This document provides an overview of common diagnostic tests used to evaluate heart disease, including symptoms, imaging, stress testing, and cardiac enzyme levels. Key points include: chest X-ray and echocardiogram are used to examine the heart and vessels, ECG detects arrhythmias and ischemia, nuclear imaging with agents like thallium-201 assess perfusion and viability, stress testing like exercise or pharmacological methods increase demand to detect ischemia, and cardiac enzymes like CK-MB and troponin rise with myocardial injury and are diagnostic of heart attack. The document provides details on techniques, normal ranges, and clinical applications of these important cardiac diagnostic evaluations.

1. Interpretation of Clinical Lab
Data [CARDIAC] for Newbies

2. Common symptoms of heart disease
 Chest pain (dull, aching tightness rather than tight
stabbing sensation);
 Dyspnoea; Palpitations; Dizziness; Syncope; Oedema;
Diagnostic Testing
 Chest X-Ray (CXR): Provides info. about heart size,
pulmonary circulation, and aortic abnormalities.
 Echocardiogram: provides more reliable info. about
chamber size, hypertrophy, valvular and congenital
abnormalities.
 Electrocardiogram (ECG): Indicates the cardiac rhythm;
reveals conduction abnormalities; provides evidence of
ventricular hypertrophy, MI, Ischemia.

3. ECG
 Angina Pectoris: ST depression; Flat (inverted) T-wave
 STEMI:
• 1st ECG change during STEMI is ‘hyperacute T waves’ which
appear peaked and are related to localized hyperkalemia. These
changes are rarely seen as they are transient and frequently
occur prior to hospital arrival.
• ST segment elevation (pertaining to the affected myocardium).
• 1 mm of ST elevation in 2 contiguous leads is required
to diagnose STEMI,
• ST elevations are indicative of the ischemic area.

4. Q
R
S

5.  NSTEMI and Unstable angina:
• ST-segment depression≥ 0.5 mm; negative (inverted or flat) T-
waves≥ 1.0 mm
• ST depressions do NOT localize to the ischemic area
• ECG cannot be used to determine the location of ischemia in
patients w/ NSTEMI and unstable angina.

6. Q
R
S

7. Ischemic ST depression is characterized by horizontal or
downward sloping (if not, then ischemia is unlikely to be the
cause).

8. If QRS….
• > 100/min. → Tachycardia;
• < 60/min. → Bradycardia;

9. Q
R
S

10. Exercise Stress Testing (EST or ET or ETT)
 Is a test of myocardial perfusion; also determines
the adequacy of CV functions;
 Evaluates clinical and CV responses to exercise;
 Used as a diagnostic and prognostic assessment in
patients with known or suspected IHD.
 Non-invasive test (conducted on a tread mill or bicycle
ergometer);
 Treadmill walking is preferred over the ergometer as it
involves more muscle mass.

11. EST (contd’.)
 Principle: Controlled method to assess the balance between
myocardial O2 demand and coronary blood flow under ‘stress’
(exercise is the stressor).
 A (+) ET is defined as ‘1mm horizontal or downsloping
depression, or elevation of the ST segment for 60-80
milliseconds after the QRS complex’.

12. Nuclear Imaging
 Used to detect MI or to measure myocardial function,
perfusion or viability depending on the
radiopharmaceutical used and the technique of
imaging.
 Thallium-201 (TL-201):
• Rapidly taken up by the myocardium;
• An image taken immediately after injection reflects the
distribution of blood flow to the myocardium.
• Areas of ischemia or infarction receive less TL-201 and
appear dark.
• Around 2 - 6 hrs. post-injection, TL-201 redistributes so
that all cardiac myocytes contain a comparable
concentration. Images at this time show dark areas
(infarction) but normal density in ischemic areas.

13.  The hypoperfused areas of the viable myocardium
which had little or no TL-201 initially are called ‘Partial
Defects’.
 Redistribution occurs because there is a delayed
washout of TL-201 from the poorly perfused
myocardium resulting in less contrast between the
density of TL-201 in different areas of the heart. This
gives the appearance of redistribution into the
previously ischemic areas.

