• Also known as Coronary Artery Disease

(CAD)
• Ischemic heart disease (IHD) is a condition in
which there is an inadequate supply of blood
and oxygen to a portion of the myocardium
• Imbalance between myocardial oxygen supply
and demand.
• Caused mainly by Atherosclerosis of
Coronary Artery
• It includes
– Angina: Stable & Unstable
– Myocardial infarction
– Сhronic ischemic heart disease
• Can affect any artery
in the body
• Heart: angina, MI
and sudden
death;
• Brain: stroke and
transient
ischaemic attack;
• Limbs: claudication
and critical limb
ischaemia.
• Progressive inflammatory disorder of the
arterial wall characterised by focal lipid rich
deposits of atheroma
• Remain clinically assymptomatic until
– large enough to impair tissue perfusion,
– Ulceration and disruption of the lesion result in
thrombotic occlusion
– Distal embolisation of the vessel.
• Clinical manifestations depend upon the site of
the lesion and the vulnerability of the organ
supplied
• Second and third decades of life
• Tend to occur at sites of altered arterial shear stress such as
bifurcations
• Starts with any abnormal endothelial function
• Inflammatory cells, predominantly monocytes, bind to
receptors expressed by endothelial cells,
• Migrate into the intima
• Take up oxidised low-density lipoprotein (LDL) particles
• Become lipid-laden macrophages or foam cells.
• As Foam cells dies, it releases its lipid pool in intimal
space with
cytokines and growth factor
• In response, smooth muscle cells migrate from the media of the
arterial wall into the intima
• Lipid core will be covered by smooth muscle cells and matrix
• Forms stable atherosclerotic plaque that will remain
asymptomatic until it becomes large enough to obstruct
• In established atherosclerotic plaque, macrophages
mediate inflammation and smooth muscle cells
promote repair
• Cytokines released by macrophage starts degrading
smooth muscle layered over plaque
• Now lesion remains vulnerable to mechanical stress that
ultimately causes erosion, fissuring or rupture of the
plaque surface.
• Any breach in the integrity of the plaque will
expose its contents to blood
• Trigger platelet aggregation and thrombosis
• That extend into the atheromatous plaque and the
arterial lumen.
– cause partial or complete obstruction at the site of the
lesion
– distal embolisation resulting in infarction
– ischaemia of the affected organ
• Effect of risk factors is multiplicative rather
than
additive.
• It is important to distinguish between
relative risk and absolute risk.
• Absolute Risk
– Age
– Male sex
– Positive family history
• Relative Risk
– Smoking
– Hypertension
– Diabetes mellitus
– Haemostatic
factors.
– Physical
activity
– Obesity
– Alcohol
– Other dietary
factors
– Personality
• Age & Sex
– Premenopausal women have lower rates
of disease than men
– Although this sex difference disappears after the
menopause
• Positive family history
– Runs in families,
– Due to a combination of shared
genetic, environmental and
lifestyle factors.
• Smoking
– strong consistent
– Dose linked relationship between cigarette smoking and
IHD, especially in younger (< 70 years)
individuals
• Hypertension: directly proportional
• Hypercholesterolaemia: directly proportional to
serum cholesterol concentrations (LDL)
• Diabetes mellitus: potent risk factor for all
forms of atherosclerosis
– Men with type 2 diabetes: two- to four-
fold greater annual risk
of CAD,
– Women with type 2 diabetes: (3–5-fold)
risk
• Haemostatic factors
• Platelet activation and high levels of fibrinogen
• Antiphospholipid antibodies - recurrent arterial
thromboses
• Physical activity
• Physical inactivity roughly doubles the risk of coronary
heart
disease
• Regular exercise
– Increased serum HDL cholesterol concentrations,
– Lower BP,
– Collateral vessel development

• Obesity: often associated with HTN

and cardiovascular disease
• Alcohol: excess consumption
• Other dietary factors
• Diets deficient in fresh fruit, vegetables and
polyunsaturated fatty acids (PUFA)
• Personality: little or no evidence to support
the popular belief that stress is a major cause
of CAD
• Social deprivation
• Strategies taken before onset of disease in
high risk individual.
• Two complementary strategies
• Population strategies
– modify the risk factors of the whole population
– through diet and lifestyle advice
– For ex: Public restricting of smoking
• Targeted strategies
– identify and treat high risk individuals who
usually have a combination of risk
factors
– can be identified by using composite scoring
• Already have evidence of atheromatous
vascular disease are at high risk of
future cardiovascular events.
• Various secondary measures in this case
– energetic correction of modifiable risk factors,
• Smoking
• Hypertension
• Hypercholesterolaemia,
– Statin therapy irrespective of their serum
cholesterol concentration
– Target BPof ≤ 140/85 mmHg
– Aspirin and ACE inhibitors
– Beta-blockers: h/o MI or heart failure.
