JACC Vol. 20, No.5
November I, 1992:1149-55
1149
Target Lesion Calcification in Coronary Artery Disease:
An Intravascular Ultrasound Study
GARY S. MINTZ, MD, FACC, PHILLIPE DOUEK, MD, AUGUSTO D. PICHARD, MD, FACC,
KENNETH M. KENT, MD, PHD, FACC, LOWELL F. SATLER, MD, FACC,
JEFFREY J. POPMA, MD, FACC, MARTIN B. LEON, MD, FACC
Washington, D.C.
Objectives. The purpose of this study was to evaluate the
frequency, amount and distribution of target lesion calcification in
patients undergoing transcatheter therapy for symptomatic coronary artery disease.
Background. Coronary artery target lesion calcification may be
an important determinant of response to transcatheter therapy:
balloon angioplasty causes dissections in calcified lesions, directional atherectomy cuts calcium poorly, rotational atherectomy
causes preferential ablation of calcium and laser irradiation effect
may vary. Intravascular ultrasound imaging is a highly sensitive
technique for detection of plaque calcification in vivo.
Methods. We performed intravascular ultrasound imaging
before or after, or both, various transcatheter therapies in 110
patients. These 84 men and 26 women had a mean age of 60 years
and a duration of angina of 22 ± 34 months. Forty-nine patients
had one-vessel, 29 had two-vessel, 25 had three-vessel and 7 had
left main coronary disease. Vessels treated and imaged were the
left main (n = 7), left anterior descending (n = 47), left circumflex
(n = 18) and right (n = 38) coronary arteries.
Results. Eighty-four patients (76%) had target lesion calcifica-
tion; 29 patients had one-quadrant, 25 had two-quadrant, 17 had
three-quadrant and 13 had four-quadrant calcification. The calcification was superficial in 42 patients, deep in 13 and both
superficial and deep in 31. The axial length of calcium could be
measured in 29 patients; it was ::;5 mm in 11 and 2:6 mm in 18.
Fluoroscopy detected calcification in 50 patients (48%, p < 0.001
vs. detection by ultrasound); this proportion increased to 74% in
patients with calcification of two or more quadrants and to 86% in
patients with calcification 2:6 mm in length of two or more
quadrants. Calcification was more common in patients who
smoked and tended to be more common in patients with multivessel d!sease or previous coronary artery bypass graft surgery.
Conclusions. We conclude that target lesion calcification occurs
in 75% of patients with symptomatic coronary artery disease
requiring angioplasty. Target lesion calcification is best detected,
localized and quantified by intravascular ultrasound. These observations may be important in selecting devices for transcatheter
therapy.
(J Am Coli CardioI1992;20:1149-55)
Coronary artery calcification, particularly target lesion calcification, may be an important determinant of the arterial
response to transcatheter therapy for coronary artery disease (I). The barotrauma of balloon angioplasty causes
dissections in calcified target lesions (2); the calcific deposits
act as a wedge in creating cleavage planes through atherosclerotic plaque (3). Directional atherectomy does not cut
target lesion calcium well, and adjacent vessel calcification
impedes passage of the device (4,5). Rotational atherectomy
causes preferential ablation of calcified atherosclerotic
plaque (6). Continuous wave laser irradiation is ineffective
against calcium; in contrast, pulsed wave laser devices may
partially ablate calcium (7).
All conventional methods of detecting and localizing
coronary artery calcification have limitations. Intravascular
ultrasound imaging permits analysis of coronary artery
structure and atherosclerotic lesion morphology in a manner
not possible previously. In'this study we report the use of
this technique to determine the incidence and severity of
target lesion calcification in patients undergoing transcatheter therapy for symptomatic coronary artery disease.
From the Department of Medicine, Cardiology Division, Washington
Hospital Center, Washington, D.C.
Manuscript received January 31, 1992; revised manuscript received April
9, 1992, accepted April 16, 1992.
Address for correspondence: Martin B. Leon, MD, Washington Cardiol·
ogy Center, 110 Irving Street, Northwest, No. 4B·14, Washington, D.C.
