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CORONARY ARTERY DISEASE
Dr.S.Vinoth Kumar
Assistant Professor
Internal Medicine
IGMC&RI
CAD
Risk factors and Pathophysiology
Clinical spectrum
Clinical features
Investigations and treatment
Complications of MI
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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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PathoPhysiology
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IHD – Clinical Spectrum Acute
• Unstable Angina
• Acute Myocardial
Infarction (NSTEMI,
STEMI)
• Prinzmetal Angina
• Sudden Cardiac Death
Chronic
• Stable Angina
• Microvascular Angina
(Syndrome X)
• Silent Ischemia
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• 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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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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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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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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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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Differential Diagnosis
Acute Coronary Syndrome 5/24/2021
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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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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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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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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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V1
V2
V3
V4
V5
V6
I
II
III
aVR
aVL
aVF
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Localisation of Infarction
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AWMI
IWMI
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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
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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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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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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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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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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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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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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Statins
• Loading dose of Statin – Atorvastatin 80
mg/Rosuvastatin 20-40 mg
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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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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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• 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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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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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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Thrombolysis
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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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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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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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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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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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Antiplatelets
Fibrinolytic
Anticoagulants
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Unstable Angina/NSTEMI
Treatment
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Indications for PCI in NSTEMI
• Refractory angina
• Recurrent angina
• Clinical symptoms of heart failure or hemodynamic instability
• Life-threatening arrhythmias (ventricular fibrillation or
ventricular tachycardia)
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Complications of MI
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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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Cardiac Rupture:
- Occurs within 2 weeks
- After transmural MI
- Electromechanical dissociation and sudden
death
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Ventricular Aneurysm:
- Transmural anteroseptal infarct
- Persistent ST segment elevation > 6 weeks
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Cardiogenic Shock:
- Females,diabetics,AWMI,prior MI,old age
- Atleast 40% of Lt Ventricle should be
affected
Causes:
-Extensive LV infarction
-Extensive RV infarction
-VSD,Acute MR
-Cardiac tamponade with free wall rupture
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RV Failure:
- After IWMI
-Hypotension,JVD,absence of dyspnea
-Fluid administration
-Nitrates should be avoided
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Arrhythmias
Electrical instability Pump failure, excessive
sympathetic stimulation
Bradyarrhythmias and
conduction disturbances
Ventricular premature
beats
Sinus tachycardia Sinus bradycardia
Ventricular tachycardia
Atrial fibrillation and/or
atrial flutter
Junctional escape rhythm
Ventricular fibrillation
Paroxysmal
supraventricular
tachycardia
Atrioventricular block
and intraventricular
block
Accelerated
idioventricular rhythm
Nonparoxysmal
atrioventricular junctional
tachycardia
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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
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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Post-MI Medical Therapy
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Lifestyle modification
• Diet (weight control,lipid-lowering,‘Mediterranean
diet’)
• Cessation of smoking
• Regular exercise
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• 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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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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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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INVESTIGATIONS
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• Resting ECG
• Exercise ECG
• Stress Echocardiography
• Myocardial perfusion scanning
• CT Angiography
• Coronary arteriography
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Resting ECG 5/24/2021
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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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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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AT REST
AFTER EXERCISE
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Stress Echocardiography
• Uses transthoracic echocardiography
• Identify ischaemic segments of
myocardium and areas of infarction
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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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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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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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Left Coronary Artery
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Right Coronary Artery
Treatment of Stable Angina
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Anti-anginal
