definition of IHD - introduction - types Atherosclerosis definition and risky factors Angina diagnosis : types - investigation and management Acute coronary syndromes: types - investigation and management

1. ISCHEMIC
HEART DISEASES
Dr. Sameh Ahmad Muhamad abdelghany
Lecturer Of Clinical Pharmacology
Mansura Faculty of medicine

2. 2
Introduction
Asthersclerosis
Angina
Acute coronary
syndromes
Treatment
CONTENTS

3. INTRODUCTION

4. 4
Introduction
 Definiton:
 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
 Also known as Coronary Artery Disease (CAD)

5. 5
Introduction
 Caused mainly by Atherosclerosis of
Coronary Artery
 It includes
o Angina: Stable & Unstable
o Myocardial infarction

6. 6
Introduction
 In 2015 CAD affected 110 million people and resulted in 8.9
million deaths.
 It makes up 15.9% of all deaths making it the most common
cause of death globally.
 The risk of death from CAD for a given age has decreased
between 1980 and 2010, especially in developed countries.
 Rates are higher among men than women of a given age

7. ATHEROSCLEROSIS

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Atherosclerosis
 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

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Atherosclerosis
 Progressive inflammatory disorder of the arterial wall
characterized by focal lipid rich deposits of atheroma
 Remain clinically asymptomatic until
o large enough to impair tissue perfusion,
o Ulceration and disruption of the lesion result in
thrombotic occlusion
o Distal embolization of the vessel.
 Clinical manifestations depend upon the site of the
lesion and the vulnerability of the organ supplied

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Atherosclerosis

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Astherosclerosis
 Risk Factors:
 Absolute Risk
o Old age
o Male sex
o Positive family history

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Astherosclerosis
 Relative Risk
o Smoking
o Hypertension
o Diabetes mellitus
o Hypercholesterolaemia
o Hemostatic factors.
o Obesity
o Physical in-activity
o Alcohol

13. ANGINA

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Angina
 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

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Classical or Exertional
Angina Pectoris
 Characterized by
o constricting discomfort in the front of the chest,
arms,neck, jaw
o provoked by physical exertion, especially after meals and
in cold, windy weather or by anger or excitement
o relieved (usually within minutes) with rest or glyceryl
trinitrate. Occasionally, it disappears with continued
exertion (‘walking through the pain’).

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Classical or Exertional
Angina Pectoris
 Typical angina: all three features,
 Atypical angina: two out of the three,
 Non-anginal chest pain: one or less of these features

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Types of Angina
I. Stable Angina:
 episodic clinical syndrome where there is no change in
severity of attacks.
II. Unstable angina:
 Deterioration(24 hrs) in previous stable angina with
symptoms frequently occurring at rest, i.e. acute
coronary syndrome

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Types of Angina
III. Refractory angina:
 patients with severe coronary disease in whom
revascularization is not possible and angina is not
controlled by medical therapy.
IV. Variant (Prinzmetal’s) angina:
 occurs without provocation, usually at rest, as a result of
coronary artery spasm, more frequently in women

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Stable Angina
 Characterized by central chest pain, discomfort or
breathlessness that is precipitated by exertion or
other forms of stress and is promptly relieved by
rest

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Stable Angina

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Stable Angina
 Activities precipitating angina
 Common
o Physical exertion
o Cold exposure
o Heavy meals
o Intense emotion
 Uncommon
o Lying flat (decubitus angina)
o Vivid dreams (nocturnal angina)

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Clinical Features
 History is the most important factor in making the
diagnosis
 Physical examination is unremarkable
 Careful search for evidence of underlying
o valve disease - left ventricular dysfunction -
arterial disease
o unrelated conditions that may exacerbate angina
(anemia, thyrotoxicosis).
 Important assessment of risk factors

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Investigations
 Resting ECG
 often normal
 Reversible ST segment depression or
elevation, with or without T-wave
inversion, at the time the patient is
experiencing symptoms

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Investigations
 Exercise ECG
 Use standard treadmill or bicycle
while monitoring the patient’s
ECG, BP and general condition.
 Planar or down-sloping ST
segment depression of ≥ 1mm is
indicative of ischemia
 Up-sloping ST depression is less
specific and often occurs in
normal individuals

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Investigations
 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

26. TREATMENT

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Treatment
Management of angina pectoris involves:
 careful assessment of the extent and severity of arterial
disease
 identification and control of risk factors such as smoking,
hypertension and hyperlipidemia
 use of measures to control symptoms
 Identification of high-risk patients for treatment to improve
life expectancy.

