• Non—Q wave MI: Area of ischemic necrosis is limited to the
inner one third to half of myocardial wall.
• Q wave MI: Area of ischemic necrosis penetrates the entire
thickness of the ventricular wall.
• Coronary artery spasm
• Coronary embolism (caused by infective endocarditis, rheumatic
heart disease, intracavitary thrombus)
• Periarteritis and other coronary artery inflammatory diseases
• Dissection into coronary arteries (aneurysmal or iatrogenic)
• Congenital abnormalities of coronary circulation
• MI with normal coronaries (MINC syndrome): more frequent in
younger patients and cocaine addicts
• Crushing substernal or retrosternal chest pain usually lasts
longer than 30 min.
• Pain is unrelieved by rest or sublingual nitroglycerin or is rapidly
• Pain radiates to the left or right arm, neck, jaw, back, shoulders,
or abdomen and is not pleuritic in character.
• Pain may be associated with dyspnea, diaphoresis, nausea, or
• There is no pain in approximately 20% of infarctions (usually in
diabetic or elderly patients).
• Skin may be diaphoretic, with pallor (because of decreased
• Rales may be present at the bases of lungs (indicative of CHF).
• Cardiac auscultation may reveal an apical systolic murmur
caused by mitral regurgitation secondary to papillary muscle
dysfunction; S3 or S4 may also be present.
• Physical examination may be completely normal.
• Serum cardiac enzyme studies: damaged necrotic heart
muscle releases cardiac isoenzymes (CK, LDH) into the
blood stream in amounts that correlate with the size of the
infarct. Electrophoretic fractionation of the enzymes can
pinpoint certain isoenzymes (CK-MB and LDH-1) that are
more sensitive indicators of MI than total CK or LDH.
• Cardiac troponin levels: cardiac-specific troponin T (cTnT)
and cardiac- specific troponin I (cTnI) are new markers for
acute Ml. Rapid whole blood bedside assays are now
available. Increases in serum levels of cTnT and cTnI may
occur relatively early after muscle damage and may be
present for several days after MI (up to 7 days for cTnI and
up to 10 to 14 days for cTnT).
Fig.26. Time course of elevations of serum markers after MI.
Traditionally total CK, CK-MB, and lactic dehydrogenase
(LDH [with isoenzymes]) are measured. The smaller
molecule myoglobin is released quickly from infarcted
myocardium. Troponin I rises more slowly than myoglobin
and may be useful for diagnosis of infarction even up to 3 to
4 days after the event. Assays for cardiac-specific troponin I
and troponin T using monoclonal antibodies are now
ECG In Q wave infarction, there is development of:
a. Inverted T waves, indicating an area of ischemia
b. Elevated ST segment, indicating an area of injury
c. Q waves, indicating an area of infarction (usually develop
over 12 to 36 hr)
ECG in non-Q wave MI
Q waves are absent, but:
a. History and myocardial enzyme elevations are compatible
b. ECG shows ST segment elevation, depression, or no
change followed by T wave inversion.
Superacute and acute stage of non-Q-wave MI
• Chest radiography is useful to evaluate for pulmonary
• Echocardiography can evaluate wall motion abnormalities
and identify mural thrombus or mitral regurgitation, which
can occur acutely after MI.
• Limit patient’s activity: bed rest in the initial 24 hr; if the
patient remains stable, gradually increase activity.
• Diet: NPO until stable, then no added salt, low-cholesterol
• Patient education to decrease the risk of subsequent cardiac
events (proper diet, cessation of smoking, regular exercise)
should be initial when the patient is medically stable.
1. Nasal oxygen
3. Adequate analgesia: morphine sulfate IV
5. β-Adrenergic blocking agents
7. Primary angioplasty (PTCA) may be performed as an excellent
alternative to thrombolytic therapy. Prompt access to emergency
coronary artery bypass graft (CABG) surgery is mandatory if
primary PTCA is to be undertaken.
Prognosis after MI
The prognosis after MI depends on multiple factors:
• Presence of arrhythmias,
• Use of β-blockers: the mortality of patients on a regular regimen
of β- blockers is significantly decreased when compared with that
of control groups.
• Size of infarct: the larger it is, the higher the post-MI mortality
• Site of infarct: inferior wall MI carries a better prognosis than
anterior wall MI.
• Type of infarct: although the in-hospital mortality rate is higher
for patients with Q wave infarcts, the long-term prognosis for non
—Q wave MI may be worse because these patients have a higher
incidence of sudden cardiac death after hospital discharge.