Download Transmural Myocardial Infarction with Arteriographically Normal

Transmural Myocardial Infarction with
Arteriographically Normal Appearing
Coronary Arteries*
Kent H. Potts, M . D . ,
Paul C. Houk, M.D.%
0 0
Paul D. Stein, M.D., F.C.C.P„f
and
Two patients with electrocardiographic and clinical manifestations of transmural
myocardial infarction, who subsequently were shown to have arteriographically
normal appearing coronary arteries, are described. The etiology of the apparent
myocardial infarction in these patients was not determined.
k substantial number of patients with documented
angina and arteriographically normal appearing coronary arteries have been reported. " However, few patients have been reported with apparent transmural myocardial infarctions who subsequently were shown to have normal coronary
arteriograms and no other form of heart disease.
The following is a report of two such patients.
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CASE REPORTS
CASE 1
A 28-year-old man, previously in good health, was
awakened D e c 19, 1 9 7 1 , with severe chest pains which
radiated to the neck and xiphoid area. This was associated
with shortness of breath, diaphoresis, and a feeling of numbness in the upper extremities. T h e pain persisted for more
than two hours. T h e electrocardiogram ( E C G ) at that time
showed prominent S T segment and T wave changes ( F i g 1 ) .
Later that day, Q waves were present in leads I I , I I I , and
a V F and there was a prominent R wave in V j ( F i g 2 ) . Serial
E C G s showed evolutionary changes. These changes were
compatible with an acute inferior and direct posterior transmural myocardial infarction. A subsequent vectorcardiogram
was also compatible with this diagnosis. W h e n initially seen,
the patient did not appear acutely ill, and physical examination was within normal limits. T h e serum glutamic oxaloacetic transaminase ( S G O T ) level was 1 8 0 units on the first
day and subsequently dropped to 5 0 , 3 4 , and 42 units on
subsequent days. T h e serum lactic dehydrogenase, level was
2 2 5 units on the first day, with subsequent daily values of
" F r o m the Department of Medicine, University of Oklahoma
School of Medicine and Veterans Administration Hospital,
Oklahoma City.
"Assistant Clinical Instructor in Medicine.
tAssociate Professor of Medicine.
JProfessor of Medipine.
Supported in part from V.A. Research Service and Oklahoma Heart Association.
Reprint requests: Dr. Stein, Veterans Administration
Hospital,
921 NE 13th St., Oklahoma City, Okla,
73104
a
CHEST, VOL.
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320, 2 4 8 , and 2.52 (normal in this laboratory is 4 0 - 1 4 0
international units [ l u ] ) . T h e serum creatine phosphokinase
was not measured on the first day, but on subsequent days
was 128, 92, 5 2 and 6 0 (normal in this laboratory is 9 - 9 0 I u ) .
Serum cholesterol, triglyceride, lipoproteins, lupus erythematosis preparation, glucose tolerance test, blood urea nitrogen,
serologic test for syphilis, uric acid, protein bound iodine,
erythrocyte and leukocyte count, and urine analysis were
normal, as were posterior-anterior and lateral chest films. T h e
hospital course was uncomplicated and the patient was discharged after four weeks. On the day after discharge, he
suffered a 4 0 minute episode of chest pain and was readmitted to the hospital, but physical examination, E C G and
serum enzymes were unchanged. Selective coronary arteriography (utilizing 35 mm c i n e ) four months after the apparent acute infarction showed normal appearing coronary
arteries ( F i g 3 ) . L e f t ventricular end-diastolic pressure was
elevated at 18 mm Hg. Hypokinesia of the inferior border of
the left ventricle was seen on the ventriculogram ( F i g 3 ) .
Coronary sinus lactate and pyruvate levels were normal at
rest and after pacing at 150 beats/min. For a period of six
months following cardiac catheterization, the patient complained of occasional right upper quadrant and epigastric
pain not related to exertion. Roentgenograms of the gall
bladder showed multiple stones. T h e r e has been no angina.
CASE 2
A 28-year-old man, in previously good health, developed
severe substernal chest pain during heavy exertion on July
2 3 , 1 9 6 2 . Examination one hour after the onset of symptoms
showed an anxious, hyperventilating patient who was acutely
ill. During the examination, two brief episodes of unconsciousness occurred. An E C G at that time showed paroxysms
of "totally irregular rhythm of ventricular origin."'" T h e following day an E C G showed no arrhythmia, but a distinct current
of injury was present in the anterior precordial leads with
Q R S changes of an acute anteroseptal myocardial infarction.
Typical evolutionary changes followed. T h e S G O T level rose
to 2 2 8 units and returned to normal by the third day after
admission. T h e patient had an uneventful recovery. Later
" T h i s electrocardiogram is not available.