20010.
©1992 by the American College of Cardiology
Methods
Patient group. We studied 110 patients undergoing transcatheter therapy for symptomatic native coronary artery
disease. Patients with a recent myocardial infarction and
patients with saphenous vein graft disease were excluded.
The clinical, angiographic and intravascular ultrasound records from these patients form the basis of this report.
There were 84 men and 26 women with a mean age of
60 ± 10 years (range 38 to 77) and a duration of angina of 22
± 34 months (range <1 month to 12 years). Hypertension
was present in 63 patients and insulin·dependent diabetes in
13. There was a history of remote myocardial infarction in 38
0735·1097192/$5.00
1150
MINTZ ET AL.
TARGET LESION CALCIFICATION IN CORONARY ARTERY DISEASE
patients and of previous coronary artery bypass graft surgery in 18. Thirty-eight patients were smokers; two were on
maintenance dialysis.
Forty-nine patients had one-vessel, 29 had two-vessel, 25
had three-vessel and 7 had left main coronary disease.
Vessels treated and imaged were the left main (n == 7), left
anterior descending (n == 47), left circumflex (n == 18) and
right (n == 38) coronary arteries. Transcatheter therapeutic
modalities were balloon angioplasty in 36 patients, stent
placement (Johnson and Johnson Interventional Systems or
Medtronic) in 8, excimer laser coronary angioplasty (Advanced Interventional Systems) in 9, directional coronary
atherectomy (Devices for Vascular Intervention) in 29, high
speed rotational atherectomy (Heart Technology) in 25 and
transluminal extraction catheter atherectomy (Interventional
Technologies) in 3. All patients with sten! placement underwent imaging before the intervention.
Patients were studied after giving written, informed consent. Intravascular ultrasound imaging is performed as part
of ongoing protocols approved by the Institutional Review
Board of the Washington Hospital Center.
Fluoroscopic-angiographic study. The presence of calcification in the target lesion was evaluated during fluoroscopy
before the ultrasound study was performed or by persons
who did not know the ultrasound results. With use of digital
electronic calipers, the percent angiographic diameter stenosis was measured in orthogonal projections. The angiographic target lesion was defined as the entire length of
lesion SUbjected to transcatheter device therapy. The mean
percent angiographic diameter stenosis was 79 ± 12% (range
58% to 100%) before intervention.
Intravascular ultrasound imaging systems. We used the
InterTherapy intravascular ultrasound imaging system incorporating either a 20-MHz transducer-tip catheter within a
4.9F sheath or a 25-MHz transducer-tip catheter within a
3.9F sheath. Point to point resolution along the ultrasound
beam axis was calculated to be 100 pm for the 20-MHz and
80 /-Lm for the 25-MHz catheter; the calculations are based on
transducer frequency and wavelength and the speed of
ultrasound transmission in tissue. The maximal penetration
depth was 8 mm, which was also a function of the tissue type
being imaged. Planar two-dimensional images were formed
in real time by motor rotation of the entire transducer-tip
catheter within the polyethylene imaging sheath at 1,800
rpm. In 40 patients, the 25-MHz tipped catheter was withdrawn within the imaging sheath at 0.5 mmis by a prototype
motorized pullback device. At this pullback rate, contiguous
image slices were 17 JLm apart. Studies performed in this
manner provided source material for many of the illustrations in this study. Studies were recorded on high resolution
0.5-in. (1.27-cm) videotape for off-line analysis.
Three-dimensional reconstruction of the planar intravascular ultrasound images was possible in the 40 patients in
whom imaging was performed with the motorized pullback
mechanism. We used software developed by Pura and hardware from Image Comm. The software-encoded algorithm
JACC Vol. 20, No.5
November 1,1992:1149-55
Figure 1. Intravascular ultrasound images from six patients illustrating patterns of calcium distribution. A, C and F, Superficial calcification (solid arrows). D, Deep calcification (open arrow). Band E,
Superficial (solid arrow) and deep (open arrow) calcification. In A,
the adventitia shadowed by the lesion calcification is reconstructed
by a dotted line; the ultrasound catheter is shown by the long white
arrow.
uses thresholding to render the three-dimensional image.