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Medical Treatment
Antiplatelet therapy
 Low-dose (75 mg) aspirin
o reduces the risk of adverse events such as MI
o prescribed for all patients with CAD indefinitely
 Clopidogrel (75 mg daily)
o ALTERNATIVE if aspirin causes dyspepsia or other
side-effects

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Medical Treatment
Antianginal drugs
 Five groups of drug
o Nitrates
o β-blockers
o calcium antagonists
o potassium channel activators
o If channel antagonist

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Medical Treatment
1. 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
o avoided by a 6–8-hour nitrate-free period
o Nocturnal angina: long acting nitrates can be given at the end
of the day

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Medical Treatment
2. β-blockers
 lower myocardial oxygen demand by reducing heart rate, BP
and myocardial contractility
 May provoke bronchospasm in patients with asthma
3. 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

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Medical Treatment
4. Potassium channel activators
 arterial and venous dilating properties
 do not exhibit the tolerance seen with nitrates.
 E.g Nicorandil
5. If channel antagonist
 Ivabradine is the first of this class of drug
 Induces bradycardia by modulating ion channels in the sinus
node
 not have other cardiovascular effects
 Safe to use in patients with heart failure

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Medical Treatment
 It is conventional to start therapy with
o low-dose aspirin,
o a statin,
o sublingual GTN
o β-blocker,
 And then add a calcium channel antagonist or a
long-acting nitrate later if needed

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Medical Treatment
 goal is the control of angina with minimum side-
effects and the simplest possible drug regimen
 little evidence that prescribing multiple anti-
anginal drugs is of benefit
 Revascularisation : if an appropriate combination
of two or ore drugs fails to achieve an acceptable
symptomatic response

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Percutaneous Coronary
Intervention(PCI)
 Passing a fine guide-wire across a coronary stenosis
under radiographic control
 Balloon is placed and then inflated to dilate the stenosis
 Then a coronary stent is deployed on a balloon
 Mainly used in single or two-vessel disease

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Percutaneous Coronary
Intervention(PCI)

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Coronary artery bypass grafting
(CABG)
 Stenosed artery is by-passed with
o internal mammary arteries
o radial arteries
o reversed segments of the patient’s own saphenous vein
 Major surgery under cardiopulmonary bypass

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Coronary artery bypass grafting
(CABG)

39. ACUTE CORONARY
SYNDROMES

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ACUTE CORONARY SYNDROMES
 Myocardial Infarction: ST-elevation myocardial infarction
(STEMI) or Non-ST-elevation myocardial infarction
(NSTEMI)
o symptoms occur at rest
o evidence of myocardial necrosis - increased cardiac troponin or
Creatine kinase
 Unstable angina (UA).
o new-onset or rapidly worsening angina (crescendo angina)
o angina on minimal exertion
o or angina at rest in the absence of myocardial damage

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ACUTE CORONARY SYNDROMES
 Present as a new phenomenon or against a background
of chronic stable angina.
 Complex ulcerated or fissured atheromatous plaque
with adherent platelet rich thrombus and local coronary
artery spasm.
 Without treatment, the infarct-related artery remains
permanently occluded in 20–30% of patients

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Myocardial Infarction (MI)
 Evidence of myocardial necrosis in a clinical setting consistent
with myocardial ischemia, in which case any one of the
following meets the diagnosis for MI:
a) Detection of rise and/or fall of cardiac biomarkers (preferably
troponin)
b) ECG changes indicative of new ischemia (new ST-T changes
or new left bundle branch block)
c) Development of pathological Q waves
d) Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality

