Presentasi Slide Terakhir
Presentasi Slide Terakhir
Presentasi Slide Terakhir
Myocardial
• The diagnosis of MINOCA, like the diagnosis of MI, indicates
infarction with that there is an ischaemic mechanism responsible for the
myocyte injury (i.e. non-ischaemic causes such as myocarditis
non-obstructive have been excluded).
coronary arteries
Myocardial injury • The mechanisms include increased ventricular
and/or infarction pressure, small-vessel coronary obstruction,
anaemia, hypotension, and possibly direct toxic
associated with effects on the myocardium associated with the
kidney disease uraemic state.
Operationalizing
• To establish the diagnosis of an acute MI, a rise and/or fall in
criteria for cTn values with at least one value above the 99th percentile URL
myocardial injury is required, coupled with a high clinical and/or ECG likelihood of
myocardial ischaemia. hs-cTn assays shorten the time to
and infarction diagnosis in many patients towithin 3 h ofonset of symptoms
Application of
supplemental • Supplemental leads, as well as serial ECG recordings, should be
deployed with a very low threshold in patients who present
electrocardiogram with ischaemic chest pain and a non-diagnostic initial ECG.
leads
Electrocardiographic detection
of myocardial infarction
Electrocardiographic • It is not possible to initially distinguish ECG manifestations of
detection acute or chronic myocardial injury from acute myocardial
ischaemia.
of myocardial injury
Conditions that • A QS complex in lead V1 is normal. A Q wave < 0.03 s and < 0.25
confound the of the R wave amplitude in lead III is normal if the frontal QRS
axis is between -30 and 0. A Q wave may also be normal in aVL
electrocardiographic if the frontal QRS axis is between 60–90. Septal Q waves are
diagnosis of small, nonpathological Q waves < 0.03 s and < 0.25 of the R-
wave amplitude in leads I, aVL, aVF, and V4–V6.
myocardial infarction
Silent/unrecognized
myocardial infarction in • An annual ECG is reasonable in clinical trials to monitor
for silent Q wave MI events if the study population is
epidemiological studies expected to have an accelerated rate of atherosclerotic
and quality events.
programmes
• clinical findings,
• patterns on the ECG,
• laboratory data,
• observations from imaging procedures,
• and on occasion pathological findings,
• all viewed in the context of the time horizon over
which the suspected event unfolds.