The hardware can digitize 6 frames/so Parameters were set so
that 12 image slices were stacked per mm of arterial length;
230 digitized images were used to reconstruct a segment of
artery 19 mm long. Regions of interest were set to include all
arterial structures between the adventitia and intima and to
exclude the imaging sheath. The threshold was set just low
enough to exclude blood echoes. Each arterial segment
either was viewed as an intact cylinder or was split in half to
be viewed as two hemicylinders.
Qualitative ultrasound. Calcification is detected as bright
dense echoes (brighter than the reference adventitia) with
acoustic shadowing of underlying tissue. Calcification is
differentiated from dense fibrous tissue by the presence of
acoustic shadowing. Dense fibrous tissue also causes bright
echoes (as bright as or brighter than those of the reference
adventitia but usually less bright than those of calcium), but
usually without acoustic shadowing (8-1 Calcification was
classified as 1) superficial if it involved the lumen-intimal
interface, 2) deep if it was within the plaque with 2:0.3 mm of
overlying noncalcified plaque, or 3) both (Fig.
Quantitative ultrasound. The circumference of atherosclerotic plaque in the target iesion occupied by calcium was
measured as an arc (in 0) with a protractor centered on the
imaging catheter (Fig. 2). The target lesion was identified by
using a fluoroscopic reference for the ultrasound catheter
position to ensure accurate comparison with angiographic
data. If there was more than one calcific deposit in a given
imaging slice, the arcs of calcium were added. If the arcs
overlapped, they were measured as a single continuous arc.
JACe Vol. 20, No.5
November I, 1992:1149-55
1151
MINTZ ET AL.
TARGET LESION CALCIFICATION IN CORONARY ARTERY DISEASE
tration) was confirmed by relating the three-dimensional
reconstruction to the corresponding two-dimensional image
slices.
was performed by
Statistical analysis. Statistical
using chi-square analysis, the Student test, the Fisher exact
test, analysis of variance or correlation coefficients where
appropriate. Results are reported as mean value ± 1 SD.
Results
Figure 2. Intravascular ultrasound images from four patients, illustrating the measurement of the circumferential arc of calcium. A,
Noncalcified artery. B, Fibrotic-calcific atherosclerotic plaque with
an arc (arrows) of calcium measuring 74° (note the shadowing of the
deeper tissues beyond the calcium). C, Artery with an arc of calcium
measuring 271°. D, Complete (360°) circumferential intimal calcification.
With the motorized pullback device, the length of each
calcific deposit or the overall length of contiguous and
overlapping calcific deposits was measured in 40 patients.
With the imaging catheter moving at 0.5 mm/s, each second
of recorded videotape represents a segment of artery 0.5 mrn
long. Two contiguous imaging slices are 17 ,urn apart. For the
purposes of this study, the length of a calcified arterial
segment was calculated from the number of seconds or the
number of frames of videotape in which it appeared (Fig. 3
and
With three-dimensional reconstruction, the area of intimal surface occupied by calcification could be visualized.
When visualizing the artery from outside the adventitia,
adventitial dropout represented underlying calcification (Fig.
5). Confirmation that adventitial dropout was caused by
underlying calcification (rather than by weak acoustic pene-
Figure 3. Intravascular ultrasound images of a
short calcific deposit (shown by open arrows)
that is circumferential in the second image slice
and 1O{)0 in the third image slice. The study was
performed with the motorized pullback device.
Image slices shown are I mm apart at center;
the most distal slice is at left, and the most
proximal slice is at right. The calcific deposit
occupies <2 mm of axial vessel length. No
calcium was detected on fluoroscopic study.
Fluoroscopic analysis. By fluoroscopy, 50 patients (48%)
had calcification in the region of the target lesion treated by
transcatheter therapy.
