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Transcript
Heart Block Complicating Acute Inferior Wall
Myocardial Infarction*
Prem K. Gupta, M.D.;"" Edgar Lichstein, M.D.;t and
Kul D. Chuddu, M.D.S
Heart block was noted in 60 (35 complete and 25 seconddegree) of 410 patients with acute inferior wall myocardial infarction. This group with heart Mock was compared to a control grow of 30 patients with acute
inferior wall infarction without heart Mock. The incidences of prior myocardial infarction and hypertendon,
in addition to the highest level of serum creatine phospholdnase and a maximum degree of !ST-segment elevation in the inferior leads, were all greater in patients with
heart Mock, as compared to the controls. The incidences
of various complications, including dizziness and syncope,
transient hypotension, cardiogenic shock, and congestive
heart failure, were also higher in the group with heart
Mock, while sinus nodal disturbances and atrial arrhythmias occurred with equal frequency. The mortality in
those with heart Mock was 28 percent compared to 13
percent for the control. It is concluded that patients with
heart Mock complicating acute inferior myocardial infarction have a greater amount of myocardial necrosis,
a higher incidence of complications, and a higher mortality. Insertion of a temporary pacemaker shoold be considered when spedllc indications are present and not rootineb.
concerning heart block complicating acute
Studies
myocardial infarcti~n~-~O
have emphasized the
period of 1970 to 1974. Most patients were monitored in the
coronary care unit for four to six days, except those who
required longer periods because of various complications.
Daily 12-lead electrocardiograms and determinations of
serum creatine phosphokinase levels were performed during
this period. In addition to constant electrocardiographicmonitoring and hourly rhythm strips, repeat ECGs were obtained
whenever changes in atrioventricular conduction were noted.
Patients in whom heart block appeared as a terminal event or
transiently during cardiac resuscitation were not included in
this study.
A history of hypertension was recorded if the patient had
previously had more than one blood-pressure determination
greater than 160/90 mm Hg or if the patient was receiving
antihypertensive medication. Diabetes mellitus was considered to be present if a fasting blood glucose level greater
than 120 mg/100 ml had been recorded prior to hospitalization or if the patient was receiving antidiabetic medication.
Previous myocardial infarction was diagnosed by the history
of typical precordial pain and the presence of significant Q
waves on the ECG. Serial 12-lead ECGs were reviewed for
the maximum degree of ST-segment elevation in the inferior
leads. In addition, rhythm strips were reviewed to determine
the time of onset and the disappearance of heart block and to
determine the presence of sinus nodal abnormalities and
atrial arrhythmias. Maximum serum creatine phosphokinase
values were recorded as multiples of the upper limit of
normal for our laboratory.
The presence of cardiogenic shock was recorded if the
systolic blood pressure was persistently lower than 80 mm Hg
and was accompanied by the clinical features of cool moist
skin, mental confusion, and a fall in urinary output. A
transient fall in blood pressure not accompanied by these
clinical features and usually associated with bradyarrhythmias was classified as transient hypotension. Congestive heart
failure was considered to be present if bilateral basal rales
were heard which were not related to a history of chronic
pulmonary disease and were accompanied by radiographic
appearance of bundle-branch block and the higher
mortality associated with anterior wall infarction,
and the more benign prognosis of atrioventricular
block associated with inferior wall myocardial infarction. The indications for insertion of a temporary
pacemaker in patients with heart block complicating
acute inferior wall myocardial infarction remain unsettled.7,8.12.1421.2e
This study reports our experience with 60 patients
with heart block complicating acute inferior wall
myocardial infarction. Significant clinical features,
serum creatine phosphokinase levels, ST-segment
elevations, and various complications are compared to a group of control patients with inferior
myocardial infarction without heart block. An attempt is made to clarify the indications and value
of temporary-pacemaker insertion.
Heart block was noted in 60 (35complete and 25 seconddegree) of the 410 patients with acute inferior-wall myocardial infarction seen in our coronary care unit during the
"From the Department of Medicine, Division of Cardiology,
Mount Sinai Ho ital Senices, City Hospital Center at
E I m h m NY, an3 Mount Sinai School of Medicine, City
University of New York, New York.
""Assistant Professor of Clinical Medicine.
tAssociate Professor of Medicine.
$Assistant Professor of Medicine.
Manuscript received September 9; revision accepted December 1.
