SHAPE Society

1. Editorial Slides
VP Watch –July 10, 2002 - Volume 2, Issue 27
Coronary Pan-Artritis;
How Specific Is Inflammation to Culprit Lesions?

2.  Atherogenic diet in animals induces
monocytes adhesion to vascular
endothelium and accumulation in lesion-
prone arterial sites. 1
 Davis et al. showed that coronary plaques
with positive remodeling have a higher lipid
content and macrophage count which
explain why plaque rupture is often
apparent at sites with only modest luminal
stenoses. 5

3.  Macrophage-rich areas are more frequently
found in patients with unstable angina and
non-Q-wave MI.
 Moreno, Falk, and others suggested that
macrophages are a marker of vulnerable
plaques and play a significant role in
pathophysiology of acute coronary
syndromes.3

4.  Libby et al. have shown that inflammation
links atherosclerosis to thrombosis. 12
 Inflammation of atherosclerotic plaque
seems to be a feature in a cascade of
events that eventually lead to plaque
rupture. 7,8

5. • In 1997 Boyle studied the extent of
inflammation in 351 coronary ruptured and
unruptured plaques. He found a prevalence
of inflammation of 5% to 10% in superficial
plaque of control group. 9
• Boyle described that inflammation was
common ( 40%) in deeper layers of the
atherosclerotic plaque and was associated
with lipid but not with rupture. 9

6.  Pasterkamp and coworkers found that
inflammation of cap and shoulder of the
plaque is a common feature, locally
observed, in atherosclerotic femoral and
coronary arteries. 6
 They suggest that high prevalence of
local inflammatory responses should be
considered if they are used as a
diagnostic target to detect vulnerable,
rupture-prone lesions. 6

7. • Casscells, Willerson, and coworkers found
a temperature rise in 37% of 50 samples of
carotid artery specimens. 10
• Temperature differences were correlated
significantly with cell density in the
plaques. 10
• They showed that temperature differences
could be observed very close to one
another (<1 mm). 10

8.  As reported in VP Watch of this week,
Buffon, Maseri, and colleagues by measuring
neutrophil myeloperoxidase found that patients
with unstable angina had evidence of
inflammation in left coronary artery even if it
was free of substantial atherosclerosis and
culprit stenosis was in the right coronary artery.
 They found that neutrophil myeloperoxidase
content of aortic blood was lower in unstable
angina compared to stable angina.

9.  Maseri et al. found no significant increase in
neutrophil activation in the great cardiac vein in
controls, in patients with stable angina and
documented left anterior descending coronary
stenosis, or in patients with active variant angina
and recurrent ischemia in the territory of the left
anterior descending coronary artery.
 They also did not detect any elevation in
neutrophil activation through femoral circulation
in any of their groups studied (unstable angina,
stable angina, coronary stenosis, variant angina,
and healthy controls).

10. Conclusion
 Subjects with an increased risk of acute
coronary events are likely to have many
vulnerable plaques throughout the
coronary tree.
 Patients who are prone to unstable angina
will have widespread coronary
inflammation.

11. Questions:
• How specific is inflammation to
vulnerable plaque? In other
words, if a site of inflammation
is found in coronary artery,
what is the likelihood of
becoming a culprit plaque?

12. • Are stable (non-vulnerable)
plaques equally inflamed like
vulnerable plaques?
• Given widespread coronary
inflammation (pan-artritis) how
can coated stent stand as the
treatment of choice?
Questions:

13. 1) Ross R. Atherosclerosis -- an inflammatory disease. N Engl J Med 1999;340:115-126.
2) van der Wal AC, Becker AE, van der Loos CM, Das PK. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is
characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation 1994;89:36-44.
3) Moreno PR, Falk E, Palacios IF, Newell JB, Fuster V, Fallon JT. Macrophage infiltration in acute coronary syndromes: implications for plaque
rupture. Circulation 1994;90:775-778.
4) Shah PK, Falk E, Badimon JJ, et al. Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic
plaques: potential role of matrix-degrading metalloproteinases and implications for plaque rupture. Circulation 1995;92:1565-1569.
5) Varnava AM, Mills PG, Davies MJ. Relationship between coronary artery remodeling and plaque vulnerability. Circulation. 2002 Feb
26;105(8):939-43.
6) Gerard Pasterkamp; Arjan H. Schoneveld; Allard C. van der Wal; Dirk-Jan Hijnen; Willem J. A. van Wolveren; Simon Plomp; Hans L. J. M.
Teepen; Cornelius Borst Inflammation of the atherosclerotic cap and shoulder of the plaque is a common and locally observed feature in
unruptured plaques of femoral and coronary arteries. Arterioscler Thromb Vasc Biol. 1999 Jan;19(1):54-8
7) Davies MJ, Thomas AC. Plaque fissuring: the cause of acute myocardial infarction, sudden ischaemic death, and crescendo angina. Br Heart
J. 1985;53:363–373
8) Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation. 1995;92:657–671
9) Boyle JJ. Association of coronary plaque rupture and atherosclerotic inflammation. J Pathol. 1997;181:93–99
10) Casscells W, Hathorn B, David M, Krabach T, Vaughn WK, McAllister HA, Bearman G, Willerson JT. Thermal detection of cellular infiltrates
in living atherosclerotic plaques: possible implications for plaque rupture and thrombosis. Lancet. 1996;347:1447–144
11) Davies MJ, Bland JM, Hangartner JRW, Angelini A, Thomas AC. Factors influencing the presence or absence of acute coronary artery
thrombi in sudden ischemic death. Eur Heart J. 1989;10:203–208
12) Peter Libby; Vasc Med 1998;3(3):225-9 The interface of atherosclerosis and thrombosis: basic mechanisms.
References