- Myocardial infarction is caused by inadequate oxygen supply to the heart muscle, usually due to blockage of a coronary artery. - The classic symptom is chest pain or discomfort that may radiate to the shoulder, neck or arm. - An electrocardiogram (ECG) within 10 minutes of symptoms can help diagnose myocardial infarction and determine prognosis. ST segment elevations on ECG strongly indicate acute ischemia. - Biomarkers of cardiac injury like cardiac troponins and creatine kinase MB fraction rise in the bloodstream following myocardial infarction and can help with diagnosis.

1. Analysis of various investigations
in myocardial infarction

2. • The most common serious cause of acute chest discomfort is
myocardial ischemia or myocardial infarction.
• Occurs when the supply of myocardial oxygen is inadequate
for the demand.
• The classic manifestation of ischemia is angina, which is
usually described as a heavy chest pressure or squeezing, a
burning feeling, or difficulty breathing.

3. • The discomfort often radiates to the left shoulder, neck, or
arm.
• It typically builds in intensity over a few minutes.
• The pain may begin with exercise or psychological stress, but
ACS most frequently occurs without obvious precipitating
factors.

5. • One third of patients who experience STEMI will die within 24 hours
of the onset of ischemia, and many of the survivors will suffer
significant morbidity.
• For many patients, the first manifestation of CHD will be sudden
death.
• The difficulty lies in discriminating patients with ACS or other life-
threatening conditions from those with noncardiovascular, non–life-
threatening chest pain.
• The diagnosis of ACS is missed in approximately 2% of patients.

7. ECG
• An ECG, a source of decisive data, should be obtained within
10 minutes after arrival for individuals with ongoing chest
discomfort and as rapidly as possible in those who have a
history of chest discomfort consistent with ACS.
• The ECG helps to define both diagnosis and prognosis.

8. • New persistent or transient ST-segment abnormalities (≥0.05 mV)
that develop during a symptomatic episode at rest and resolve when
the symptoms resolve strongly suggest acute ischemia and severe
CAD.
• Nonspecific, ST-segment changes or T wave abnormalities of 0.2 mV
or less are not as helpful for risk stratification

15. ST SEGMENT ELEVATION
• Most patients who present with acute STEMI have underlying
atherosclerotic coronary artery disease.
• The usual pathophysiology of STEMI, sometimes evolving into a Q
wave MI, relates to blockage of one of the major epicardial coronary
arteries by a ruptured or eroded (ulcerated) atherosclerotic plaque,
an event followed by the formation of a clot (thrombus) at this intra-
coronary site.

16. • The earliest ECG changes seen with acute transmural
ischemia/infarction typically occur in the ST-T complex in the two
major, sequential phases:
• The acute phase is marked by the appearance of ST segment
elevations and sometimes tall positive (so-called hyperacute) T waves
in multiple (usually two or more) leads.
• The term “STEMI” refers specifically to MIs with new or increased
elevation of the ST segment, sometimes with prominent T waves,
which are usually associated with complete or near complete
occlusion of an epicardial coronary artery.

18. • Reciprocal ST depressions may occur in leads whose positive poles
are directed about 180° degrees from those showing ST elevations.
• Thus, an inferior MI may be marked by ST elevations in leads II, III,
and aVF, along with ST depressions in I, and aVL.
• Elevation of any degree in two contiguous inferior leads with any
amount of ST depression in aVL is highly suspicious for inferior MI.

21. • The evolving phase occurs hours or days later and is characterized by
deep T wave inversions in the leads that previously showed ST
elevations.

23. QRS Changes:
• Q Waves of Infarction MI, particularly when large and transmural, often
produces distinctive changes in the QRS (depolarization) complex.
• The characteristic depolarization sign is the appearance of new Q waves.
• With a transmural infarction, necrosis of heart muscle occurs in a localized
area of the ventricle.
• As a result the electrical voltages produced by this portion of the myocardium
disappear.
• Instead of positive (R) waves over the infarcted area, Q waves are often
recorded (either a QR or QS complex)

24. • The new Q waves of an MI generally appear within the first day or so
of the infarct.
• With an anterior wall infarction these Q waves are seen in one or
more of leads V1 to V6, I, and aVL.
• With an inferior wall MI the new Q waves appear in leads II, III, and
aVF.