Reprint requests: Dr. Cupta, Mt. Sinai Hospital S e d e s , 7901 Broadway, Elmhurst, New York 11373
CHEST, 69: 5, MAY, 1976
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of the upper limit of normal are shown in Figure 2.
Time of Onset and Duration of Heart B b c k
DIABETES
HYPERENSION
OLD M I
FIGURE
1. Diabetes, hypertension, and old myocardial infaro
tion ( MI) in patients with heart block ( HB ) and controls,
Numbers in bars are numbers of patients.
evidence of increasing pulmonary vascular congestion.
Similar historic and clinical data were obtained on a
control group of 30 patients with acute inferior wall my-dial infarction who did not show evidence of heart block.
The incidence of heart block (second-degree and
third-degree) in patients with acute inferior wall
myocardial infarction was 15 percent. The average
age of the patients with heart block (61 years) was
similar to that of the control group (62 years), as
was the malelfemale ratio ( 2 : l ) . The incidences of
previous myocardial infarction, hypertension, and
diabetes mellitus in the patients with heart block
and the control group are shown in Figure 1. The
maximum ST-segment elevation measured in millimeters in the inferior leads and the maximum serum
creatine phosphokinase level expressed in multiples
Heart block was present on admission or developed within 24 hours in 35 patients (early heart
block) and appeared late (two to seven days after
admission) in 25 patients (late heart block). Of the
group with early heart block, the block was noted at
the time of admission in 26 patients and appeared
within 24 hours in nine patients. There were no
deaths in ten of the patients with early heart block in
whom the defect was transient ( a few minutes to
one hour), while there were ten deaths in the remaining 25 patients with early heart block patients
in whom the block lasted from two hours to 14 days.
In the 25 patients with late block, the block lasted
from two hours to 16 days, and seven deaths occurred in this group. The duration of block varied
and was noted to be intermittent and unstable in 11
patients and present for more than six days in nine
others. In four patients in whom the block was
present transiently on admission, it reappeared on
the third and fourth days of hospitalization.
The incidences of various complications for those
with heart block and the controls are shown in
Figure 3. The greater incidences of transient hypotension and cardiogenic shock in the group with
heart block were statistically significant ( P < 0.05).
The mortality of 28 percent (17160) in the patients
with heart block was higher than the 13 percent
(4130) noted in the controls and was not affected by
the degree of heart block. The 56-percent incidence
(34160) atrial arrhythmias and sinus nodal abnormalities was similar to the 53-percent incidence
( 16/30) noted in the control group.
Rate and Morphologic Appearance of Escape
Rhythm
ST SEGMENT
SERUM CPK
RGURE2. Maximum height of ST-segment elevation measured in millimeters and highest level of serum creatine phosphokinase ( CPK) measured in multiples of upper limit of
normal. HB, heart block.
The average rate of the escape rhythm in those
patients with complete heart block was 45 beats per
minute, with a range of 24 to 70 beats per minute.
There was no relationship between the rate of this
escape pacemaker and the morphologic appearance
of the escape beats, the time of occurrence of heart
block, the associated complications, or the mortality.
The escape beats were wide in seven patients
(Table 1). In three of these patients, bundle-branch
block was not present in the conducted beats, and
the morphologic appearance of the escape beats was
consistent with right bundle-branch block and left
anterior hemiblock, suggesting an escape focus in
the posterior division of the left bundle branch (Fig
4). A His-bundle electrogram recorded in one of
these patients showed a markedly prolonged atrioHis (A-H) interval, in addition to block distal to the
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CHEST, 69: 5, MAY, 1976
CHF
MORTALITY
HYFOTENSION
FIGURE 3. Incidences of various complications in patients with heart block (HB)and controla.
Numbers in bars are numbers of patients. CHF, congestive heart failure.
a SmCQeL
His-bundle potential (Fig 5). One of these patients
died, and two survived. The four remaining patients
with wide escape beats all had evidence of bundlebranch block during periods of normal conduction.
In one patient, who ultimately survived, a pattern of
right bundle-branch block was present during normal conduction and in the escape beats. In the
remaining three patients, the morphologic appearance of the escape complex was different from that
of the normally conducted beats, and all three died,
despite pacemaker insertion. An additional patient
developed trifascicular block manifested by periods
of right bundle-branch block and left posterior
hemiblock and of left bundle-branch block. Ventricular asystole occurred, requiring insertion of a
temporary pacemaker. A permanent pacemaker was
inserted at four weeks after hospitalization, but the
patient died suddenly of a possible arrhythmia at
seven weeks.
