2. CAD
Risk factors and Pathophysiology
Clinical spectrum
Clinical features
Investigations and treatment
Complications of MI
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3. Traditional risk factors:
-Age
-Male gender
-Dyslipidemia
High LDL cholesterol
Low HDL cholesterol
-DM
-HTN
-Smoking
-Family history of
premature CAD
Emerging risk factors:
-Lp(a)
-Fibrinogen
-Homocysteine
-Urine
microalbuminuria
-Hs CRP
-Markers of subclinical
ASCVD
ABI
Carotid IMT
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6. • Remarks on Angina Pectoris” by John Warren, M.D.,
appeared in 1812
• Warren’s description of angina pectoris (derived from
the Latin angina, “infection of the throat”; from the
Greek ά́γχο′νη, “strangling”; and from the Latin pectus,
“chest”)
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7. Angina Pectoris
Retrosternal chest pressure, burning, or heaviness
Radiating to neck, jaw, epigastrium, shoulders,along the
ulnar surface of the left arm; the right arm and the outer
surfaces of both arms may also be involved
Precipitated by exercise, cold weather,emotional stress
Begins gradually and reaches its maximum intensity over
a period of minutes
Duration 2-10 min.Relieved within minutes by rest or the
use of nitroglycerin
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10. Unstable angina more severe Typically
<20 min,present even at rest;crescendo pattern
Acute myocardial infarction more severe
Sudden onset, usually lasting ≥30 min; often
associated with shortness of breath, weakness,
nausea, vomiting
Variant Angina occurs at rest but not with
exertion - focal spasm of an epicardial coronary
artery
Levines
Sign
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11. Anginal equivalents (i.e., symptoms of myocardial
ischemia other than angina)
- dyspnea, faintness,fatigue,eructations particularly
in older patients and diabetics
Nausea,vomiting,diarrhea,epigastric pain seen in IWMI
Silent MI
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12. Clinical Classification of Chest Pain
Typical angina (definite)
Typical angina (definite)
Substernal chest discomfort: characteristic quality,
duration
Provoked by stress
Relieved by rest or nitroglycerin
Atypical angina (probable)
Meets 2 of the above characteristics
Noncardiac chest pain
Meets ≤1 of typical angina characteristics
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15. Definition of MI
Detection of a rise and/or fall of cardiac biomarker values with at
least one value above the 99th percentile (URL) and with at least one
of the following:
Symptoms of ischaemia
New or presumed new significant ST-segment–T wave (ST–T) changes
or new left bundle branch block (LBBB)
Development of pathological Q waves in the ECG
Imaging evidence of new loss of viable myocardium or new regional
wall motion abnormality
Identification of an intracoronary thrombus by angiography or
autopsy
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16. Examination
• Signs of sympathetic activation: pallor, sweating,
tachycardia
• Signs of vagal activation: vomiting, bradycardia
• Signs of impaired myocardial function
Hypotension, oliguria, cold peripheries
Narrow pulse pressure
Raised JVP
Third heart sound
Systolic murmurs,pericardial rub
Lung crepitations
• Signs of tissue damage: fever
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17. ECG
Initial ECG may be normal or
nondiagnostic in one-third of cases
Repeated ECG’s are important,
especially where the diagnosis is
uncertain or patient has recurrent or
persistent symptoms
Difficult to interpret if there is bundle
branch block or previous MI
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18. STEMI
ST elevation
• New ST elevation at the J point in two
contiguous leads with the following cut points:
≥0.1 mV in all leads (except V2-V3)
In leads V2-V3 the following cut points apply:
• ≥0.2 mV in men ≥40 years
• ≥0.25 mV in men <40 years
• ≥0.15 mV in women
Sequential features are reliable for the
approximate age of the infarct to be deduced
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23. CAUSES OF ST ELEVATION
Ischemia/myocardial infarction
Noninfarction, transmural ischemia (Prinzmetal's angina, and possibly tako-tsubo
syndrome)
Acute myocardial infarction
Postmyocardial infarction (ventricular aneurysm pattern)
Acute pericarditis
Normal variant ("early repolarization" pattern)
Left ventricular hypertrophy/left bundle branch block
Other (rarer)
Brugada pattern (right bundle branch block-like pattern with ST elevations in right