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Myocardial Infarction (MI)

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Clinical features
 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

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Investigations
 Confirmatory diagnosis
 difficult to interpret if there is bundle branch block
or previous MI.
 Repeated ECGs are important:
o initial ECG may be normal or non-diagnostic in
one-third of cases

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Investigations
 ECG
 Non-ST segment elevation ACS
 Partial occlusion of a major vessel or complete
occlusion of a minor vessel,
 unstable angina or partial thickness (subendocardial)
MI.
o ST-segment depression and T-wave changes.
 Presence of infarction: loss of R waves in the absence
of Q waves

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Investigations
ECG
 ST segment elevation ACS
 Myocardial infarction with presence of cardiac
biomarkers e.g creatine kinase (CK), a more sensitive
and cardiospecific isoform of this enzyme (CK-MB),
and the cardiospecific proteins, troponins T and I

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Investigations

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Investigations
 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 may be cardiomegaly due
to pre-existing myocardial damage

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Investigations
 Echocardiography
 assessing left and right ventricular function
 detecting important complications such as mural
thrombus, cardiac rupture.

51. TREATMENT

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Management
 Early Medical treatment
 Admitted urgently to hospital because of significant risk
of death or recurrent myocardial ischemia
 Reduce the incidence by at least 60%
 Oxygen : nasal cannula 2–4 L/min if hypoxia is present

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Management
 Early Medical treatment
 Brief history/risk factors and immediate
o Intravenous access + blood for markers
o 12-lead ECG
 Aim of early management
 Analgesia
 Antithrombotic therapy
 Anti-anginal therapy
 Reperfusion therapy

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Anti-anginal Therapy
 Sublingual glyceryl trinitrate :
o valuable first-aid measure
 IV nitrates (GTN or isosorbide dinitrate ):
o left ventricular failure and the relief of recurrent or
persistent ischemic pain

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Analgesia
 Essential to relieve distress and to lower adrenergic
drive
 IV opiates:
o initially morphine sulphate 5–10mg
 IV Antiemetics:
o initially metoclopramide 10mg

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Antithrombotic Therapy
 Antiplatelet therapy
 Aspirin: within the first 12 hour.
 Aspirin + clopidogrel : early (within 12 hours
 Ticagrelor: more effective than clopidogrel
 Antiplatelet treatment with i.v. glycoprotein IIb/IIIa
inhibitors :
o reduces the combined endpoint of death or MI and used
in context of PCI

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Antithrombotic Therapy
 Anticoagulants therapy
 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.
 Continued for 8 days or until discharge from hospital or
coronary revascularisation

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Reperfusion therapy
 Depending on type of MI, outcome of reperfusion therapy
varies
o NSTEMI: No demonstrable benefit
o STEMI: restores coronary artery patency and preserves left
ventricular function and improves survival
 Medium- to high-risk patients do benefit
 Primary percutaneous coronary intervention (PCI)

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Reperfusion therapy
 Thrombolysis
 reduce hospital mortality by 25–50%
 Alteplase (human tissue plasminogen activator)
o better survival rates than other thrombolytic agents, such as
streptokinase,
 Analogues of tPA (tenecteplase and reteplase):
o longer plasma half-life than alteplase and can be given as an
intravenous bolus

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Late Management of MI
 Risk stratification and further investigation lifestyle
modification
 Cessation of smoking
 Regular exercise
 Diet (weight control, lipid-lowering)

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Late Management of MI
 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 antagonist
 Rehabilitation devices:
 Implantable cardiac defibrillator (high-risk patients)

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Complications of Acute Coronary
Syndrome
 Arrhythmias
 Ischemia
 Acute circulatory failure
 Pericarditis
 Mechanical complications e.g rupture of the ventricle
 Embolism
 Impaired ventricular function, remodeling and ventricular
aneurysm

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thanksF o r W a t c h i n g