Intravascular ultrasound analysis. By intravascular ultrasound, 84 patients (76%) had target lesion calcification (p <
0.001 vs. the number detected with fluoroscopy). Fortyseven patients (56%) had a single calcific deposit; the other
37 had two or more calcific deposits. In these 84 patients the
arc of calcium measured 100 ±
(range 00 to 360°); in 29
patients it measured ~90°, in 25 patients 91° to 180°, in 17
patients 181° to 270° and in 13 patients 271 to 360 (Fig. 6).
In 42 patients (50%) the calcification was superficial, in 13
(15%) it was deep and in 31 (35%) it was both superficial and
deep.
In 40 patients the longitudinal length of single or mUltiple
contiguous calcific deposits could be measured. Twenty-nine
of these patients (73%) had target lesion calcification. The
mean length was 15 ± 9 mm (range to 40). In 11 patients,
the length was :55 mm, in 6 it was 6 to 10 mm, in 7 it was 11
to 20 mm and in 5 it was >20 mm. In these 29 patients there
was no significant correlation between the arcs and length of
target lesion calcification (Fig. 7).
Typically, there was significant axial variability in the
circumferential arc of calcification within each lesion site
(Fig. 8 and 9).
Clinical correlates (Table
Target lesion calcium did
not correlate with patient age, duration of angina or a history
of hypertension, diabetes or a remote myocardial infarction.
Calcification was more common in smokers (37 of 38) than in
nonsmokers (49 of72, p < 0.001) and the arc of calcium was
larger in smokers than in nonsmokers (157 ± 1260 VS. 83 ±
91°, p < 0.02). Calcification tended to be more common in
0
0
1152
lAce Vol. 20, No.5
November 1, 1992:1149-55
MINTZ ET AL.
TARGET LESION CALCIFICATION IN CORONARY ARTERY DISEASE
Figure 4. Intravascular ultrasound images of a long, circumferential
calcium deposit (arrows). Image slices shown are 5 mm apart at
center; the most distal slice is at left and the most proximal slice is
at right. The uninterrupted calcific deposit occupies 40 mm of axial
vessel length. Extensive calcium was evident on fluoroscopic study.
patients with multivessel or left main disease (53 of 61) than
in patients with single-vessel disease (35 of 49, p = 0.060)
and the arc of calcification tended to be larger in the former
Figure 5. Three-dimensional reconstruction of intravascular ultrasound images, showing the circumferential and the axial distribution
of calcium. The artery is shown as two hemicylinders and is viewed
from outside so that only the outermost layer (or adventitia) is seen
normally. A and F show hemicylinders, 20 mm long. Adventitial
dropout (short thin arrows) represents acoustic shadowing from
underlying calcification. The axial length of the largest calcium
deposit is from point G to point H. Panels D, C, D and E are
two-dimensional image slices from this artery. The calcium in these
two-dimensional image slices is shown by the open arrows. The long
arrows locate these image slices within the axial length of the artery
shown in F.
groups (137 ± 1180 vs. 81 ± 79°, p <
Similarly, target
lesion calcification tended to be more common in patients
with than in those without previous coronary artery bypass
graft surgery
of 18 vs. 70 of 92, p =:
and the arc of
group (137 ± 118 0 vs.
calcification tended to be larger in
81 ± 79°, p < 0.05). There were too few patients with
insulin-dependent diabetes mellitus or chronic renal insufficiency for statistical analysis. Target lesion calcification did
not correlate with the angiographic percent diameter stenosis before intervention or with lesion location or morphology.
Fluoroscopic-ultrasound correlations. Fluoroscopic target
lesion calcification was more common in patients whose arc
of calcification measured ;;::91 0 (36 (74%] of 51) than in
patients whose arc measured ::;90 (10 [29%] of 33, p <
0.001).
In 40 patients, both the arc and the length of calcification
could be measured. When both of these variables were
fluoroscopy in no
considered, calcium was detected
patient with an arc ::;900 and a length ::;5 mm, 0 of 5 patients
with an arc 91° to 360 and a length ::;5 mm, 2 of 3 patients
with an arc ::;900 and a length ;;::6 mm and 13 (86%) of 15 of
patients with an arc 91° to 3600 and a length ;;::6 mm.