14.  To enhance the evaluation of the partial defects, a
second injection of TL-201 can be used.
 Areas of nil distribution are called ‘Cold Spots’ or ‘Fixed
defects’ (representing infarcted myocardium).
Scope of TL-201 imaging:
 Useful for patients w/
• atypical chest pain to determine if IHD is the cause of
symptoms.
• ambiguous or false-positive ETT to determine the ETT
abnormalities.
 The finding of redistribution is a marker of jeopardized
but viable myocardium that has important prognostic
value.

15.  Tc-99: To detect myocardial viability.
 Antimyosin Abs: Highly specific, so, should be more
better markers of myocyte necrosis. But, uptake into
myocardial tissues is very low; localization is more
dependent on blood flow rather than on myosin conc.
 Phyenylpentadecanoic acid: assesses both myocardial
perfusion and metabolism by virtue of it’s affinity for
fatty acid metabolism.

16. Pharmacological Stress Testing
 Alternative to ETT
 For patients who are unwilling or unable to undergo
ETT;
 Used to assess coronary perfusion;
 P’cological agent produces stress by…
• hyperemic (vasodilator) response,
[OR]
• ↑es myocardial O2 demand (heart rate and myocardial
contractility);
 Agents used:
• Dipyridamole and Adenosine (hyperemic stress), and
• Dobutamine (cardiac stress)

17. Principle of Dipyridamole and Adenosine TL-201 scanning:
 Related to the coronary arteriolar vasodilator props.
 Dipyridamole inhibits adenosine reuptake by cells;
causing an ↑ ed conc. of adenosine.
 Adenosine is a very potent coronary artery vasodilator
(↑es the perfusion).
 Areas distal to the coronary will be hypoperfused; but
these areas will get filled on redistribution indicating
viable but jeopardized myocardium.
 Optimal dose (based on numerous research articles):
• Dipyridamole 0.142 mg/kg per min. over 4 mins.
• Adenosine 0.140 mcg/kg per min. over 6 mins.

18.  TL-201 (2.5 – 4 mCi) is administered…
• immediately after inf. of dipyridamole,
(or)
• after 3 mins. of Adenosine inf.
 Onset of action:
• Dipyridamole (5-7 mins. post-inf.);
• Adenosine (approx. 30 secs. post-inf.);

19. Dobutamine:
 Synthetic catecholamine;
 ↑es heart rate and cardiac output ↑es myocardial
O2 demand.
 Ischemia develops in areas where there is ↑ in O2
demand (by stenosis which prevents the blood flow to
those areas).
 This can be detected by the TL-201 scanning….
• Dobutamine dose 10 – 20 mcg/kg per min.
• TL-201 is administered 2-3 mins. before inf. ends.
 β-blockers and CCBs may interfere w/ the heart’s
response to the Dobutamine stress test.
(Recommendation: Discontinue the Tx prior to the
test).
 Contraindicated: Aortic stenosis, uncontrolled HTN,
severe ventricular arrhythymias;

20. Dobutamine stress testing…
 Post-MI, this test identifies patients at high risk of
subsequent cardiac events.
 For patients w/ suspected or k/c/o IHD,…
• a positive result is an independent predictor of ‘cardiac
events’;
• a negative result indicates protection from cardiac death.
 Showed higher diagnostic accuracy (82%) for IHD;
against 87% for ETT, and 77% for dipyridamole;
 Showed high sensitivity (80%) – review of 14 studies;
942 IHD patients;
 Cardiac catheterization
 CT scan; MRI scan

21. Cardiac Enzymes
Lactate Dehydrogenase (LDH1 to LDH5)
 Highly distributed throughout the body w/ high concs.
in the heart muscle, skeletal muscle, liver, kidney,
brain, and RBCs.
 LDH1, LDH2 (mainly in the heart);
 LDH3 (lungs);
 LDH4, LDH5 (mainly in the liver and skeletal muscles);
 LDH1 is often measured after a suspected MI. This
isoenzyme shows greater catalytic activity combined w/
α-OH butyrate. This substrate is measured. Post-MI,
peak serum levels are achieved after 2-3 days, then
declines over 7 days or more.