precordial leads)
Class 1C antiarrhythmic drugs
DC cardioversion
Hypercalcemia
Hyperkalemia
Hypothermia (J wave/Osborn waves)
Myocardial injury
Myocarditis
Tumor invading left ventricle
Trauma to ventricles
24. NSTEMI/Unstable Angina
ST Depression and T Wave Changes
• New horizontal or downsloping ST depression
≥0.05 mV in two contiguous leads
• T-wave inversion ≥0.1 mV in two contiguous leads
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26. Plasma cardiac biomarkers
MI causes a rise in the plasma concentration of
enzymes and proteins that are normally concentrated
within cardiac cells
Biochemical markers:
Creatine kinase (CK)
Cardio-specific isoform (CK-MB)
Cardio-specific proteins, Troponins T and I
Serial estimations are helpful because it is the
change in plasma concentrations of markers that
confirms the diagnosis of MI
Unstable angina - no detectable rise in
cardiac biomarkers or enzymes
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28. Chest X-ray
• Demonstrate pulmonary oedema that is not evident
on clinical examination
• Heart size is often normal
Echocardiography
• Useful for assessing ventricular function
• Detecting important complications such as mural
thrombus,cardiac rupture, VSD, mitral regurgitation
and pericardial effusion
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29. Goals Of Immediate Management
Identify candidates for reperfusion therapy
Relief of ischemic pain as well as recognition
and treatment of hypotension, pulmonary
edema, and arrhythmia
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30. Treatment
▫ Supplemental oxygen should be administered if
saturation is <90%
▫ Serial ECGs should be obtained for patients who
do not have ST segment elevation on the initial
ECG
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31. Analgesia
To relieve distress
To lower adrenergic drive and thereby reduce
vascular resistance, BP, infarct size and susceptibility
to ventricular arrhythmias
Intravenous opiates (initially, morphine sulphate 5–
10 mg or diamorphine 2.5–5 mg) and antiemetics
should be administered
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32. Antiplatelet therapy and Statins
• ASA effectively blocks platelet aggregation within
minutes and should be administered immediately
Aspirin (ASA) 162-325 mg Nonenteric coated formulations
(chewed or crushed) given
orally or rectally facilitate rapid
drug absorption and platelet
inhibition.
Clopidogrel 300-600 mg loading dose, 75-150
mg daily
600 mg loading dose followed by 7
d of 150 mg maintenance dose
may reduce the incidence of stent
thrombosis and MI
Prasugrel 60 mg loading dose 10 mg daily quicker acting and more potent
antiplatelet agent with improved
efficacy
should not be used in patients
greater than 75 yr old, less than
60 kg, or with a history of
stroke/TIA
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34. Antianginal
Sublingual glyceryl trinitrate (300–500 μg) is a
valuable first-aid measure in unstable angina or
myocardial infarction
Intravenous nitrates (glyceryl trinitrate 0.6–1.2 mg/hr
or isosorbide dinitrate 1–2 mg/hr) are useful for the
treatment of left ventricular failure and the relief of
recurrent or persistent ischaemic pain
Intravenous β-blockers (metoprolol 5–15 mg given
over 5 mins) relieve pain,reduce arrhythmias
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35. Reperfusion Therapy
All patients who present with a STEMI within 12 to 24
hours of symptom onset should be considered for
immediate reperfusion therapy
Choice of reperfusion strategy includes
Thrombolysis
Primary PCI
Emergent CABG
NSTEMI patients - Immediate emergency reperfusion
therapy has no demonstrable benefit and
thrombolytic therapy may be harmful
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36. • Door to needle time- 30 min
(for patients receiving thrombolytic
therapy)
• Door to balloon time-90 min
(for patients undergoing primary
angioplasty)
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37. Primary Percutaneous Coronary
Intervention (PCI)
Treatment of choice for STEMI
Outcome is best when it is used in combination with
glycoprotein iib/iiia receptor antagonists and
intracoronary stent
Greater reduction in the risk of death, recurrent MI or
stroke
Primary PCI has been limited by availability of the
necessary resources
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38. PCI is preferred over thrombolysis in patients who:
• Presented within 12 hours of symptom onset and