• A type of chest pain
• Not a disease, its a
symptom of an
underlying heart
problem specially IHD
• Described as ‘heavy’, ‘tight’ or
‘gripping’.
• Typically,
central/retrosternal
• Mild ache to most severe
that provokes sweating
and fear
• Associated breathlessness.
 CLASS Characteristic
Class I No angina with ordinary activity. Angina with
strenuous activity
Class II Angina during ordinary activity, e.g. walking up
hills, walking rapidly upstairs, with mild
limitation of activities
Class III Angina with low levels of activity, e.g. walking
50– 100 yards on the flat, walking up one flight
of stairs, with marked restriction of
activities
Class IV Angina at rest or with any level of exercise
• Characterized by
– constricting discomfort in the front of the chest,
arms, neck, jaw;
– provoked by physical exertion, especially after meals
and in cold, windy weather or by anger or excitement
and
– relieved (usually within minutes) with rest or
glyceryl trinitrate. Occasionally, it
disappears with continued exertion (‘walking
through the pain’).
• Typical angina: all three features,
• Atypical angina: two out of the three,
• Non-anginal chest pain: one or less of these
features
• Stable Angina: episodic clinical syndrome where
there is no change in severity of attacks.
• Unstable angina: Deterioration(24 hrs) in
previous stable angina with symptoms frequently
occurring at rest, i.e. acute coronary
syndrome
• Refractory angina: patients with severe coronary
disease in whom revascularization is not possible
and angina is not controlled by medical therapy.
• Variant (Prinzmetal’s) angina: occurs
without provocation, usually at rest, as a
result of coronary artery spasm, more
frequently in women
• Characterised by central chest pain, discomfort or
breathlessness that is precipitated by exertion or other
forms of stress and is promptly relieved by rest
• Activities precipitating angina
– Common
• Physical exertion
• Cold exposure
• Heavy meals
• Intense emotion
– Uncommon
• Lying flat (decubitus angina)
• Vivid dreams (nocturnal angina)
• History is by far the most important factor in
making the diagnosis
• Physical examination is frequently
unremarkable
• But careful search for evidence of
– valve disease (particularly aortic),
– left ventricular dysfunction (cardiomegaly, gallop
rhythm)
– arterial disease (carotid bruits, peripheral vascular
disease)
– unrelated conditions that may exacerbate angina
(anaemia, thyrotoxicosis).
• Important assessment of risk factors
e.g. hypertension, diabetes mellitus
• Resting ECG
– may show evidence of previous MI but is often normal, even in
patients with severe CAD.
– Occasionally, there is T-wave flattening or inversion in some leads,
providing non-specific evidence of myocardial ischaemia or
damage.
– The most convincing evidence of myocardial ischaemia - reversible ST
segment depression or elevation, with or without T-wave inversion, at
the time the patient is experiencing symptoms
• Exercise ECG
– Exercise tolerance test (ETT) - standard treadmill or bicycle while
monitoring the patient’s ECG,BPand general condition.
– Planar or down-sloping STsegment depression of ≥ 1mm is
indicative of ischaemia (A, B)
– Up-sloping ST depression is less specific and often occurs in
normal individuals (C)
• Other forms of stresstesting
– Myocardial perfusion scanning
– Stress echocardiography
• Coronary arteriography
– detailed anatomical information about the extent
and nature of coronary artery disease
– indicated when non-invasive tests have
failed to establish the cause of atypical
chest pain
– under local anaesthesia
– requires specialised radiological equipment,
cardiac monitoring and an experienced
operating team
• Management of angina
pectoris involves
– careful assessment of
the
likely extent and
severity of arterial disease
– identification and control of
risk
factors such as smoking,
hypertension and
hyperlipidaemia
– use of measures to
control symptoms
– Identification of high-risk
patients
• Antiplatelet therapy
– Low-dose (75 mg) aspirin
• reduces the risk of adverse events such as MI
• prescribed for all patients with CAD indefinitely
– Clopidogrel (75 mg daily)
• equally effective ALTERNATIVE
• if aspirin causes dyspepsia or other side-effects
• Anti-anginal drug treatment: Five groups
of drug
– Nitrates
– β-blockers
– calcium antagonists
– potassium channel activators
– If channel antagonist
• Nitrates
– act directly on vascular smooth muscle to produce
venous
and arteriolar dilatation
– reduction in myocardial oxygen demand
– Increase in myocardial oxygen supply
– prophylactically before taking exercise that is
liable to provoke symptoms.
– Continuous nitrate therapy can cause
pharmacological tolerance
• avoided by a 6–8-hour nitrate-free period
• Nocturnal angina: longacting nitrates can be given at the end of
the day
• β-blockers: lower myocardial
oxygen demand by reducing
heart rate, BP and
myocardial contractility
• provoke bronchospasm in
patients
with asthma.