• Help to relieve or prevent the symptoms of angina
Nitrates
Β-blockers
Calcium antagonists
Potassium channel activators
If channel antagonist
Ranolazine
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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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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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-Bare metal stent
-Drug Eluting Stent
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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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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PCI AND CABG
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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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PRINZMETAL OR VARIANT
ANGINA
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Pathophysiology: Dynamic small vessel constriction (vasospasm)
(positive stress testing)
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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CAD-ACS

  • 1. CORONARY ARTERY DISEASE Dr.S.Vinoth Kumar Assistant Professor Internal Medicine IGMC&RI
  • 2. CAD Risk factors and Pathophysiology Clinical spectrum Clinical features Investigations and treatment Complications of MI 5/24/2021 2 MEU_IGMC&RI_ITP
  • 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 5/24/2021 3 MEU_IGMC&RI_ITP
  • 5. IHD – Clinical Spectrum Acute • Unstable Angina • Acute Myocardial Infarction (NSTEMI, STEMI) • Prinzmetal Angina • Sudden Cardiac Death Chronic • Stable Angina • Microvascular Angina (Syndrome X) • Silent Ischemia 5/24/2021 5 MEU_IGMC&RI_ITP
  • 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”) 5/24/2021 6 MEU_IGMC&RI_ITP
  • 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 5/24/2021 7 MEU_IGMC&RI_ITP
  • 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 5/24/2021 10 MEU_IGMC&RI_ITP
  • 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 5/24/2021 11 MEU_IGMC&RI_ITP
  • 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 5/24/2021 12 MEU_IGMC&RI_ITP
  • 14. Acute Coronary Syndrome 5/24/2021 14 MEU_IGMC&RI_ITP
  • 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 5/24/2021 15 MEU_IGMC&RI_ITP
  • 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 5/24/2021 16 MEU_IGMC&RI_ITP
  • 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 5/24/2021 17 MEU_IGMC&RI_ITP
  • 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 5/24/2021 18 MEU_IGMC&RI_ITP
  • 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 5/24/2021 24 MEU_IGMC&RI_ITP
  • 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 5/24/2021 26 MEU_IGMC&RI_ITP
  • 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 5/24/2021 28 MEU_IGMC&RI_ITP
  • 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 5/24/2021 29 MEU_IGMC&RI_ITP
  • 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 5/24/2021 30 MEU_IGMC&RI_ITP
  • 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 5/24/2021 31 MEU_IGMC&RI_ITP
  • 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 5/24/2021 32 MEU_IGMC&RI_ITP
  • 33. Statins • Loading dose of Statin – Atorvastatin 80 mg/Rosuvastatin 20-40 mg 5/24/2021 MEU_IGMC&RI_ITP 33
  • 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 5/24/2021 34 MEU_IGMC&RI_ITP
  • 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 5/24/2021 35 MEU_IGMC&RI_ITP
  • 36. • Door to needle time- 30 min (for patients receiving thrombolytic therapy) • Door to balloon time-90 min (for patients undergoing primary angioplasty) 5/24/2021 36 MEU_IGMC&RI_ITP
  • 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 5/24/2021 37 MEU_IGMC&RI_ITP
  • 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 5/24/2021 38 MEU_IGMC&RI_ITP
  • 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 5/24/2021 40 MEU_IGMC&RI_ITP
  • 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 5/24/2021 41 MEU_IGMC&RI_ITP
  • 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). 5/24/2021 42 MEU_IGMC&RI_ITP
  • 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 5/24/2021 44 MEU_IGMC&RI_ITP
  • 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. 5/24/2021 45 MEU_IGMC&RI_ITP
  • 49. Indications for PCI in NSTEMI • Refractory angina • Recurrent angina • Clinical symptoms of heart failure or hemodynamic instability • Life-threatening arrhythmias (ventricular fibrillation or ventricular tachycardia) 5/24/2021 49 MEU_IGMC&RI_ITP
  • 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 5/24/2021 52 MEU_IGMC&RI_ITP
  • 54. Cardiac Rupture: - Occurs within 2 weeks - After transmural MI - Electromechanical dissociation and sudden death 5/24/2021 54 MEU_IGMC&RI_ITP
  • 55. Ventricular Aneurysm: - Transmural anteroseptal infarct - Persistent ST segment elevation > 6 weeks 5/24/2021 55 MEU_IGMC&RI_ITP
  • 56. Cardiogenic Shock: - Females,diabetics,AWMI,prior MI,old age - Atleast 40% of Lt Ventricle should be affected Causes: -Extensive LV infarction -Extensive RV infarction -VSD,Acute MR -Cardiac tamponade with free wall rupture 5/24/2021 56 MEU_IGMC&RI_ITP
  • 57. RV Failure: - After IWMI -Hypotension,JVD,absence of dyspnea -Fluid administration -Nitrates should be avoided 5/24/2021 57 MEU_IGMC&RI_ITP
  • 58. Arrhythmias Electrical instability Pump failure, excessive sympathetic stimulation Bradyarrhythmias and conduction disturbances Ventricular premature beats Sinus tachycardia Sinus bradycardia Ventricular tachycardia Atrial fibrillation and/or atrial flutter Junctional escape rhythm Ventricular fibrillation Paroxysmal supraventricular tachycardia Atrioventricular block and intraventricular block Accelerated idioventricular rhythm Nonparoxysmal atrioventricular junctional tachycardia 5/24/2021 58 MEU_IGMC&RI_ITP
  • 59. 5/24/2021 MEU_IGMC&RI_ITP 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 5/24/2021 60 MEU_IGMC&RI_ITP
  • 63. Lifestyle modification • Diet (weight control,lipid-lowering,‘Mediterranean diet’) • Cessation of smoking • Regular exercise 5/24/2021 63 MEU_IGMC&RI_ITP
  • 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 5/24/2021 64 MEU_IGMC&RI_ITP
  • 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 5/24/2021 65 MEU_IGMC&RI_ITP
  • 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 5/24/2021 66 MEU_IGMC&RI_ITP
  • 68. • Resting ECG • Exercise ECG • Stress Echocardiography • Myocardial perfusion scanning • CT Angiography • Coronary arteriography 5/24/2021 MEU_IGMC&RI_ITP 68
  • 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 5/24/2021 71 MEU_IGMC&RI_ITP
  • 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 5/24/2021 72 MEU_IGMC&RI_ITP
  • 74. Stress Echocardiography • Uses transthoracic echocardiography • Identify ischaemic segments of myocardium and areas of infarction 5/24/2021 74 MEU_IGMC&RI_ITP
  • 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 5/24/2021 75 MEU_IGMC&RI_ITP
  • 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 5/24/2021 77 MEU_IGMC&RI_ITP
  • 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) 5/24/2021 79 MEU_IGMC&RI_ITP
  • 83. Treatment of Stable Angina 5/24/2021 83 MEU_IGMC&RI_ITP
  • 85. Anti-anginal • Help to relieve or prevent the symptoms of angina Nitrates Β-blockers Calcium antagonists Potassium channel activators If channel antagonist Ranolazine 5/24/2021 85 MEU_IGMC&RI_ITP
  • 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 5/24/2021 87 MEU_IGMC&RI_ITP
  • 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 5/24/2021 88 MEU_IGMC&RI_ITP
  • 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) 5/24/2021 93 MEU_IGMC&RI_ITP
  • 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 5/24/2021 94 MEU_IGMC&RI_ITP
  • 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 5/24/2021 99 MEU_IGMC&RI_ITP
  • 101. 101 Pathophysiology: Dynamic small vessel constriction (vasospasm) (positive stress testing)
  • 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 5/24/2021 102 MEU_IGMC&RI_ITP