28. • Characteristically, completely occlusive thrombi leads to extensive
injury to the ventricular wall in the myocardial bed subtended by the
affected coronary artery.
• Infarction alters the sequence of depolarization ultimately reflected
as changes in the QRS complex.

29. Serum and Plasma Markers of Cardiac Damage
• Necrosis compromises the integrity of the sarcolemmal membrane;
intracellular macromolecules (serum and plasma cardiac markers)
begin to diffuse into the cardiac interstitium and ultimately into the
microvasculature and lymphatics in the region of the infarct.
• The rate of appearance of these macromolecules in the peripheral
circulation depends on several factors, including intracellular location,
molecular weight, local blood and lymphatic flow, and the rate of
elimination from blood.

31. Cardiac specific troponins
• The preferred biomarker to detect myocardial injury is cardiac
troponin, which consists of three subunits that regulate the calcium-
mediated contractile process of striated muscle.
• These subunits include troponin C, which binds Ca2+; troponin I (TnI),
which binds to actin and inhibits actin-myosin interactions; and
troponin T (TnT), which binds to tropomyosin, thereby attaching the
troponin complex to the thin filament

32. • In patients with MI, concentrations of cTnT and cTnI detected by
conventional assays (non–high-sensitivity) can be detected
approximately 3 hours after the onset of chest pain.
• Because of continuous release from a degenerating contractile
apparatus in necrotic myocytes, elevations in cTnI may persist for 7 to
10 days after MI.
• Elevations in cTnT may persist for up to 10 to 14 days.

33. • The prolonged time course of the elevation in cTnT and cTnI is
advantageous for the late diagnosis of MI.
• Patients with STEMI who undergo successful recanalization of the
infarct-related artery have a rapid release of cardiac troponins, which
can indicate reperfusion.

35. High-Sensitivity Cardiac Troponin.
• It’s more precise measurement of very low concentrations of cardiac-
specific troponin.
• Such assays have greater sensitivity,also have diminished clinical
specificity for MI because they detect true myocardial injury in a
variety of other clinical settings.
• The rapidly changing concentration of troponin over periods of 1-3
hours helps in discriminating acute myocardial infarction from
structural cardiac diseases

36. Creatinine kinase MB- iso enzyme
• CK-MB measured with a mass assay is the best alternative.
• Cardiac muscle contains both the MM and the MB isoenzyme of CK.
• Other tissues can contain small quantities of CK-MB, including the
small intestine, tongue, diaphragm, uterus, and prostate.
• CK-MB may rise in circumstances involving severe skeletal muscle
injury.

37. • CK rises within 4–8 h and generally returns to normal by 48–72 h.
• CK is not specific as it can be elevated in
• cardiac surgery,
• myocarditis, and
• electrical cardioversion.

38. • The nonspecific reaction to myocardial injury is associated with
polymorphonuclear leukocytosis, which appears within a few hours
after the onset of pain and persists for 3–7 days;
• The white blood cell count often reaches levels of 12,000–15,000/μL.
• The erythrocyte sedimentation rate rises more slowly than the white
blood cell count, peaking during the first week and sometimes
remaining elevated for 1 or 2 weeks.

39. CARDIAC IMAGING
• Abnormalities of wall motion on two-dimensional echocardiography
are almost universally present.
• Although acute STEMI cannot be distinguished from an old
myocardial scar or from acute severe ischemia by echocardiography.
• Echocardiographic estimation of left ventricular (LV) function is useful
prognostically.
• Detection of reduced function serves as an indication for therapy with
an inhibitor of the renin-angiotensin-aldosterone system.

40. • Several radionuclide imaging techniques are available for evaluating
patients with suspected STEMI.
• However, these imaging modalities are used less often than
echocardiography because they are more cumbersome and lack
sensitivity and specificity in many clinical circumstances.

41. • Myocardial perfusion imaging with [201Tl] or [99mTc]-sestamibi,
which are distributed in proportion to myocardial blood flow and
concentrated by viable myocardium, reveals a defect (“cold spot”) in
most patients during the first few hours after development of a
transmural infarct.
• Although perfusion scanning is extremely sensitive, it cannot
distinguish acute infarcts from chronic scars and, thus, is not specific
for the diagnosis of acute MI.

43. Thank you.