• Calcium antagonists
• inhibit the slow inward
current
• caused by the entry of extracellular
calcium through the cell
membrane of excitable cells,
• particularly cardiac and
arteriolar smooth muscle
• lower myocardial oxygen demand
by
reducing BP and
myocardial contractility
• Potassium channel activators
– arterial and venous dilating properties
– but do not exhibit the tolerance seen with nitrates.
– Nicorandil (10–30mg 12-hourly orally) - only
drug in this class currently available for clinical
use
• If channel antagonist
– Ivabradine is the first of this class of drug
– Induces bradycardia by modulating ion channels in
the
sinus node
– Comparatively, does not have other
cardiovascular effects
– Safe to use in patients with heart
failure
• Passing a fine guide-wire across a coronary
stenosis under radiographic control
• Ballon is placed and then inflated to dilate the
stenosis
• Then a coronary stent is deployed on a balloon
– maximise and maintain dilatation of a stenosed
vessel
– reduces both acute complications and the
incidence of clinically important restenosis
• Mainly used in single or two-vessel
disease
*
• Stenosed artery is by-passed with
– internal mammary arteries
– radial arteries
– reversed segments of the patient’s own saphenous vein
• Major surgery under cardiopulmonary bypass,
• But in some cases, grafts can be applied to the beating
heart: ‘off-pump’ surgery
• Operative mortality is approximately 1.5% but risks are
higher
– elderly patients,
– with poor left ventricular function
– those with significant comorbidity, such as renal failure
• 90% of patients are free of angina 1 year after CABG surgery,
but fewer than 60% of patients are asymptomatic
after 5 or more years.
• Evidence of myocardial necrosis in a clinical
setting consistent with myocardial ischaemia,
in which case any one of the following meets
the diagnosis for MI:
– Detection of rise and/or fall of cardiac
biomarkers (preferably troponin),
– ECG changes indicative of new ischaemia (new
ST-T changes or new left bundle branch block)
– Development of pathological Q waves
– Imaging evidence of new loss of viable
myocardium or new regional wall
motion abnormality
• Pain is the cardinal symptom
• Prolonged cardiac pain: chest, throat,
arms, epigastrium or back
• Anxiety and fear of impending death
• Nausea and vomiting
• Breathlessness
• Collapse/syncope
• Sympathetic activation: pallor, sweating, tachycardia
• Vagal activation: vomiting, bradycardia
• Signs of impaired myocardial function
• Hypotension, oliguria, cold peripheries
• Narrow pulse pressure
• Raised JVP
• Third heart sound
• Quiet first heart sound
• Diffuse apical impulse
• Lung crepitations
• Tissue damage: fever
• Other complications: e.g. mitral regurgitation,
pericarditis
• There are three types of MIs:
• Type 1 – spontaneous MI with ischaemia due to a
primary coronary event, e.g. plaque
erosion/rupture, fissuring or dissection
• Type 2 – MI secondary to ischaemia due to
increased oxygen demand or decreased supply,
such as coronary spasm, coronary embolism, anaemia,
arrhythmias, hypertension, or hypotension
• Type 3,4,5 – diagnosis of MI in sudden cardiac death,
after percutaneous coronary intervention (PCI) and
after coronary artery bypass graft
(CABG),respectively.
• Confirmatory diagnosis
• But difficult to interpret if there is bundle branch
block or previous MI.
• Repeated ECGs are important: initial ECG may be
normal or non-diagnostic in one-third of cases
• ECGchanges are best seen in the leads that ‘face’
the ischaemic or infarcted area
• ST-segment deviation
– ST-segment elevation
– T wave inversion - change in ventricular
repolarisation
– persists after the ST segment has returned
to normal.
– reliable for the approximate age of the infarct to be
deduced.
a Normal ECG complex. B Acute
ST elevation (‘the current of
injury’). C Progressive loss of
the R wave, developing Q wave,
resolution of the
ST elevation and terminal T
wave inversion. d Deep Q wave
and T- wave
inversion. E Old or
established infarct pattern
• Non-ST segment elevationACS
– Partial occlusion of a major vessel
orcomplete occlusion of a minorvessel,
– unstable angina or partial
thickness (subendocardial) MI.
• ST-segment depression and T-wave
changes.
– Presence of infarction: loss of R waves
in the absence of Q waves
Recent anterior non-ST
elevation (subendocardial)
MI.
