Download Spasm of the Left Anterior Descending Coronary

Spasm of the Left Anterior
Descending Coronary ~ r t e r ~ *
Frank 1- Rose, M.D.,** A h . D. Johnson, M-D-,t and
Rfchrd A. Carleton, M.D.3 F.C.C.P.
*
~ * twith -t
whose e - a c
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a rlgM cornruterg ksion wps tormd
at coronary angiography to have transient spasm of the
left wedor descendiq cornMild
atherosclerotic dhPerse app&
to
.a a m b s w
for the kcalized coronary spasm.
m.
Since
the original description by Prinzmetal,' the
anatomic substratum of variant angina pectoris has
been felt to be significant focal coronary atherosclerosis.
However, the unusual characteristics of the syndrome
gave rise to early speculation that coronary arterial
spasm might coexist and be causally related. Recently,
coronary arterial spasm in the setting of variant angina
has been well documented, especially in the carefully
studied case reported by Oliva, Potts, and Pluss,z and in
the direct observation of MacAlpin and co-workers.8 A
patient is described with variant angina in whom transient spasm of the left anterior descending coronary
artery was demonstrated.
A 46-year-old Caucasian man, an athletic coach, was in
apparent good health until September 1973. At that time.,
'From the Cardiology Section, Department of Medicine,
Universitv of California San Diem.
- , and the Veterans Administration H ital. S& Diego.
**Cardiology F X W , Cardiology
Division, University of
California.
thsistant Professor of Medicine, University of California;
Director. Cardiac Catheterization Laboratorv. Veterans Administration H ital, San Diego.
$F'rofessor of ~ z c i n eUniversity
,
of California; Chief, Cardiology Section, Veterans Administration Hospital, San
Diego. Presently at Dartmouth Medical College, Hanover,
New Hampshire.
Reprint requests: Dr. Carleton, Dartmouth Medical School,
Hanwer, New Hampshire 03755
..
hypertension (160/110mm Hg) was documented during a
routine examination; an electrocardiogram demonstrated only
left axis deviation. Diuretic therapy was begun, and subsequent blood pressures were normal.
Approximately two weeks later, the patient experienced an
episode of lower retrosternal chest pain while restfully
seated. The pain lasted approximately two minutes and was
associated &th diaphor&is; there- was no shortness of
breath, nausea, or vomiting. Several episodes of similar pain
occurred during the succeeding weekeach without relationship to
mid~eptember,an -bode of pain lasting
approximately one half hour occurred and the patient was
placed in a coronary care unit. The admission electrocardiogram demonstrated left axis deviation. During the following
day, while in bed, the lower retrosternal pressure sensation
recurred. The e l d o g r a m monitor showed sinus
bradycardia and frequent premature ventricular contractions.
Subsequendy, an e l e c t d o g r a m demonstrated complete
heart block, a junctional escape rhythm, and occasional
Dremature ventricular contractions. Leads 2. 3. and aVF
Lmonstrated marked ST segment elevation '(Fig 1 ) . The
precordial R-wave progression was less well developed than
on the prior tracing. Atropine and isoproterenol were infused;
a junctional tachycardia at a rate of 95 per minute appeared.
The ST segment elevation increased to approximately 1.1 mv
and the drugs were discontinued. Within two hours, the
patient had returned to a sinus rhythm with normal ST
segmenis but with residual T wave inversion in Vz.4.
The patient was referred to the San Diego Veterans
Administration Hospital for further evaluation, where cardiovascular examination was unremarkable save for the presence
of a fourth heart sound.
E l d o g r a p h i c monitoring demonstrated transient
ST segment elevation and premature ventricular contractions
in coniunction with each of two e~isodesof chest pain.
~eithe; serial enzymes nor elec&adiograms suggested
myocardial infarction.
With a clinical diagnosis of variant angina, cardiac catheterization was performed. Atxial pacing to a rate of 150 per
minute produced neither pain, e l d o g r a p h i c changes,
nor abnormalities of pulmonary artery wedge or left ventricular end diastolic pressure. Left ventriculography demonstrated a normal contraction pattern.