anticipated time from first medical contact to balloon
inflation of 2 hours or less
• Contraindications to fibrinolytic therapy
• Presenting 12-24 hours of symptom onset with ongoing
symptoms/signs of ischemia or hemodynamic instability
• Presenting with cardiogenic shock
• Underwent recent PCI or prior CABG
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40. Absolute Contraindications Relative Contraindications
•History of intracranial hemorrhage or
hemorrhagic stroke
•Prior ischemic stroke more than 3 mo
ago
•Ischemic stroke within 3 mo •Allergy or previous use of streptokinase
(greater than 5 d ago)
•Known structural cerebrovascular
lesion (AVMs, aneurysms, tumor)
•Closed head injury within 3 mo •Recent internal bleeding (2-4 wk)
•Aortic dissection •Prolonged/traumatic CPR more than
10 min
•Severe uncontrolled hypertension (SBP
> 180 mm Hg, DBP > 110 mm Hg)
•Major surgery within 3 wk
•Active peptic ulcer disease
•Active bleeding or bleeding diathesis •Noncompressible vascular punctures
•Severe menstrual bleeding
•History of intraocular bleeding
•Pregnancy
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41. Medication Dosage Comments
Streptokinase (SK) 1.5 million units IV
over 60 min
Produces a generalized
fibrinolytic state (not clot
specific)
Allergic reactions including
skin rashes, fever, and
anaphylaxis may be seen in
1-2% of patients
Because of the development
of antibodies, patients who
were previously treated with
streptokinase should be given
an alternate thrombolytic
agent
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42. BOLUS FIBRINOLYTICS
Recombinant tissue
plasminogen activator (rt-
PA)
15 mg IV bolus
0.75 mg/kg over 30 min
(maximum 50 mg)
0.50 mg/kg over 60 min
(maximum 35 mg)
Fibrin selective agent with
improved clot specificity
compared to SK.
Does not cause allergic
reactions or hypotension.
Reteplase (r-PA) Two 10-unit IV boluses
administered 30 min apart
Fibrin selective agent with a
longer half-life but reduced
clot specificity compared to
rt-PA.
Tenecteplase (TNK-tPA) 0.50 mg/kg IV bolus (total
dose 30-50 mg)
Genetically engineered
variant of rt-PA with slower
plasma clearance, improved
fibrin specificity, and higher
resistance to plasminogen
activator inhibitor-1 (PAI-1).
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44. Anticoagulants
Reduces the risk of thromboembolic complications and
prevents re-infarction in the absence of reperfusion
therapy or after successful thrombolysis
Should be continued for 8 days or until discharge from
hospital or coronary revascularisation
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45. Unfractionated
heparin (UFH)
60 units/kg IV bolus, 12
units/kg/hr
UFH should be given to
all patients undergoing
PCI and those receiving
thrombolytics
Enoxaparin (LMWH) 30 mg IV bolus, 1 mg/kg
SC bid
Patients greater than 75
yr of age should not be
given a loading dose and
receive 0.75 mg SC bid.
Bivalirudin 0.75 mg/kg IV bolus, 1.75
mg/kg/hr
Bivalirudin has been
validated in patients
undergoing PCI
Fondaparinux 2.5 mg IV bolus, 2.5 mg
SC daily
Shown to be superior to
UFH when used during
thrombolysis with
decreased bleeding rates.
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52. Mechanical:
Ventricular septal defect:
- Seen 2 to 5 day after MI
- common in older females,Hypertension,Anterior
infarction
Papillary muscle rupture:
- Common in inferiorwall MI
- Sudden onset pulmonary edema and cardiogenic
shock
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59
AIVR is particularly common with acute MI
Sign of reperfusion after the use of thrombolytic agents or after
interventional coronary artery procedures
Short lived, lasting minutes or less, and usually requires no specific
therapy
60. Ischemic
Infarct expansion
Post infarct angina (few hrs to 30 days after Acute
MI)
Embolic Complications
Pericarditis
Early- After Transmural MI
Late- Dresslers Syndrome - 1 to 8 weeks after
MI,due to autoimmune mechanism
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64. • Aspirin is the preferred antiplatelet agent after MI
and should be used indefinitely
• Doses of 75 to 325 mg/d have been shown to
reduce the risk of recurrent MI, stroke, and cardiac
death
• Clopidogrel (75 mg/d) or Prasugrel (10 mg/d)
should be given for a minimum of 1 month in
patients who receive a BMS and for at least 1 year
in patients who receive a DES
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65. β-Blockers confer a mortality benefit following acute MI.