Three-dimensional reconstruction of ultrasound image
slices. Intimal surface (plaque) calcification was not obviously different from a noncalcified intimal surface, and
deeper tissue calcification was not seen at all. However,
when viewed from outside the artery (Fig. 5), adventitial
dropout accurately reflected underlying superficial and deep
0
Figure 6. Distribution of target lesion calcification according to the
number of quadrants involved. Twenty-four percent of 110 patients
had no calcification, 26% had calcification of one quadrant, 23% of
two quadrants, 15% of three quadrants and 12% of four quadrants.
N=110 patients
26%
1-90
91·180
1111-270 271·360
Arc of Target Lesion Calcium (degrees)
MINTZ ET AL.
TARGET LESION CALCIFICATION IN CORONARY ARTERY DISEASE
lACC Vol. 20, No.5
1992:1149-55
;>.lovember
The normal coronary artery architecture (intima,
media and adventitia) and the major components of the
atherosclerotic plaque
loose and dense fibrous connective tissue, intimal hyperplasia and calcium) can be
studied in vivo in a manner not possible previously.
In previous studies, the acoustic signature of arterial
plaque calcium, dense fibrous tissue and soft plaque (containing lipid, loose connective tissue or intimal hyperplasia)
has been validated in vitro. Using intravascular ultrasound
imaging, we detected calcium in 84 (76%) of 110 lesions
targeted for transcatheter therapy. This proportion approximates the highest pathologic incidence reported.
Calcification can be superficial or deep and occur in single
or multiple discrete deposits. However, circumferential deposition of calcification tends to be greater than axial deposition. Short arterial segments with extensive (multi quadrant)
circumferential calcification are more common than are long
segments with single-quadrant calcification.
Within any length of calcified artery, there can be extensive axial variability in the pattern of calcium deposition.
Axial variability tends to be more pronounced than circumferential variability and is greater in heavily calcified than in
lightly calcified arteries. Both very short calcified segments
and the marked axial variability in calcium deposition are
seen best with slow movement of the transducer and careful
interrogation of the entire artery, which can be facilitated by
motorized transducer movement. Furthermore, intravascular ultrasound imaging can differentiate target lesion calcification from calcification of contiguous arterial segments.
Many studies have used X-ray techniques to detect
coronary artery calcification to screen for hemodynamically
significant coronary artery disease. A meta-analysis of 13
reports (21) suggested that 58% of patients with documented
coronary artery disease have fluoroscopic calcification. This
frequency may be increased by using digital subtraction
fluoroscopy (22), computed tomography (22-24) and ultrafast computed tomography (25,26). In our study, there was
fluoroscopic calcification in 48% of lesions targeted for
transcatheter therapy. With use of intravascular ultrasound
imaging as the standard, fluoroscopic calcification increased
with increasing amounts of target lesion calcification. Fluoroscopy detected calcium in 74% of patients with multiquadrant target lesion calcification and in 86% of patients with
(8-1
~36°1
~
~270
~
. ..
l O+---~~--~~--~--~--~~
o
5
U
U
•
~
~
9
~
Length of Target Lesion Calcium (mm)
Figure 7. There is no correlation between the circumferential arc of
target lesion calcification and its axial length.
plaque calcification in all patients. Small and large calcific
deposits were seen equally well. Contiguous calcium deposits appeared as a single large deposit unless they were
separated by 1 mm of uncalcified artery. Circumferential
calcification as short as 1 mm appeared as "napkin-ring"
adventitial dropout. Long, single-quadrant calcification appeared as a linear streak of adventitial dropout.
Discussion
Lesion-associated calcification is found frequently at necropsy in patients with coronary atherosclerosis (12,13).