Mode of Death
Seventeen patients in the group with heart block
died. The cause of death was cardiogenic shock in 11
patients; death occurred within the &st 24 hours in
seven of these and occurred between the third and
Table 14Irmocteri.tia of Patient. Showiw
wile Ewope Beds*
Patient
1
SinukConducted
QRS
Normal
Escape
&RS
Outcome
RBBB and LAH Survived (shock)
RBBB and LAH Died (shock)
3
Normal
RBBB and LAH Survived
4
RBBB
RBBB
survived
5
RBBB
LBBB
Died (CHF)
6
RBBB and LAEI RBBB and LPH;
RBBB and LAB; Died (shock)
LBBB
7
RBBB and LAH; Wide
LPH
Died (shock)
*RBBB, Right bundle-branch block; LAH, left anterior hemiblock; LBBB, left bundle-branch block; LPH, left posterior
hemiblock; and CHF, congestive heart failure.
CHEST, 69: 5, MAY, 1976
Frcm 4. Selected leads from ECGs (case 1, Table 1). A.
At time of admission. Note sinus rhythm with changes of
acute inferior-wall myocardial infarction B. Recorded soon
after admission. Note complete heart block with QRS morphologic appearance suggestive of right bundle-branch block
and left anterior hemiblock.
HEART BLOCK COMPUCATIWG ACUTE lWMl 601
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I
f
A-H = 190-220 Msec
1
I
I
FIGURE5. His-bundle electrograrns (HBE) (case 1, Table 1 ) . Complete heart block is present,
and block occurs distal to His-bundle potential. Atrio-His interval (A-H) is prolonged and
ranges from 190 to 220 msec.
the seventh days of hospitalization in the remaining
four. All of these 11 patients had heart block, and six
had temporary pacemakers at the time of their
death. In the remaining five, there was not adequate
time for pacemaker insertion. Cardiac rupture was
the cause of death in one additional patient, who
died on the eighth day of hospitalization. In the
remaining five patients, death occurred from other
causes between the fifth and 35th days of hospitalization. In four of these patients, heart block was not
present when the patients were discharged from the
coronary care unit, but in the three instances in
which death was sudden, it is not known whether
the mechanism was recurrent block or ventricular
fibrillation.
Indications for Pacemaker Insertion
Temporary transvenous pacemakers were inserted
in 31 patients (eight with second-degree and 23 with
comple'te heart block). The various indications for
pacemaker insertion were as follows: atropine-resistant symptomatic bradyarrhythmia, 19 patients;
shock, 11 patients; hypotension, eight patients; congestive heart failure, 17 patients; prolonged asystole,
two patients; control of atrial and ventricular arrhythmia, five patients; and wide escape beats, seven
patients. In many patients, two or more of these
indications existed simultaneously. Ventricular fibrillation occurred in three patients during pacemaker
insertion, and in each case, successful defibrillation
was achieved.
The reported incidence of heart block complicating acute myocardial infarction ranges from 1.5 per~ l ~ variation is due in
cent to 18 p e r ~ e n t . ~ * " ' *This
part to inclusion of both anterior and inferior wall
infarctions in some of the reports and the lack of
constant monitoring in earlier series. The incidence
of 15 percent in our series is less than the incidences
of 26 percent and 27 percent reported by ~thers.~,ll
Our finding of a higher incidence of prior myocardial infarction in the group with heart block, as
compared to the controls, suggests more extensive
coronary arterial disease and is similar to other reported r e ~ u l t s . ~ . ~ , ~
The magnitude of ST-segment elevation and
the levels of serum creatine phospholdnase have
been correlated with the extent of myocardial
n e ~ r o s i s . ~The
~ 3 ~elevation of both of these parameters in our group of patients with heart block is in
agreement with the concept that patients with heart
block complicating acute inferior-wall myocardial
infarction have a greater amount of myocardial
damage. This may also explain the higher incidences
of congestive heart failure and shock and the higher
mortality in patients with heart block.