22. LDH (contd’.)
 LDH1 and LDH2: ↑es after MI, renal infarction,
megaloblastic anaemia;
 LDH2 and LDH3: ↑es after acute leukemia;
 LDH5: ↑es after damage to liver or skeletal muscle;

23. Creatine Kinase (CK)
 Relatively high concs. in heart muscles, skeletal muscles,
smooth muscles, brain.
 Markedly ↑ed after circulation failure, MI, muscular
dystrophies, exercise, and trauma.
 CK has 2 protein subunits: M and B (which combine to form 3
isoenzymes BB, MM, and MB).
 Cardiac tissues contain more of the CK-MB isoenzyme.
 CK-MM (skeletal muscle); CK-BB (brain tissue);
 ↑ed CK-MB levels indicate myocardial necrosis.

24. Enzymes Rise (hrs.) Peak (hrs.) Falls
CK-MB 4 – 6 12 48 – 72 hrs.
LDH 12 48 – 72 7 days
AST 12 24 48 hrs.

25. Aspartate aminotransferase (AST)
 Formerly known as Serum Glutamic-Oxaloacetic
Transaminase (SGOT);
 Found mainly in the cardiac and hepatic tissues;
 To a lesser extent in the skeletal muscle, kidney
tissue and pancreatic tissue.
 ↑ed AST levels are seen 8 hrs. post-damage to the
heart from MI.

26. Alanine aminotransferase (ALT)
 Formerly known as Serum Glutamic-Pyruvic
Transaminase (SGPT);
 Mainly in the liver;
 To a lesser extent in the heart, skeletal muscles, and
kidneys;
 ALT ↑es less consistently and less markedly than
AST post-MI.

27. Cardiac Troponins ( ‘I’ and ‘T’)
 Used in the diagnosis of MI;
 Troponin-I (< 1.5 ng/ml); Troponin-T (< 0.1 ng/ml);
 Troponin-I (only in cardiac muscle);
 Troponin-T (in cardiac and skeletal muscles);
 Troponin-T has shown prognostic value in unstable
angina and detecting minor myocardial injury w/
greater sensitivity than CK-MB.

28. THE END
(FYI Snippets follow….)

33.  P-wave (2.5 mm): R and L atrial depolarization
 QRS complex (120 ms): R and L ventricular depolarization
 ST segment: phase 2 of ventricular repolarization
 T-wave: rapid phase 3 of ventricular repolarization;
 J-point: the end of QRS and beginning of ST segment is called J-point.
 PR interval: extends from beginning of P wave to beginning of the
QRS. This interval measures the time from the initial depolarization of
the atria to the initial depolarization of the ventricles, and reflects a
physiological delay in AV conduction imposed by the AV node.
Normal range is 120 – 200 ms (3 to 5 1-mm-divisions) and no longer.
 QT interval: is measured from the beginning of the QRS to the end of
the T wave. It represents the time in which the ventricles depolarize
and repolarize and is a measure of ventricular action potential (AP)
duration. Normal intervals are < 460 ms for women and < 450 ms for
men. But QT values are heart-rate dependent and can vary from 270
ms at a heart rate of 150 beats/min to 500 ms at a heart rate of 40
beats/min.

34.  FYI:
• Anterior STEMI requires 2 mm of ST elevation in V2 and V3 in men >
40 years of age (ACC/AHA definition). A total of 2.5 mm elevation is
required in men < 40 years of age, and only 1.5 mm elevation is
required in women.
• Posterior STEMI frequently has ST depression in V1-V3 instead of
elevation since the vectors are completely reversed. If a posterior
ECG were obtained, ST elevation will be seen in V7-V9, although
sometimes subtle. Since these posterior changes occur from coronary
thrombosis and urgent treatment is needed, it is classified as a
STEMI.
• (courtesy ACC and AHA)
• What is V1-V9????