These studies have shown that coronary artery calcification
increases with the extent and severity of atherosclerosis
(14), patient age (15,16) and primary or secondary chronic
hypercalcemia (17). In addition, both hyperlipidemias
(18,19) and chronic renal failure (20) may predispose to
coronary artery calcification, the former by accelerating
atherogenesis and the latter by causing chronic hypercalcemia. The highest pathologic incidence reported is 79% (4).
However, pathologic detection has limitations. Patient selection is biased and specimens usually are decalcified before
staining. In vitro X-ray analysis of pathologic tissue has
limited resolution and is only semiquantitative. With the
motorized pullback device, it is possible to slice the artery
into more and thinner slices with intravascular ultrasound
than is commonly done during pathologic analyses.
High frequency intravascular ultrasound provides detailed transmural images of human coronary arteries in vivo
Figure 8. Variability in circumferential arc of target lesion calcification
even within a short « 1
arterial
segment. Image slices shown are
0.1 mm apart at center; the most
distal slice is at left, and the most
proximal slice is at right. Arrows
point to calcific deposits in some of
the image slices.
1153
1154
MINTZ ET AL.
TARGET LESION CALCIFICATION IN CORONARY ARTERY DISEASE
JACC Vo\. 20, No.5
November I, 1992:1149-55
Table 1. Clinical Correlates in the Study Group
Calcium
(no. of
patients)
a
360
.E!
~ ';'270
d
~ 180
... u
e ..
~
o
901~===:::~====~
......
u 'C
-10 -8
A
.E!
~
·1
0
1
4
6
8
10
Distance from Center of Lesion (mm)
90 .
~{ll~ii~~~~lIliliii!l~~
.!: 'iii"170 ..
=-
"' -4
~ ~180 .
e..
a 'C .
~ ......
o
B
~
..
.10·8·6 -4
·1
0
1
4
6
8
10
Distance from Center of Lesion (mm)
I!iY
360
Arc of
Calcium (")
(mean ± SD)
Smoking
Yes
No
370f38
49 of 72
} <0.001
157 ± 126
83 ± 91
}
<0.02
Hypertension
Yes
No
48 of 63
39 of 47
} NS
95 ± 107
100 ± 97
}
NS
Remote MI
Yes
No
30 of 38
58 of 72
} NS
119 ± lOS
194 ± 106
}
NS
CABG
Yes
No
17 of 18
70 of 92
}
0.076
194 ± 106
100 ± 98
}
<0.01
CAD
I-V
2-V/3-VILM
35 of 49
53 of 61
}
0.060
81 ± 79
137 ± 118
}
<0.05
36 of 47
16 of 18
270f38
} NS
93 ± 110
lOS ± 76
86 ± 91
}
NS
LAD
LCx
RCA
Values outside braces indicate p values. CABG = coronary artery bypass
graft surgery; CAD = coronary artery disease; LAD = left anterior descending coronary artery; LCx = left circumflex coronary artery; LM = left main
coronary artery; MI = myocardial infarction; RCA = right coronary artery;
V = vessel.
<IS ..
3!'iii"170~...
~ ~180·
e ..
u'C
~
......
C
~
90
o
-10·8",
-4
.1
0
1
4
6
8
10
Distance from Center of Lesion (mm)
360
:g ';'270
90 t~~~~~~~~~~~~;7
~ ~180
e ..
u'C
<IS..
~
......
D
o
-10 -8
"' -4
·1
0
1
4
6
8
10
Distance from Center of Lesion (mm)
Figure 9. Graphs illustrating the variability in arc of calcium within
any given target lesion length. The arc of calcification is shown on
the y axis; the target lesion length is shown on the x axis as the
distance from the center of the lesion with the most distal end of the
lesion in negative numbers at left. Individual patients are shown on
the z axis. A, Four patients with calcification of one quadrant. B,
Nine patients with calcification of two quadrants. C, Seven patients
with calcification of three quadrants. D, Nine patients with calcification of four quadrants. The center of the lesion was the longitudinal middle of the most severe length of stenosis (as determined by
intravascular ultrasound imaging using the motorized pullback device).
long multiquadrant calcification and a length ~6-mm. However, fluoroscopy missed all examples of short multiquadrant calcification with a length <5 mm.
