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9A

Old Myocardial Infarction

Synopsis tion in coronary arteries have been identified as


newer risk factors for MI.
Significance
Old myocardial infarction (MI) by ECG criteria Classification Problems
has been used as evidence for coronary heart Abnormal Q waves in survivors of acute MI may
disease (CHD) in epidemiological studies for not develop and when present, they tend to dimin-
comparing cross-sectional MI prevalence and for ish or even disappear with time. In older studies
risk evaluation in contrasting populations. Myo- using ventriculography as a standard, the sensi-
cardial infarction by ECG is the only manifesta- tivity of Minnesota Code 1.1–1.3 Q waves in
tion of past silent MI. detecting wall motion abnormalities was reported
as 51% at a specificity of 84%. Equally low sensi-
Mechanism tivity has been reported in autopsy studies or
using ECG-independent evidence in the acute
Coronary arteries are endarteries. Obstruction of phase as a standard. Low specificity reduces the
an artery in the coronary bed results in acute isch- utility of some more sensitive ECG criteria such
emic injury, and if not resolved, a subsequent loss as poor R wave progression in anterior MI. Up to
of electrical activity and death of damaged myo- a quarter to a third of MIs by ECG criteria have
cardial cells. Abnormal QS or Q waves usually been found to be unrecognized, one-half of them
appear following or concomitant with ST devia- without any reported symptoms. The limited clas-
tions in acute phase and evolving ST-T changes. sification accuracy of ECG criteria based solely on
Dead or fibrosed myocardial tissue alters excita- ECG evidence reduces the utility of comparative
tion pathways around the damaged region causing evaluation of MI prevalence in contrasting
other QRS changes, and occasionally blocking populations.
conduction in major conduction pathways of the
His–Purkinje system.
Prevalence
The reported prevalence of Minnesota Code 1.1–
Risk Factors
1.3 Q waves in community-based populations at
These include CHD risk factors in general: age 40–59 years ranges from less than 1% to 6.6%
cigarette smoking, age, male gender, serum cho- in men and from 1% to 4.5% in women. In CHD-
lesterol and improper lipoprotein balance, hyper- free cohorts of 40- to 59-year-old men, the preva-
tension, impaired glucose tolerance, and heredity. lence ranges from 1.6 to 2.1%. Definite old MI
Elevated homocysteine, C-reactive protein, fibrin- prevalence by strict Q-wave criteria is low at age
ogen, and other factors promoting plaque forma- 40–59 years, even in countries with high CHD

166
Introduction 167

mortality like Finland (1.3% in men and 0.5% in the primary requirements in cardiovascular
women). epidemiological studies. Acute MI, of primary
concern in clinical applications, is rarely encoun-
tered in community health surveys. The sequels
Mortality Risk of myocardial damage following the acute MI
Independent short-term risk for CHD mortality phase, the residual abnormal Q waves and re-
for MI by the Minnesota Code 1.1–1.3 combina- polarization abnormalities, provide primary evi-
tion varies in contrasting populations from dence for an old MI. Abnormal Q waves do not
nonsignificant to over fourfold risk increase. develop in a certain fraction of patients, and when
Long-term risk is not significant. Short-term they do, they tend to become smaller or even dis-
excess mortality risk for large Q waves in CHD- appear with time because of cardiac remodeling
free and in total male cohorts has been 13- to in the healing and adaptation phase following
nearly 20-fold in some studies. For strict MI cri- acute MI. While ST elevation is the primary
teria combining major Q waves and major ST-T marker of acute ischemic injury, negative or “flat”
codes, the reported multivariable-adjusted short- T waves, often with borderline-abnormal Q waves,
term risk for CHD mortality ranges from seven- remain as chronic manifestations of old ischemic
fold up to 19-fold, and also the reported long-term injury. Some degree of residual ST elevation is
risk is over threefold. Prevalence of MI by such often retained particularly in old anterior MI. Sus-
stricter criteria is low, reducing the corresponding tained ST depression may indicate the presence of
utility in identifying high-risk subgroups. In most a chronic ischemic state.
studies, mortality risk has been similar for non- There are several other clinical conditions that
recognized and recognized MI in men. Mortality may induce secondary repolarization abnormali-
risk in women has been reported to be marginally ties, including in particular left ventricular con-
lower for unrecognized than for recognized MI. duction defects and left ventricular hypertrophy
(LVH). In CHD, repolarization abnormalities may
be secondary, due to altered sequence of ventricu-
lar excitation with scar formation and fibrosis
Abbreviations and Acronyms (often combined with compensatory LVH in post-
MI states), or they can be primary signs of derailed
BARI – Bypass Angioplasty Revascularization
ionic channel function in ischemic regions. Clini-
Investigation
cally so-called non-Q-wave MI in the acute phase
CABG – coronary artery bypass grafting
may occur particularly in smaller MIs when clearly
CAD – coronary artery disease
abnormal Q waves do not develop. Repolarization
CHD – coronary heart disease
abnormalities evolve characteristically in the
CVD – cardiovascular disease
acute phase in Q-wave and in non-Q-wave MI.
LAD – left anterior descending (coronary artery)
This chapter covers ECG abnormalities that are
LCX – left circumferential (coronary artery)
most directly associated with an old MI. Various
LBBB – left bundle branch block
studies have used quite diverse definitions for MI
LVH – left ventricular hypertrophy
and ischemic abnormalities. In the Minnesota
LPD – left posterior descending (coronary
Code, abnormal Q waves are covered under Code
artery)
1. Abnormalities in ST and T waves are coded
MI – myocardial infarction
under Codes 4 and 5. In the Minnesota Code in
RCA – right coronary artery
general, various categories are coded as indepen-
dent entities without a clear hierarchy in relation
to other coding categories. Many newer studies
9A.1 Introduction have used various combinations of Q wave and
ST-T codes to identify an old MI. At times left
Objective coding of ECG abnormalities associated bundle branch block (Code 7.1) is included with
with coronary heart disease (CHD), particularly Q wave and ST-T codes in a pooled category char-
old myocardial infarction (MI), has been one of acterized as “ischemic abnormalities”.

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