Clin. Cardiol.
19, 656-661 (1996)
Clinical Pathologic Correlations
This section edited by Bruce Wallel; M.D.
Nonatherosclerotic Causes of Coronary Artery Narrowing-Part
BRUCEF. WALLER,M.D.,* t EDWARD
T. A. FRY,M.D.,? JAMES B. HERMILLER,M.D.,"
*Cardiovascular Pathology Registry, St. Vincent Hospital; tNasser, Smith and Pinkerton Cardiology, Inc., Indianapolis, Indiana, USA
Summary:Approximately 5% of patients with acute myocar-
dial infarction do not have atheroscleroticcoronary artery dis-
ease but have other causes for their luminal narrowing. The
third part of this three-part review of nonatherosclerotic caus-
es of coronary narrowing focuses on coronary vasculitis, in-
fectious diseases, Kawasaki's disease, metabolic disorders,
metastatic disease, and substance abuse (cocaine).
Key words: coronary vasculitis, Kawasaki's disease, cocaine,
metastatic tumor
Coronary Artery Arteritis (Vasculitis)
Epicardial coronary arteritis (vasculitis) is a rare event that
has been reported in several conditions .The result-
ing coronary injury may directly lead to myocardial is-
chemidinfarction (MI) with or without associated coronary
artery thrombosis.' Baroldi2 provides a useful classification
of the arteritis conditions based upon type of coronary artery
route of entry. Coronary arteritis may result From direct exten-
sion from adjacent organ or tissue infections (e.g., epicardial
or myocardial abscess from aortic valve endocarditis, pericar-
dial tuberculosis). In this situation, the coronary artery adven-
titial layer is initially involved. Coronary arteritis may result
from a hematogenous spread through the coronary lumen or
through vasa vasorum. In this situation, the intimal layer is
initially involved. In other vasculitides, the exact mechanism
of vascular origin is not understood. Baroldi2 also considers
the following morphologic-histologic findings as signs of
Address for reprints:
Bruce E Waller. M.D.
8333 Naab Road, Suite 400
Indianapolis, IN 46260, USA
Received: February 9, 1996
Accepted: March 25, 1996
III
THOMAS
PETERS, M.D.,? JOHN D. SLACK,
M.D.,?
coronary arteritis: (1) focal artery necrosis with or without
calclfication, (2) acute coronary artery thrombosis or recanal-
ized thrombus unassociated with underlying atherosclerotic
plaque, (3) rupture of the vessel wall unassociated with trau-
ma or an interventional procedure, (4) coronary artery wall
thickening with secondary luminal narrowing, and (5) wall
thinning with aneurysm formation.3 Specific coronary le-
sions also may be seen in specific systemic diseases (e.g., pol-
yarteritis nodosa).
Tbberculosis
Tuberculosis arteritis is seen chiefly in patients with pen-
cardial or myocardial lesions. Specific coronary artery gran-
uloma may involve the adventitia, the intima, or the entire
wa11.234
PolyarteritisNodosa
Polyarteritis nodosa is probably the most common cause
of coronary angitis. It is a systemic necrotizing vasculitis that
affects medium and small vessels. Of 66 cases studied by
Holsinger et al.? 41 (62%) had involvement of the epicardial
coronary arteries and 4 1 also had myocardial infarcts of vary-
ing size. The coronary lesions resemble the necrotizing vas-
cular lesions elsewhere, with an acute cellular phase with de-
struction of the media and internal elastic membrane and sub-
sequent intimal proliferation and scar in the healed phase.
The coronary artery may dilate to form small berry-like aneu-
rysms, become occluded by thrombus, or rupture (producing
fatal pencardial tamponade).6
Giant Cell Arteritis
Giant cell arteritis affects chiefly the temporal and other
cranial arteries, but coronary artery involvement and myocar-
*
dial infarction have been reported by Ainsworth et al.'. The
arterial wall lesion is a granulomatous inflammation with gi-
ant cells found along a degenerated internal elastic mem-
 B.F. Waller o r ~ 1 . :Nonatherosclerotic causes of CA narrowing-Part
1 Some conditions associated with coronary artery arteritis
TARI.E
(vasculitis)
Tuberculosis
Polyarteritis nodosa
Giant cell
Rheumatic fever
Systcinic lupus erythematosus
Burger's disease (thrornbo-angiitisobliterans)
Wegcner's granulornatosis
Salmonella
Leprosy
Mucocutaneous lymph node syndrome
Takayasu's disease
Typhus
Infective endocarditis
Rheumatoid arthritis
Ainylosing spondylitis
Syphilis
Frcini Ref. 79 with permission.
bra~ne.~The intima becomes greatly thickened, and ultimate-
ly the vessel is converted into a fibrous cord. Luminal throm-
bus may also be present. Of I6 cases of temporal arteritis re-
ported by Harrison," only 1 case involved the epicardial
coronary arteries.