1972
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549
FIGURE 1. Electrocardiogram, patient 1,
on day of admission, showing S T segment
elevation and q waves in leads II. III. and
aVF. Depression of the S T segment and
inversii
i the T wave is shown in leads
V i - V j . Paper speed is 50 mm per second.
Some of the leads were retraced for reproduction.
that year he was given a medical discharge from military
service. Although the complete hospital records describing
this hospitalization are available, the first E C G available for
review was obtained eight months later. T h a t E C G was
incomplete, but showed prominent QS waves in V] through
V;f which were compatible with an old anteroseptal myocardial infarction.
Between the ages of 3 3 and 37, the patient was hospitalized with severe chest pain on three occasions. He did not
have clear evidence of a recurrent myocardial infarction on
those occasions, but his E C G continued to show changes
compatible with an old anteroseptal infarction ( F i g 4 ) . A
vectorcardiogram also showed changes compatible with an
anteroseptal myocardial infarction.
At age 3 6 , intermittent claudication of the left calf developed. Arteriography showed complete occlusion of the left
external iliac artery at its origin. A left iliofemoral bypass
graft with endarterectomy of the superficial and deep formoral arteries was performed.
Currently, the exercise capacity of this patient is limited by
angina pectoris, dyspnea on exertion and leg pain. He uses
approximately 30 nitroglycerin tablets per week. T h e patient
has had abnormal glucose tolerance values. His blood sugar
levels are controlled by diet therapy alone. T h e patient's
mother and five siblings also have diabetes. His mother, age
52, sister, age 47, and maternal grandmother, age 6 1 , died of
heart disease and one sister, age 4 5 , and one brother, age 4 3
have had myocardial infarctions, but are alive.
Evaluation of serum lipids has shown changes suggesting
Type 4 hyperlipoproteinemia (cholesterol 2 3 0 to 2 7 0 ml/100
ml, serum triglyceride 3 5 0 to 5 1 0 mg/100 ml, serum phospholipids 2 7 0 to 3 2 0 rag/ml). He is currently being treated with
a low fat diet and clofibrate. T h e patient has never been
hypertensive.
Cardiac catheterization and selective coronary arteriography at age 37 showed arteriographically normal appearing
coronary arteries ( Fig 5 ) . Left ventricular end-diastolic pres-
sure was elevated at 2 5 mm Hg. Akinesia of the apex and
superior border of the left ventricle was also shown ( F i g
5).
DISCUSSION
Most patients who have suffered a transmural
myocardial infarction have an occlusion of one or
more major coronary arteries. However, small, clinically undetected or subendocardial infarctions not
caused by occlusion of a major coronary artery have
been reported at autopsy. Such infarctions usually were associated with other manifestations of
illness such as aortic stenosis, pulmonary embolism,
anemia, arterial hypertension, systemic hypotension,
or an operative procedure (for unexplained reasons ) .
4,5
Unobstructed coronary arteries in six patients
with electrocardiographic evidence of a previous
transmural myocardial infarction were described by
Campeau and associates. In three patients, there
was a prosthetic heart valve, or history of a recent
cardiac catheterization which suggests the possibility of coronary embolization with subsequent recanalization. In three of these patients, there was
nothing to suggest a coronary embolism. The etiology of the infarction was unclear. An extensive list
of possible causes for this observation was enumerated.
0
Thromboembolism with recanalization was postulated to explain a transmural infarction with normal
coronary arteriograms in two women reported by
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FIGURE 2. Electrocardiogram ( E C G ) , patient 1, taken 4 - 5 hours after Figure 1.
Prominent Q S waves are shown in leads II,
III. a V F , and V«. An R wave is shown in
V ) . Q R S interval is 0.09 sec. Paper speed
is 5 0 mm per second. Some of the leads
were retraced for reproduction.
C H E S T , V O L . 6 2 , N O . 5, N O V E M B E R ,
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1972
TRANSMURAL
MYOCARDIAL
551
INFARCTION
FIGURE 3. Coronary arteriograms and ventriculogram, patient 1, five months after
acute episode. A, right coronary artery
( R C A ) , left anterior oblique position.
B, left coronary artery showing left anterior descending ( L A D ) and left circumflex ( L C i r c ) coronary artery in right anterior oblique position. C, left coronary
artery, left anterior oblique position showing L A D and L Circ. D , ventriculogram,
right anterior oblique position. Arrows
indicate area of hypokinesis.
Glancy and associates. One of these patients was
receiving treatment with oral contraceptive agents,
and the other suffered a myocardial infarction 11
days postpartum. Four patients reported by
Bruschke and associates had electrocardiographic
evidence of a transmural myocardial infarction even
though the selective coronary arteriograms showed
no obstructive disease of the major vessels. One of
these patients was 36 weeks pregnant and had an
aneurysm of the anterior descending coronary
artery without narrowing. It was suggested bv the
authors that the aneurysm may have originated as a
dissecting aneurysm which temporarily occluded
the lumen. A second patient in that series had
normal coronary arteriograms on the first study, but
complete obstruction of the anterior descending
coronary artery on a second study and patency of
the vessel on a third study. This feature was taken
as evidence of a thromboembolic process with
recanalization.