Onset and Duration of Heart Block
The time of onset and the duration of block in
acute inferior wall myocardial infarction have no
uniform pattern.5*9.11.12.20
We observed block
within the &st 24 hours following admission in 58
percent (35160) of our cases, which is similar to
the experience of
The duration of
heart block varied markedly in our series and lasted
from a few minutes to 16 days. Persistence of heart
block to this degree was noted by Norrisl' and by
Kostuk and Beanlands,12 but not by Simon et a1.20
It appears that different mechanisms may be in
operation, producing heart block with different
times of onset and different periods of duration.
Heart block occumng early and transiently during
periods of chest pain might be related to inappropriate vagal tone; or transient ischemia of the atrioventricular node might occur, as is seen in patients
602 GUPTA, LICHSTEIN, CHADDA
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CHEST, 69: 5, MAY, 1976
with Prinzmetal's angina and heart b l o ~ k . In
~~,~~
ples of this discrepancy are the exceptionally low
those patients with heart block appearing later and
mortality of 20 percent without pacing described by
Jackson and Bashour," while Rotman et all3 relasting for longer periods of time, edema and inflammation of the atrioventricular node is likely.
ported a 30 percent mortality despite pacing. In the
Massive necrosis of the atrioventricular node has
series of Friedberg et al,9 three deaths were related
been demonstrated in patients with block who died
to Stokes-Adams attacks, and it was thought that
pacemaker therapy might have been useful. Other
of cardiogenic shock.' This concept of different
investigatorssg.%have reported beneficial effects of
mechanisms may explain the reappearance of block
pacing in patients who had experienced syncope.
on the third and fourth days of hospitalization in
It is our policy to insert a temporary pacemaker in
four of our patients who showed transient block at
a patient with heart block only if symptoms are
the time of admission. Kostuk and bean land^'^
present. These symptoms include dizziness or synfound, as we did, that patients with early and trancope, hypotension, cardiogenic shock, and congessient block had a more benign prognosis.
tive heart failure. In addition, we insert a pacemaker
Significance of Wide Escape Beats
if sigdicant ventricular arrhythmias requiring overdrive are present, or if the patient is completely
The site of block in acute inferior wall myocardial
asymptomatic and there is complete heart block
infarction has been localized to the region of the
with a wide QRS escape complex.
atrioventricular node or within the His bundle.2728
Although the majority of these patients show narrow
ACKNOWLEDGMENT: We are grateful to Mr. Manuel
escape beats, a small percentage does show an esBeckeman for the art work and to Mrs. Frances Schlesinger
a p e rhythm with a wide QRS c ~ m p l e x . In
~ ~the
~ ~ ' ~ for secretarial assistance.
study by Lie et a1,28 12 out of 35 patients admitted
REFERENCES
with heart block complicating acute inferior-wall
infarction showed a wide QRS esdape complex.
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2: 19681969, 1937
Kostuk and Beanlands12 noted four patients with a
2
Master
AM, Dack S, JafFe HL: Bundle branch and
wide QRS escape rhythm and observed that their
intraventricular blodc in acute coronary artery occlusion.
mortality was similar to those with narrow escape
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beats. Earlier studies by Lassers and Julian8 and by
3 Penton GB, Miller H, Levine SA: Some clinical features
Friedberg et ale found a higher mortality in those
of complete heart b l d . Circulation 13:801-824, 1956
4 Cohen DB, Doctor L, Pick A: The significance of ahiopatients with wide escape beats. We believe that the
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to mortality rather than the QRS width alone. Prog5 Courter SR, Moffat J, Fowler NO: Advanced atriovennosis in patients with prior bundle-branch block
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trifascicular block, the mortality increases sign$7 Paulk EA Jr, Hurst JW: Complete heart block in acute
cantly and resembles those with anterior myocardial
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cardiac bipolar catheter pacemaker. Am J Cardiol 17:695706, 1966
who do not have bundle-branch block in sinus beats
8 Lassers BW, Julian DG: Artificial pacing in management
but show wide escape beats during heart block are
of complete heart block complicating acute myocardial
most likely to have block in the area of the His
infarction. Br Med J 2: 142-148, 1968
bundle and show a variable p r o g n o s i ~ . ~ ~ ~ ~ ~
9 Friedberg CK, Cohen H, Donoso E: Advanced heart
The benefit of routine pacemaker therapy for pablock as complication of acute myocardial infarction: Role
of pacemaker therapy. Prog Cardiovasc Dis 10:466-481,
tients with heart block complicating inferior wall
1968
infarction has not been established.§ There does not
10 Brown RW, Hunt D, Sloman JG: The natural history of
appear to be a direct relationship between a policy
atrioventricular conduction defect in myocardial infarcof pacemaker insertion and mortality. The death
tion. Am Heart J 78:460-466, 1969
rates of 40 percent7 and 45 percent12were noted by
11 Nonis RM: Heart block in posterior and anterior infarction. Br Heart J 31352-356,1969
groups who implanted pacemakers in all patients
12
Kostuk WJ, Beanlands DS: Complete heart block assowith block, while mortalities of 37 percent,' 39 perciated with .acute myocardial infarction. Am J Cardiol
cent,5 and 44 percent9 were reported by groups who
26:380-384, 1970
did not use prophylactic pacemakers. Further exam13 Rotman M, Wagner GS, Wallace AG: Bradyarrhythmias
$References 7,8, 12,14,15,21,22,32,33.