Limitations. Our study has several limitations.
1. On pathologic study, calcific deposits have width,
length and thickness. Because of acoustic shadowing artifacts, our method may minimize the true amount of calcium
present. Most often, ultrasound studies were performed
after transcatheter therapy, and some trans catheter therapies (for example, rotational atherectomy) remove calcium.
Thus, calcification may be even more common and more
extensive than our data suggest.
2. From the standpoint of impact on transcatheter therapy, the most important measurement may be the intimal
surface area occupied by calcium. By measuring the intimal
arc and axial length of calcium, we can approximate its
surface area. Current algorithms for three-dimensional reconstruction of intravascular ultrasound images do not permit a true measurement of the intimal surface occupied by
calcium. However, the surface area of adventitial dropout
does reflect the surface area of underlying plaque calcification. Also, it is not possible to measure the thickness of the
calcific deposits; the inner edge shadows the outer edge.
Similarly, superficial plaque calcification obscures deep
plaque calcification. Calcification thickness may also play an
important role in arterial responses to transcatheter therapy.
JACC Vol. 20, No.5
November I, 1992:1149-55
MINTZ ET AL.
TARGET LESION CALCIFICATION IN CORONARY ARTERY DISEASE
3. Few of our patients had chronic total occlusions. The
plaque composition in such patients may differ from that of
our study group. Plaque calcification in chronic total occlusions is important if a truly effective transcatheter therapy is
to be developed, especially if this therapy is based on laser
technology.
4. Our observations are limited to native vessel target
lesion morphology in symptomatic patients. We did not
image nontarget lesion vessels or vessels in asymptomatic
patients. We have not included data on saphenous vein
bypass grafts, and we also excluded patients with an acute
infarction.
5. With current imaging systems, all plaque calcium looks
alike. Calcium may be incorporated into atherosclerotic
plaque in more than one way; the way it is incorporated may
influence the structural integrity of the plaque and the
arterial response to transcatheter therapy (27).
6. We did not attempt to relate procedural success to the
amount or distribution of target lesion and adjacent vessel
calcification. This important study needs to be done.
Implications. Calcification is a major determinant in how
target lesions respond to various transcatheter therapies.
Recently developed low profile imaging catheters (such as
the 3.9F catheter used in 40 of our studies) makes imaging
feasible before intervention. As more trans catheter therapies
become available, it may become important to use intravascular ultrasound to analyze target lesion composition to
select among them.
References
I. Potkin BN, Mintz GS, Matar FA, et aI. A mechanistic comparison of
transcatheter therapies assessed by intravascular ultrasound (abstr).
Circulation 1991;84(suppl I1):II·541.
2. Potkin BN, Mintz GS, Keren G, Douek PC, Matar FA, Satler LF.
Ultrasound assessment of lesion composition predicts mechanisms of
PTCA (abstr). Circulation 1991;84(suppl I1):II·722.
3. Fitzgerald PJ, Sudhir K, Sykes CM, Ports TA, Strunk BL, Yock PG.
Localized calcium is a major risk factor for arterial dissection during
angioplasty: a catheter ultrasound study (abstr). Circulation 1991 ;84(suppl
II):II·722.
4. Robertson GC, Horihara T, Selmon MR, Johnson DE, Simpson JB.
Directional coronary atherectomy. In: Topol EJ, ed. Textbook of Inter·
ventional Cardiology. Philadelphia: WB Saunders, 1990:563-79.
5. Matar FA, Mintz GS, Potkin BN, et aI. Ultrasound plaque composition
determines directional coronary atherectomy effect (abstr). Circulation
1991;84(suppl II):II·154.
6. Bertrand ME, Fourrier JL, Auth DC, Lablanche JM, Gommeaux AF.
Percutaneous coronary rotational angioplasty. In: Ref 4:580-9.
7. Isner JM. Pathology in cardiovascular laser therapy. In: Isner MJ, Clarke
RH, eds. Cardiovascular Laser Therapy. New York: Raven, 1989:63-87.
