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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”.