Coronary arteriograms were performed by the Sones technique after premeditation with 1 mg of intravenous atropine
and 0.4 mg of sublingual nitroglycerin. The initial injection
into the left coronary artery showed minimal lumenal irregularity in the proximal left anterior descending coronary artery. The remeder of the left comnary artery was normal.
The right coronary artery was dominant and gave rise both to
the sinus nodal and AV nodal arteries. A small marginal
=
FIGURE1. Electrocardiogramduring an episode of chest pain.
CHEST, 66: 6, DECEMBER, 1974
SPASM OF LEFT ANTERIOR DESCENDING CORONARY ARTERY 719
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The nature and origin of coronary arterial spasm is
unknown. In turn, the role of coronary arterial spasm in
the production of some or, perhaps, mast instances of
variant angina remains unclea~.~J~
Coronary arterial
spasm has been demonstrated as a sequel to stimulation
of the coronary ostium6by a catheter tip. In the present
case, the catheter tip was never within 2 cm of the point
of spasm.
Coronary arterial spasm has also been demonstrated
by Lange and his co-workers7 in individuals subjected to
long-term industrial nitroglycerin exposure. The present
patient had no such known exposure. However, the
observations of Lange may have direct pertinence in the
management of patients with coronary arterial spasm in
the sense that it may be deleterious to attempt perpetual
medication with nitrata in the event that therapy is
suddenly withdrawn.
The observation of mild atheromatous disease at the
site of spasm in our patient supports the original notion
of F'rinzmetal and co-workers' that spasm may contribute a reversible, obstructive, and transient factor in
the setting of coexistent atheromatous disease. Further
study will be needed to clarify the role of coronary
arterial spasm >invariant and traditional angina pectoris,
so that appropriate medical or surgical therapy can be
designed.
FIGURE
2. Left coronary injection one hour after nitroglycerin
administration. Note segmental spasm in the proximal anterior
descending vessel.
branch of the right coronary artery had apparent plaquing;
the remainder of the right comnary artery was normal.
The absence of meaningful coronary obst~~ction
and the
variant character of the pain led to a dedsion to repeat the
arteriograms 50 minutes later without the dmhistntim of
atropine or nitroglycerin. Early total occlusion of the proximal
left anterior descending ccnmary artery at the site of the previous minor lumenal irregularities was present (Fig 2). The
right cvronary artery showed a minor deawure in c a l i i , but
was otherwise not different. Sublingual nitroglycerin, 0.4 mg,
was then administered and selective left amnrary arteriograms were repeated at intervals.The left anterior dsgoending
coronary obstruction gradually disappeared until the appearance was identical to that seen on the initial study (Fig 3).
It is notable that the patient experienced neither chest pain
nor ST segment elevation during the procedure. The usual
transitory T-wave inversions occurred during each coronary
injection.
The patient has subsequently been maintained on nitroglycerin as needed for chest discomfort. Several episodes of
chest pain have occurred at rest, each subsiding promptly
with nitroglycerin administration.
The present case shows typical clinical and elechocardiographic features of variant angina. The initial
presumption, based upon the associated arrhythmia, was
that a lesion would be found in the right coronary artery.
Instead, transitory left coronary arterial spasm was demonstrated in the absence of clinical symptoms or of
electrocardiographic changes. We infer that this patient
may, at other times, develop arterial spasm in the right
coronary artery.
720 ROSE, JOHNSON, CARLETON
ACKNOWLEDGMENT: The patient described in this case
report was kindly referred after the initial excellent observations by Dm. Quentin L. Wood and Peter E. Pool of Solana
Beach, California.