1155
8. Tobis JM, Mallery JA, Gessert J, et al. Intravascular ultrasound crosssectional arterial imaging before and after balloon angioplasty in vitro.
Circulation 1989;80:873-82.
9. Potkin BN, Bartorelli AL, Gessert JM, et aI. Coronary artery imaging
with intravascular high-frequency ultrasound. Circulation 1990;81:157585.
10. Nishimura RA, Edwards WD, Warnes CA, et al. Intravascular ultrasound
imaging. In vitro validation and pathologic correlation. J Am Coli Cardiol
1990;16:145-54.
11. Gussenhoven EJ, Essed CE, Lancee CT, et aI. Arterial wall characteristics determined by intravascular ultrasound imaging. An in vitro study.
J Am Coli CardioI1989;14:947-52.
12. Blankenhorn DH. Coronary arterial calcification. A review. Am J Med
Sci 1961;242:4-49.
13. Warburten RK, Tampas JP, Soule AB, Taylor HE III. Coronary artery
calcification: its relationship to coronary artery stenosis and myocardial
infarction. Radiology 1968;91:109-15.
14. Frink RJ, Achor RWP, Braun AL Jr, Kincaid OW, Brandenburg RO.
Significance of calcification of the coronary arteries. Am J Cardiol
1970;26:241-7.
15. Waller BF, Roberts WC. Cardiovascular disease in the very elderly.
Analysis of 40 necropsy patients aged 90 years or over. Am J Cardiol
1983;51:403-21.
16. Gertz SD, Malekzadeh S, Dollar AL, Kragel AH, Roberts WC. Composition of atherosclerotic plaques in the four major epicardial coronary
arteries in patients ~90 years of age. Am J Cardioll99I;67:1228-33.
17. Roberts WC, Waller BF. Effect of chronic hypercalcemia on the heart.
Am J Med 1981;71:371-84.
18. Sprecher DL, Schaefer EJ, Kent KM, et al. Cardiovascular features of
homozygous familial hypercholesterolemia: analysis of 16 patients. Am J
CardioI1984;54:20-30.
19. Dinsmore RE, Lees RJ. Vascular calcification in types II and IV hyperIipoproteinemia: radiographic appearance and clinical significance. Am J
Roentgenoll985;144:895-9.
20. Meema HE, Oreopoulos 00, deVeber GA. Arterial calcifications in
severe chronic renal disease and their relationship to dialysis treatment,
renal transplant, and parathyroidectomy. Radiology 1976;121:315-21.
21. Gianrossi R, Detrano R, Colombo A, Froelicher V. Cardiac fluoroscopy
for the diagnosis of coronary artery disease: a meta analytic review. Am
Heart J 1990;120:1179-88.
22. Detrano R, Markovic D, Simpfendorfer C, et al. Digital subtraction
fluoroscopy: a new method of detecting coronary calcification with
improved sensitivity for the prediction of coronary disease. Circulation
1985;71:725-32.
23. Moore EH, Greenberg RW, Merrick SH, Miller SW, McCloud TC,
Shepard 10. Coronary artery calcification: significance of incidental
detection on CT scans. Radiology 1989;172:711-6.
24. Masuda Y, Naito S, Aoyagi Y, et al. Coronary artery calcification
detected by CT: clinical significance and angiographic correlates. Angiology 1990;41:1037-47.
25. Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamante M Jr,
Detrano R. Quantification of coronary artery calcium using ultrafast
computed tomography. J Am Coli Cardioll990;15:827-32.
26. Tanenbaum SR, Kondos GT, Veselik KE, Prendergast MR, Brundage
BH, Chanka EV. Detection of calcific deposits in coronary arteries by
ultrafast computed tomography and correlation with angiography. Am J
CardioI1989;63:870-2.
27. Foreman DW, Mitchell JC, Baker PB. Physical chemical evidence of
structural weakness in coronary arterial calcification. Cardiovasc Res
1989;23:64-9.