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in acute myocardial infarction. Circulation 45:703-722,
1972
HEART BLOCK COMPLICATING ACUTE lWMl 603
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14 Jackson AE, Bashour FA: Cardiac arrhythmias in acute
myocardial infarction: 1. Complete heart block and its
natural history. Dis Chest 51:31-38, 1967
15 Waugh RA, Wagner GS, Haney TL, et al: Immediate and
remote prognostic significance of fascicular block during
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Engl J Med 282237-240, 1970
17 Scheidt S, Killip T: Bundle branch block complicating
acute myocardial infarction. JAMA 222:919-924, 1972
18 Atkins JM, Leshin SJ, Blomgvist G, et al: Ventricular
conduction blocks and sudden death in acute myocardial
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Med 288:281-284, 1973
19 Scheinman M, Brenman B: Clinical and anatomic implications of intraventricular conduction blocks in acute
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20 Simon AB, Steinke WE, Curry JJ: Atrioventricular block
in acute myocardial infarction. Chest 62: 156-161, 1972
21 Chatteqee K, Harris A, Leatharn A: The risk of pacing
after infarction and current recommendations. Lancet
2: 1061-1063, 1969
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23 Maroko PR, Libby P, Covell JW, et al: Precordial S-T
segment elevation mapping: An atraumatic method for
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24 Sobel BE, Bresnaman GF, Shell WE, et al: Estimation of
infarct size in man and its relation to prognosis. Circulation 46:640-648, 1972
25 Prinzmetal M, Kennamer R, Merliss R, et al: Angina
26
27
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1966
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block in acute myocardial infarction. Circulation 42:925933, 1970
Schuilenburg RM, Durrer D: Conduction disturbances
located within the His bundle. Circulation 45:612-628,
1972
Lie KI, Wellens HJ, Schuilenburg RM, et al: Mechanism
and significance of widened QRS complexes during complete atrioventricular block in acute inferior myocardial
infarction. Am J Cardiol33:833-839, 1974
Schamroth L, Ziady F, deKock J: Acute inferior wall
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Bashour TT,Fahdul H, Cheng TO: Complete heart block
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Sutton R, Chattejee K: Heart block in myocardial infarction. Lancet 1:94, 1968
Beregovich J, Fenig S, Lasser J, et al: Management of
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1965
Modern Wood Engraving
Apart from lithography and etching, the post-war
period saw the rebirth of wood engraving, especially in
Switzerland. In 1953, an international society of wood
engravers was founded in Zurich, under the name of
Xylon. This group looks back to fifteenth-century engraving, especially colored wood engraving, for its
members d o not want just "grim black and white." In the
introduction of the catalogue at the exhibition at Vienna
in October 1961, they pointed out that wood engraving
should draw its inspiration from the Gargas cave in the
Pyrenees, "where you can see imprints of mutilated
hands done with a primitive paint made of iron oxide
and animal fat." In spite of their manifesto, several
artists hesitated between nineteenth-century traditionalism and the influence of Gauguin, but there are among
them marked personalities like HR Bosshard (born in
1929 in Zurich), Werner H o h a n n (born in 1935 in
Affoltem), and Heinz Keller (born in 1928 in Wintherthur). Nearly all of them are Expressionists, for wood
does not lend itself well to Abstract art, and moreover, they say their forebears of the fifteenth century had
such power of expression that they were the ancestors of
modem Expressionism.
AdhBmar, J: Twentieth-Century Graphics,
New York, Praeger, 1971
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CHEST, 69: 5, MAY, 1976