Systemic Lupus Erythematosus
Pericardial and myocardial involvement are common
complications in systemic lupus erythematosus. Several
young patients with lupus and absent coronary atherosclero-
sis have suffered acute myocardial infarction (AMI).
Necropsy examination of the coronary arteries in these pa-
tients showed intimal fibrous proliferation, which may repre-
sent healed arteritis. In a 16-year-old girl with lupus studied
by Bonfiglio etal.,13 AM1 was associated with recent throm-
botic occlusion of all three major arteries. Tsakraklides et al. Is
studied a 29-year-old woman with lupus and fatal AM1 who
had severe coronary atherosclerosis. This case suggested that
lupus and other conditions causing arteritis may predispose to
premature coronary atherosclerosis. Smaller intramyocardial
coronary arteries are involved frequently in the diffuse vas-
culitis with fibrinoid necrosis and fibrosis.16
Burger's Disease (ThromboangitisObliterans)
In a few patients with Burger's disease, the epicardial coro-
nary arteries have shown focal polymoiphonuclear infiltrates,
histiocytes, and giant cells with or without coronary artery
thrombosisi7or with only coronary thrombosis.I* In 30 cases
studied by Saphir,I7only 1 patient had coronary involvement,
whereas in 19 cases studied by Averbuck and S i l b e ~6~pa- ,~~
tients had coronary thrombosis.
I11 651
Wegener 's Granulomatosis
Wegener's granulomatosis is a necrotizing vasculitis com-
monly affecting renal and pulmonary systems. Fibrinoid
necrosis of the small and medium-sized coronary arteries has
been reported by Panillo and Fauci. l o Larger epicardial coro-
nary artery occlusion and MI was reported by Gatenby et al. l 9
Infectious Diseases
Various infectious diseases have been associated with
coronary arteritis: syphilis1, 20 infective endocarditis,"
salmonellosis,22q23 typhus,24and leprosy.23Syphilis is stated
to be one of the most common infectious diseases affecting
the coronary arteries.15Up to one quarter of patients with ter-
tiary syphilis may have ostial stenosis2"The first 3 to 4 mm
ofthe left and right coronary arteries may be involved with an
obliterative arteritis.16Rarely does acoronary artery contain a
gumma.I6 Angina and AM1 may result from syphilic coro-
nary disease.2" Malarial parasites and parasitized red blood
cells also may plug larger coronary arteries.2s,2s6 Schisto-
soma hematobium has been found in a major epicardial coro-
nary artery unassociated with MI.26
MucocutaneousLymph Node Syndrome
(Kawasaki's Disease)
This acute febrile illness affects infants and young chil-
dren. In about 20% of patients, a vasculitis of the coronary
vasa vasorum leads to coronary arterial aneurysm formation,
thrombosis, and MI. Death may result from MI or ventricular
arrhythmia in 1-2%. Late presentation with MI secondary to
dislodged aneurysmal thrombus may also occur. 27-29 Oc-
I s
casional death may result from coronary artery aneurysm
rupture.
Takayasu's Disease (PulselessDisease)
This disease results in granulomatous panarteritis and fi-
brosis of the aorta and its large branches, which in turn lead to
luminal narrowing.2s Involvement of the coronary artery os-
tia and proximal main coronary artery segments has been de-
scribed in several patients. 2. 30, i Angina pectoris and AM1
may result from these coronary lesions.
