association of sex, physical size, and operative
15. Gould KL, Lipscomb K, Hamilton GW: Physiologic basis for mortality after coronary artery bypass in the Coronary Artery
assessing critical coronary stenosis: Instantaneous flow response Surgery Study (CASS). J Thorac Cardiovasc Surg 1982;84:334-341
and regional distribution during coronary hyperemia as measures 36. Kahn SS, Nessim S, Gray R, Czer LS, Chaux A, Matloff J:
of coronary flow reserve. Am J Cardiol 1974;33:87-94 Increased mortality of women in coronary artery bypass surgery:
16. Gould KL, Kelley KO: Physiological significance of coronary flow Evidence for referral bias. Ann Intern Med 1990;112:561-567
velocity and changing stenosis geometry during coronary vasodi- 37. Rodriguez FL, Robbins SL: Capacity of human coronary arteries.
lation in awake dogs. Circ Res 1982;50:695-704 Circulation 1959;19:570-578
17. MacAlpin RN, Abbasi AS, Grollman JH, Eber L: Human coronary 38. Rowe GG, Afonso S, Lugo JE, Castillo CA, Boake WC, Crumpton
artery size during life. Radiology 1973;108:567-576 CW: Coronary blood flow and myocardial oxidative metabolism at
18. Dodge JT, Brown BG, Bolson EL, Dodge HT: Intrathoracic spatial rest and during exercise in subjects with severe aortic valve disease.
location of specified coronary segments on the normal human Circulation 1965;32:251-257
heart. Circulation 1988;78:1167-1180 39. Henry PD, Eckberg D, Gault JH, Ross J Jr: Depressed inotropic
19. Brown BG, Bolson E, Frimer M, Dodge HT: Quantitative coro- state and reduced myocardial oxygen consumption in the human
nary arteriography: Estimation of dimensions, hemodynamic resis- heart. Am J Cardiol 1973;31:300-306
Downloaded from http://ahajournals.org by on September 16, 2019
tance, and atheroma mass of coronary artery lesions using the 40. Kennedy JW, Twiss RD, Blackmon JR, Dodge HT: Quantitative
arteriogram and digital computation. Circulation 1977;55:329-337 angiocardiography: III. Relationships of left ventricular pressure,
20. Dixon WJ, Massey FJ Jr: Introduction to Statistical Analysis. New volume, and mass in aortic valve disease. Circulation 1968;38:
York, McGraw-Hill Book Co, Inc, 1969, pp 335-340 838-845
21. Heiss G, Tamir I, Davis CE, Tyroler HA, Rifkind BM, Schonfeld 41. Benjamin JI, Schuster EH, Bulkley BH: Cardiac hypertrophy in
G, Jacobs D, Frantz ID Jr: Lipoprotein-cholesterol distributions in idiopathic dilated congestive cardiomyopathy: A clinicopathologic
selected North American populations: The Lipid Research Clinics study. Circulation 1981;64:442-447
Program prevalence study. Circulation 1980;61:302-315 42. Fallen EL, Elliott WC, Gorlin R: Mechanisms of angina in aortic
22. Wahl PW, Warnick GR, Albers JJ, Hoover JJ, Walden CE, Berge- stenosis. Circulation 1967;36:480-488
lin RO, Olgilvie JT, Hazzard WR, Knopp RH: Distribution of 43. Bertrand ME, LaBlanche JM, Tilmant PY, Thieuleux FP, Delforge
lipoprotein triglyceride and lipoprotein cholesterol in an adult MR, Carre AG: Coronary sinus blood flow at rest and during
population by age, sex, and hormone use. Atherosclerosis 1981;39: isometric exercise in patients with aortic valve disease. Am J Car-
111-124 diol 1981;47:199-205
23. Brown BG, Bolson EL, Dodge HT: Dynamic mechanisms in 44. Hutchins GM, BuLldey BH, Miner MM, Boitnott JK: Correlation
human coronary stenosis. Circulation 1984;70:917-922 of age and heart weight with tortuosity and caliber of normal
24. Liu LB, Richardson T, Holt JH, Taylor CB: Luminal eccentricity human coronary arteries. Am Heart J 1977;94:196-202
and deformity in atherosclerotic coronary arteries. ParoiArterielle 45. Gross L: The Blood Supply of the Heart. New York, Hoeber, 1921,
1976;3:167-169 p 151
25. Brown BG, Petersen RB: Computer-assisted measurements of cor- 46. Ganz W, Tamura K, Marcus HS, Donoso R, Yoshida S, Swan
onary artery stenosis. (reply) Circulation 1979;60:1196 HJC: Measurement of coronary sinus blood flow by continuous
26. Kimball BP, LiPreti VL, Bui S, Wigle ED: Comparison of proximal thermodilution in man. Circulation 1971;44:181-195
left anterior descending and circumflex coronary artery dimen- 47. Reiber JHC, Kooijman CJ, den Boer A, Serruys PW: Assessment
sions in aortic valve stenosis and hypertrophic cardiomyopathy.Am of dimensions and image quality of coronary contrast catheters
J Cardiol 1990;65:767-771 from cineangiograms. Cathet Cardiovasc Diagn 1985;11:521-531