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In two otherwise healthy teenage boys and a
middle aged man with evidence of a transmural
myocardial infarction, arteriographically normal or
minimally abnormal coronary vessels were found. '
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1
No etiology was shown, though thromboembolism
with recanalization was postulated in the later case.
Patients with arteriographically normal appearing coronary arteries and clinical or electrocardiographic evidence of an non-transmural myocardial
infarction appear to be somewhat more frequently
reported than those with a transmural myocardial
infarction. Occulusion of coronary arterial twigs or
recanalization of previously occluded vessels was
postulated as a possible cause of the clinical manifestations in three such patients. Subsequently, a
variety of diseases affecting small coronary arteries
was discussed by James. Abnormalities of hemoglobin oxygen dissociation were described in young
women with non-transmural infarction or ischemia.
In three of these patients who subsequently died, subendocardial infarctions of the left
ventricle were found in spite of normal coronary
arteries.
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hi summarv. two patients with electrocardiographic and clinical manifestations of a transmural
myocardial infarction who subsequently were
shown to have arteriographically normal appearing
coronary arteries are described. Reports of such
L
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FIGURE 4. Electrocardiogram ( E C G ) , patient 2, taken five years after apparent
acute myocardial infarction. E C G is compatible with old anteroseptal myocardial
infarction. Recent injury cannot be excluded. E C G taken at time of recurrent
episode of chest pain.
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POTTS, S T E I N ,
HOUK
FIGURE 5. Coronary arteriograms and ventriculogram, patient nine years following
apparent acute myocardial infarction. A,
right coronary artery ( R C A ) , right anterior oblique position. B, left coronary artery, right anterior oblique position,
showing left anterior descending coronary
artery ( L A D ) and left circumflex coronary artery ( L C i r c ) . C, left coronary
artery, left anterior oblique position showing L A D and L Circ. D, ventriculogram,
right anterior oblique position, showing
area of akinesis ( a r r o w s ) .
patients are rare and are distinguished from reports
of individuals with angina and mild ischemic disease who were also shown to have arteriographically normal coronary arteries. It appears that a
spectrum of severity of ischemic myocardial disease
can occur that simulates occlusion of a major
coronary artery. The etiology of the apparent myocardial infarctions in these patients has not been
determined, although a variety of etiologies have
been postulated by others.
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REFERENCES
1 Kemp HG, Elliott \VC, Gorlin R: T h e anginal syndrome
with normal coronary arteriography. Trans Assoc Am
Physicians 8 0 : 5 9 - 7 0 , 1967
2 Likoff W, Segal B L , Kasparian H : Paradox of normal
selective coronary arteriograms in patients considered to
have unmistakable coronary heart disease. N E n g J Med
2 7 6 : 1 0 6 3 - 1 0 6 6 , 1967
3 Neill W A , Kassebaum D G , Judkins M P : Myocardial hypoxia as the basis for angina pectoris in patients with
normal coronary arteriograms. N E n g J Med 2 7 9 : 7 8 9 7 9 2 , 1968
4 Friedberg CK, Horn H : Acute myocardial infarction not
due to coronary artery occlusion. J A M A 1 1 2 : 1 6 7 5 - 1 6 7 9 ,
1939
5 Allison R B , Rodriguez F L , Higgins E A Jr, et al: Clinicopathological correlations in coronary atherosclerosis: four
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hundred thirty patients studied with postmortem coronary
angiography. Circulation 2 7 : 1 7 0 - 1 8 4 , 1963
Campeau L, Lesperance J , Bourassa M G , et al: Myocardial infarction without obstructive disease at coronary
arteriography. Can Med Assoc J 9 9 : 8 3 7 - 8 4 3 , 1968
Clancy D L , Marcus M L , Epstein S E : Myocardial infarction in young women with normal coronary arteriograms.
Circulation 4 4 : 4 9 5 - 5 0 2 , 1 9 7 1
Bruschke A V C , Bruyneel K J J , Block A, et al: Acute
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Sidd J J , Kemp H G , Gorlin R : Acute myocardial infarction
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Pierre M N , Robertson L : Normal coronary arteriogram
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Dear H D , Russell R O , Jones W B , et al: Myocardial
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Ross RS, Friesinger G C : Coronary arteriography. Am
Heart J 7 2 : 4 3 7 - 4 4 1 , 1966
James T N : Pathology of small coronary arteries. Am J
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Eliot RS, Bratt G : T h e paradox of myocardial ischemia
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NO.
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