Treatment should begin as soon as possible (preferably
within the first 24 hours) and continued indefinitely
ACE inhibitors provide a reduction in short-term mortality
and incidence of CHF and recurrent MI when initiated
within the first 24 hours of an acute MI
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66. HMG-CoA reductase inhibitors should be started in all
patients in the absence of contraindications. The goal is
at least 50% reduction in LDL or LDL less than 70 mg/dL
Aldosterone receptor antagonists have shown benefit in
post-MI patients with LV ejection fraction of less than
40%
Therapy for control of diabetes and hypertension
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71. T-wave flattening or inversion in some leads,
providing non-specific evidence of myocardial
ischaemia or damage
Evidence of previous MI
Normal even in patients with severe CAD
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72. Exercise ECG
Assessing the severity of coronary disease and
identifying high-risk individuals
Performed using a standard treadmill or bicycle
ergometer protocol
Monitoring the patient’s ECG, BP and general
condition
Planar or down-sloping ST segment
depression of 1 mm or more is indicative of
ischaemia
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74. Stress Echocardiography
• Uses transthoracic echocardiography
• Identify ischaemic segments of
myocardium and areas of infarction
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75. Myocardial perfusion scanning
• Evaluation of patients with an equivocal or uninterpretable
exercise test and those who are unable to exercise
• Scintiscans of the myocardium at rest and during stress
• 201 Thallium
• 99mTc-MIBI
• 99mTc-Tetrofosmin
• 99mTc-Teboroxime
• Perfusion defect present during stress but not at rest provides
evidence of reversible myocardial ischaemia
• Persistent perfusion defect seen during both phases of the
study is usually indicative of previous MI
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77. CT Angiography
▫ Noninvasive approach to imaging atherosclerosis and its
consequences
▫ Detecting coronary calcification, which is a good
marker of the total coronary atherosclerotic burden
▫ Angiography of the coronary arterial tree, assessment of
myocardial perfusion and quantification of ventricular
function
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79. Coronary arteriography
• Detailed anatomical information about the
extent and nature of coronary artery disease
• Performed with a view to coronary artery bypass
graft (CABG) surgery or percutaneous coronary
intervention (PCI)
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87. Antiplatelet therapy
ASPIRIN (75 mg)
• Reduces the risk of MI
• Prescribed for all patients with CAD indefinitely
CLOPIDOGREL (75 mg daily)
• Prescribed if aspirin causes troublesome dyspepsia or
other side-effects
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88. Percutaneous coronary intervention
(PCI) is performed by passing a fine guidewire across a
coronary stenosis under radiographic control and using it to
position a balloon, which is then inflated to dilate the stenosis
(Ballon Angioplasty )
A coronary stent is a piece of coated metallic‘scaffolding’ that
can be deployed on a balloon and used to maximise and
maintain dilatation of a stenosed vessel
Mainly used in single- or two-vessel disease
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93. Acute complications:
Occlusion of the target vessel or a side branch by
thrombus
Coronary artery dissection
Long-term complications:
Re-stenosis - due to a combination of elastic
recoil and smooth muscle proliferation (neo-
intimal hyperplasia)
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94. Coronary Artery Bypass Grafting
Under cardiopulmonary bypass or ‘off-pump’ surgery
Internal mammary arteries, radial arteries or reversed
segments of the patient’s own saphenous vein used to
bypass coronary artery stenosis
INDICATED IN
Three-vessel disease
Two-vessel disease that includes the proximal LAD and
impaired global LV function
Diabetes mellitus
Left main coronary artery disease
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99. Prinzmetal / Variant Angina
• Younger and have fewer coronary risk factors
• Detection of transient ST-segment elevation with rest pain
• Coronary angiography demonstrates transient coronary
spasm ,most common in the right coronary artery
• Nitrates and calcium channel blockers are the main
agents used to treat acute episodes and to abolish recurrent
episodes of PVA
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102. Summary
A Aspirin and anti-anginals
B Beta-blockers and blood pressure
control
C Cholesterol and cigarettes
D Diet and diabetes
E Education and exercise
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