Rheumatoid Diseases
Rarely, arteritis and intimal thickening associated with
rheumatoid disease severely narrow major epicardial coro-
nary arteries. More commonly, diffuse arteritis involves
smaller coronary arteries (including conduction system ves-
sels) in 10-20% of necropsy patients with rheumatoid arthri-
tis.32-34Small myocardial vessels may also be narrowed
658 Clin. Cardiol. Vol. 19, August 1996
severely in patients with ankylosing spondylitis. Grismer er
LII. have described a patient with ankylosing spondylitis who
had occlusion of the left main o ~ t i u m . ~ ~
Metabolic Disorders Narrowing Coronary Arteries
Specific metabolic substances may accumulate in the walls
of large and small coronary arteries as a result of inborn errors
of metabolism. The deposition of this material may severely
narrow the coronary artery lumen and produce AMI.25 In-
herited inborn errors of metabolism that are known to affect
major epicardial coronary arteries include Hunter's and
Hurler's diseases (mocopolysaccharidoses).3s-37The in-
volvement of the coronary arteries in these disorders may be
so severe as to occlude totally the vessel and to produce my-
ocardial ischemidM1. Other disorders of metabolism such as
primary oxalosis,3x Fabry's disease,I6 Sandhoff's disease
(gangliosidoses),39and homocystinuria may affect smaller
coronary vessels by severe intimal proliferation!()
Intimal Proliferation
Fibrous hyperplasia of the coronary arteries may severely
narrow the lumen and produce myocardial ischemiaM1.
The process may be associated with mediastinal irradia-
tion,." fibromuscular hyperplasia of the renal arteries?5 the
use of methysergide,"?. J3 ostial cannulation during cardiac
surgery or following aortic valve repIacement.44.45 Up to
50% of patients undergoing cardiac transplantation develop
significant epicardial coronary artery luminal narrowing or
total occlusion by intiinal fibrous proliferation within 3 to 5
years after tran~plantation.~~ Myocardial infarction and sud-
den death inay result from this chronic rejection process.
Fibrosis of the intramural vessels may also occur. Intimal
damage from immunologic rejection is believed to be the ba-
sis for the accelerated intiinal fibrous hyperplasia involving
the coronary arteries.I
A similar histologic picture of intimal fibrous proliferation
is seen in epicardial coronary arteries late after undergoing
percutaneous balloon a~igioplasty.~~~ 48 Waller et recent-
ly reported intimal fibrous proliferation of the left main coro-
nary artery occurring late after balloon angioplasty of a lesion
in the proximal left anterior descending coronary artery. They
postulated that the left main intimal reaction (identical to that
seen at the left anterior descending coronary artery angioplas-
ty site) resulted from balloon rubbing of the intimal surface
and/or extension of the fibrous process from the angioplasty
dilation site.
External Compression
External compression of the epicardial coronary arteries
may result in severe luminal narrowing and progressive my-
ocardial ischemia. External compression of a major epicardial
coronary artery has been reported in patients with sinus of
Valsalva aneurysms and epicardial tumor metastases."" s1
Myocardial bridging (external muscle compression during
ventricular systole) has been reviewed earlier.
MetastaticImplants
Myocardial metastatic lesions from various tumors (carci-
nomas, sarcomas, lymphomas) may mimic a healed myocar-
dial infarct at necropsy.' The discrete location or locations of
these metastatic deposits generally are unrelated to specific
coronary arterial supply zones, and the lesions are usually sur-
rounded by normal myocardium. These two gross observa-
tions suggest the lesions are metastatic tumor implants rather
than healed myocardial infarcts.'
Coronary Artery Thrombosiswithout Underlying
Atherosclerotic Plaque (ThrombosisIn Situ)
Thrombotic occlusion of the coronary system unassociated
with underlying atherosclerotic plaque may be seen with sev-
eral hematologic diseases: thrombocytopenia purpura, I h leu-
kemia?* polycythemia ~ e r a sickle
? ~ cell anemia, I 6 and prima-
ry thronibocytosis.s4 Occasionally, AM1 inay be the initial
manifestation of these hematologic disorders. A main factor
responsible for the myocardial ischemia in these conditionc is
blockage of small intramural coronary vessels by platelet ag-
gregates.ss These platelet aggregates initially niay form in
the major coronary arteries and then embolize distally.'