1 Primmetal M, Kennamer R, Merliss R, et al: Angina
pectoris: I. A variant form of angina pectoris: Preliminary
1
FIGURE
3. Subsequent left coronary injection 30 minutes following sublingual nitroglycerin administration.
CHEST, 66: 6, DECEMBER, 1974
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report. Am J Med 27:375-388, 1959
2 Oliva PV, Potts DE, Pluss RG: Coronary arterial spasm in
Prinzmetal angina: Documentation by coronary arteriography. N Engl J Med 288:745-751,1973
3 MacAlpin RN, Kattus AA, Alvaro AB: Angina pectoris at
rest with preservation of exercise capacity. Circulation
47:948,1973
4 Carleton RA, Johnson AD: Coronary arterial spasm: A
clinical entity? Mod Conc Cardiovasc Dis 43:87-91,1974
5 Demany MA, Tamb A, Zimmerman HA: Coronary arterial
spasm. Dis Chest 53:714-721, 1968
8 O'ReiUy RJ, Spelberg RD, King TW: Recognition of proximal right coronary artery spasm during coronary arteriography. Radiology 95:305309, 1970
7 Lange RL, Reid MS, Tresch DD, et al: Nonatheromatous
ischemic heart disease following withdrawal from chronic
industrial nitroglycerin 7.
Circulation 46:888878,
1972
The subject of this report is a 63-year-old woman who had
been in good health until she developed typical episodes of
variant angina pectoris, occasionally associated with high
degree AV block and ventricular tachycardia. Third and
fourth heart sounds were heard. Despite adequate medical
therapy, increasingly frequent chest pain occurred; cardiac
catheterization was performed. Two tapering areas of 50
percent narrowing were seen in the diagonal branch of the
anterior descending and proximal portion of the circumflex
arteries. These lesions were unchanged following nitroglycerin. The right coronary artery was initially widely patent
(Fig 1A). During the procedure she spontaneously developed ST segment elevation and typical pain. Visualization of
this vessel now revealed 95 percent luminal narrowing 3 cm
distal to the ostium extending to, and including, the posterior
descending branch (Fig 1B). Clinical improvement has occurred with use of nitroglycerin ointment.
Prinzmetal's Angina with Extensive
There is good evidence that coronary arterial spasm
Spasm of the Right Coronary ~ r t e r ~ * exist~.6-~
Previously reported cases had spasm limited to
Mark M . Applefield, M.D. and James A. R a n , Jr., M.D.
A pntient with Prinmetclrs angina had extensive sp&m
of the right coronary artery, demonstrated by coronary
arteriogmphy. Additionally, then were kss severe narrowing~(50 percent) h the diagonal and circndex
arteries probably due to atherosckmsk Improvement ha8
occurred on long-actingnitrite therapy.
N
-
umerous cases of variant angina pectoris have been
reported and the topic has been reviewed.'-' We
have studied a patient with this syndrome who had
spasm involving most of the length of the right coronary
artery.
'From the Department of Medicine, Division of Cardiology,
Georgetown University School of Medicine, Washington,
D.C.
This study was supported in part by U.S. Public Health
Grant HE 05433-14, the Benjamin May Memorial Fund, the
Metropolitan Heart Guild, and the Special Cardiac Research
Fund.
short arterial segments. Our patient had involvement of
most of the length of the right coronary system.
Therapy of coronary artery spasm seems to be medical
rather than surgical because the artery distal to the
obstruction may become spastic. Of six patients dethree have had bypass grafting.
scribed thus far,l~5-~
One patient died six weeks postoperation during chest
pain; the graft was patent. Both survivors, though pain
free, have occluded grafts; one, an inferior infarction. All
three patients treated medically are improved. Although
myocardial infarction may occur in 25 percent of patients with this syndrome, in many cases pain either
completely subsides or stabilizes after about three
months.1.J
1 MacAlpin RN, Kattus AA, Alvaro DB: Angina pectoris at
rest with preservation of exercise capacity. Circulation
47:948,1973
2 Whiting RB, Klein MD, Vanderveer J, et al: Variant
WIVJ LLLWIJ,
-V
VEW.
-8
-W
111uarmuzi main right V-1;
short m,
acute marginal branch. Note relative vessel sizes before (A, left) and during (B, rfght)vasospasm.
rluunv a.
~UWL
CHEST, 66: 6, DECEMBER, 1974
PRINZMETAL'S ANGINA WITH EXTENSIVE SPASM 721
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