There is deep symmetrical T-wave
inversion together with a reduction in
the height of the R wave in leads V1,
V2, V3 and V
• Unstable Angina: no detectable rise in
cardiac markers or enzymes
• Myocardial Infarction: creatine kinase (CK),
a more sensitive and cardiospecific isoform of
this enzyme (CK-MB), and the cardiospecific
proteins, troponins Tand I
• Also present in skeletal muscle but not CK-
MB
– intramuscular injection,
– vigorous physical exercise
– particularly in older people,
– a fall
Creatine kinase (CK) and
troponin T (TnT) are the first to
rise, followed by aspartate
aminotransferase (AST) and then
lactate
(hydroxybutyrate)
dehydrogenase
(LDH)
• Other blood tests: erythrocyte sedimentation rate (ESR)
and C- reactive protein (CRP) are also elevated
• Chest X-ray
– pulmonary oedema that is not evident on clinical examination
– heart size is often normal
– But there may be cardiomegaly due to pre-existing myocardial
damage
• Echocardiography
– assessing left and right ventricular function
– detecting important complications such as
• mural thrombus,
• cardiac rupture,
• ventricular septal defect,
• mitral regurgitation and
• Pericardial effusion.
• Admitted urgently to hospital because of significant
risk of death or recurrent myocardial ischaemia
• Reduce the incidence by at least 60%
• Oxygen – nasal cannula 2–4 L/min if hypoxia is
present
• Brief history/risk factors and immediate
– Intravenous access + blood for markers
– 12-lead ECG
• Aim of early management
– Analgesia
– Antithrombotic therapy
– Anti-anginal therapy
– Reperfusion therapy
• Sublingual glyceryl trinitrate (300–500 μg): valuable first-
aid measure
• IV nitrates (GTN 0.6–1.2mg/hour or isosorbide dinitrate 1–
2mg/hour): left ventricular failure and the relief of recurrent or
persistent ischaemic pain
• IV β-blockers (Atenolol 5–10mg or Metoprolol 5–15 mg
given over 5mins) : relieve pain, reduce arrhythmias and improve
short- term mortality. Contraindicated in
– Heart failure (pulmonary oedema),
– Hypotension (systolic BP < 105mmHg)
– Bradycardia (heart rate < 65/min).
• Dihydropyridine calcium channel antagonist: nifedipine
or amlodipine can be added to the β-blocker if there is
persistent chest discomfort
– but may cause an unwanted tachycardia if used alone.
– Because of their rate-limiting action, verapamil and diltiazem are the
calcium channel antagonists of choice if a β-blocker is
contraindicated.
• Essential not only to relieve distress, but
also to lower adrenergic drive
• IV opiates: initially morphine sulphate
5– 10mg or diamorphine 2.5–5 mg)
• IV Antiemetics: initially metoclopramide
10mg
• Intramuscular injections should be
avoided
– Poor skeletal muscle perfusion
– Painful haematoma
• Antiplatelet therapy
– Aspirin: oral dose of 300mg first tablet within the
first 12 hour, followed by 75 mg.
– Aspirin + clopidogrel 600 mg: early
(within 12 hours), followed by 150 mg daily for 1
week and 75mg daily thereafter
– Ticagrelor (180 mg followed by 90 mg 12-hourly):
more effective than clopidogrel
– Antiplatelet treatment with i.v. glycoprotein IIb/IIIa
inhibitors reduces the combined endpoint of
death or MI and used in context of PCI
• Anticoagulants
– reduces the risk of thromboembolic complication
– prevents reinfarction in the absence of
reperfusion therapy or after successful
thrombolysis
– Unfractionated heparin, fractioned (low
molecular weight) heparin or a
pentasaccharide.
– Continued for 8 days or until discharge from
hospital or coronary revascularisation
• Depending on type of MI, outcome of
reperfusion therapy varies
– NSTEMI: No demonstrable benefit
– STEMI: restores coronary artery patency and
preserves left ventricular function and improves
survival
• Medium- to high-risk patients do benefit but
this does not need to take place in the first 12
hours.
• Primary percutaneous coronary
intervention (PCI)
• Thrombolysis
• reduce hospital mortality by 25–50%
• this survival advantage is maintained for at least 10
years
• Alteplase (human tissue plasminogen activator)
– over 90 minutes (bolus dose of 15 mg)
– Followed by 0.75 mg/kg body weight, but
not exceeding 50mg, over 30 mins
– then 0.5mg/kg body weight, but not exceeding
35mg, over 60mins
– better survival rates than other thrombolytic
agents, such as streptokinase,
• Analogues of tPA (tenecteplase and
reteplase):longer plasma half-life than alteplase and
can be given as an intravenous bolus
• Risk stratification and further investigation
lifestyle modification
– Cessation of smoking
– Regular exercise
– Diet (weight control, lipid-lowering)
• Secondary prevention drug therapy
– Antiplatelet therapy (aspirin and/or clopidogrel)
– β-blocker
– ACE inhibitor
– Statin
– Additional therapy for control of diabetes and
hypertension
– Aldosterone receptor antagonis
• Rehabilitation devices: Implantable
cardiac defibrillator (high-risk patients)