Substance Abuse (Cocaine)
Cocaine abuse is a major health hazard with more than 22
million Americans having tried cocaine at least once, and 5
million who are current uses.s6 Recent reports have document-
ed that cocaine abuse can result in myocardial ischemia and
MI in the absence of coronary artery disease.5"-62Cocaine-in-
duced coronary artery vasoconstruction has been reported in
patients following intranasal cocaine.hl-h'4"h
Several instances of coronary artery thrombosis and spasm
have been reported in patients with cocaine abuse.wx Acute
coronary thrombosis in association with cardiac events (angi-
na, AMI, sudden death) has been reported by Rod and Zuck-
er,64Smith et ul.,66and Isner et ~ 1In some
. ~ instances,
~ there is
underlying atherosclerotic plaque and in others the coronary
arteries are normal. Coronary thrombosis occumng in coro-
nary arteries free of atherosclerotic plaque suggests the role of
cocaine-induced spasm or possible primary thrombogenicity
of cocaine or its metabolites.63
Coronary spasm has been associated with cocaine usage
and has been postulated as a mechanism of MI in those users
with clean coronary a r t e r i e ~ . ~Simpson
~ - ~ ~ -and
~~
reported coronary artery narrowing in a young patient with-
out underlying atherosclerotic plaque. The coronary artery
 B.F. Waller rt 01.: Nonatherosclerotic causes of CA narrowing-Part
was severely narrowed by fibrointimal proliferation that was
attributed to underlying coronary artery spasm that caused fo-
cal vessel endothelial injury, and platelet adherence and ag-
gregation. Platelets liberate platelet-derived growth factor
(PDGF) which induces intimal proliferation lesions. In pa-
tie,nts with underlying coronary plaque, cocaine-induced
spasm also may produce endothelial disruption at the surface
of the plaque and promote platelet aggregation and further
vasoconstriction from the release of platelet pr~staglandins.~~
Myocardial Oxygen DemandSupply Disproportion4
In this category are disease states in which there is failure
to deliver adequate oxygen to the myocardium over a pro-
longed period or increased myocardial wall tension requiring
‘
increased oxygen supply. The classic example of the first sit-
uation is carbon monoxide poisoning,” which has been asso-
ciated with extensive nontransmural infarction in the pres-
ence of normal epicardial coronary arteries. Prolonged shock
(from any cause) can also result in extensive nontransmural
necrosis and frequently is associated with transmural necrosis
of the papillary muscles. The classic example of the situation
in which there is increased myocardial wall tension requiring
increased coronary oxygen supply is aortic valve stenosis.23
In the face of increased oxygen demand (increased muscle
mass), coronary blood supply is limited by poor perfusion re-
sulting from lower coronary arterial pressure. In addition,
poor perfusion results from high coronary resistance caused
by increased wall pressure on the intramural coronary arteries
and high left ventricular end-diastolic pressure from a stiff
ventricle.23Excessive myocardial oxygen demand exceeding
supply (resulting in myocardial ischemia/MI) may also be
seen in thyrotoxicosis.‘
Intramural Coronary Artery Disease (Small Vessel
Disease)
Acute myocardial infarction may result froin abnormally
thickened or totally occluded intramural coronary arteries in
the presence of normal extramural (epicardial) coronary arter-
ies. Some conditions in this category include: ( 1 ) hypertrophic
cardiomyopathy, (2) diabetes mellitus, (3)amyloid heart dis-
ease, (4) neuromuscular disorders (Friedreich’s ataxia; pro-
gressive muscular dystrophy). (5)cardiac transplantation. (6)
rheumatoid arthritis, (7) collagen-vascular disorders (sclero-
demia; systemic lupus erythernatosus), (8) metabolism abnor-
malities (niucopolysaccharidoses;gangliosidoses), and (9)
polyxteritis nodosa.
Normal Epicardial Coronary Arteries
Relatively few necropsy reports have evaluated patients
with AM1 who had angiographic normal coronary arteries
and normal coronary arteries at n e c r ~ p s y . Of
~ ~100
-~~
consec-
I11 659
utive necropsy cases of AM1 studied by Eliot and Baroldi,7x
7% had infarcts without evidence of coronary luminal nar-
rowing. Eliot and B a r ~ l dstudied
i ~ ~ 10 necropsy patients who
died with a typical picture of AM1 within 25 days of onset of
symptoms. The coronary arterial systems showed minimal or
no luminal narrowing by atherosclerosis. No thrombotic ma-
terial was observed in the coronary arteries despite the fact
that AM1 was 2 days old in five patients and 3 to 4 days old in
three other patients. Numerous theories have been proposed
to explain the occurrence of AM1 in these patients: coronary
artery spasm; coronary artery disease in vessels too small to be
visualized angiographically (i.e., small vessel disease); coro-
nary artery thrombosis or embolus with subsequent clot lysis,
retraction, or reconciliation; congenital coronary anomalies;
and myocardial oxygen supply-demand disproportion.
Acknowledgment
The authors wish to thank McGraw Hill Publisher for per-
mission to use previously published material from Reference
No. I .
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