‫بسم الله الرحمن‬

‫الرحيم‬
Ischemic Heart disease
Definition
Clinical presentation
Etiology
Epidemiology
Diagnosis
Treatment
Prognosis
Definition
• myocardial ischemia caused by an
imbalance between myocardial blood
supply and oxygen demand
• usually caused by a critical coronary
artery narrowing
• CAD is the leading cause of death
worldwide.
• When ischemia is severe and
prolonged, it causes myocyte death
and results in loss of contractile
function and tissue infarction. In
cases of less severe ischemia, some
myocytes remain viable but have
depressed contractile function.
• Patients with ischemic heart IHD fall
into 2 groups
• 1)patients with chronic coronary artery
(CAD) who most commonly present
with stable angina and
• patients with Acute Coronary
Syndromes (ACSs)
• acute coronary syndromes (ACSs) is
composed of patients with
• acute myocardial infarction (MI) with
ST-segment elevation on their
presenting ECG(STEMI) and
• those with unstable angina and non-
ST-segment elevation MI
(UA/NSTEMI)
Angina pectoris
• is symptomatic reversible myocardial
ischaemia. Features:
• 1 Constricting/heavy discomfort to the
chest, jaw, neck, shoulders, or arms.
• 2 Symptoms brought on by exertion.
• 3 Symptoms relieved within 5min by
rest or GTN.
• All 3 features = typical angina;
• 2 features = atypical angina;
• 0–1 features = nonanginal chest
pain.
O/E
• For most patients with stable angina,
physical examination findings are
normal
• Pain produced by chest wall pressure is
usually of chest wall origin
• Signs of abnormal lipid metabolism or
of diffuse atherosclerosis may be
noted(xanthelasma, xanthoma)
O/E
Assess the vital signs, especially for
hypertension,
tachycardia,
bradycardia,
arrhythmia, and tachypnea
signs of anemia, thyroid disease,
hypercholesterolemia & atherosclerosis (carotid
bruit)
Sn PAD, CVS examinations,
Causes of angina pectoris
• Atheroma.
• Rarely: anaemia; coronary artery
spasm; AS; tachyarrhythmias;
• HCM;
• arteritis/small vessel disease
Types of angina
pectoris
• Stable angina
• Unstable angina
• Variant (Prinzmetal) angina
• Decubitus angina
• Stable angina: Induced by effort,
relieved by rest. Good prognosis.
• Unstable angina: (Crescendo angina.)
Angina of increasing frequency or
severity occurs on minimal exertion or
at rest; associated wit⬆️risk of MI.
• Decubitus angina:Precipitated by lying
flat
• Variant (Prinzmetal) anangina(Vasospastic
angina’)
• Caused by coronary artery spasm
• Risks : Smoking increases risk but
hypertension and hypercholesterolemia do
not. Probable triggers include cocaine,
amphetamine, marijuana, low magnesium,
and artery instrumentation (eg during
angiography
Prevalence
• Angina pectoris is more often the
presenting symptom of coronary artery
disease in women than in men, with a
female-to-male ratio of 1.7:1. It has an
estimated prevalence of 4.6 million in
women and 3.3 million in men.
• prevalence of angina pectoris increases
with age. Age is a strong independent risk
factor for mortality
Risk factor s
• Hypertension
• smoking,
• diabetes mellitus
• hypercholesterolemia
• Family history
• Obesity
• Insulin resistance
Risk factor s
• LV hypertrophy
• elevated serum levels of homocysteine,
lipoprotein (a)
• Oral contraceptive.
Diagnostic workup

• ECG
• Blood tests: FBC, U&E, TFTs, lipids,
HbA1c
• Consider echo
• chest X-ray.
• Further investigations are usually
necessary to confirm an IHD diagnosis.
Diagnostic workup

• Angiography—either using cardiac

CT with contrast, or transcatheter
angiography (more invasive but can
be combined with stenting,
Diagnostic workup

• Resting ECG taken when the patient is

not in pain may be normal 50% of
patient resting ECG.
• but may show ST depression; fl at or
inverted T waves; signs of past MI
• ST segment elevation associated with
pain which returns to normal as the
pain wanes suggest variant angina
Diagnostic workup

• Exercise Stress Testing

• Graded exercise stress testing is the most
widely used test for the evaluation of
patients presenting with chest pain. In
patients with established stable angina
pectoris, it also can provide prognostic
information about the extent of disease.
Diagnostic workup

• Absolute contraindications
include symptomatic cardiac
arrhythmias
• severe aortic stenosis
• acute MI within the previous 2days
• acute myocarditis, or pericarditis
• Active endocarditis
• Aortic dissection
• Uncontrolled heart failure
• Comorbidity : renal failure,
Thyrotoxicosis
Diagnostic workup

• Discontinue the exercise stress test in the

presence of chest pain
• a drop in systolic blood pressure of more
than 10 mm Hg
• severe shortness of breath
• fatigue, dizziness or near syncope
Diagnostic workup

• ST depression of more than 2 mm, ST

elevation of at least 1 mm without
diagnostic Q waves, or development
of ventricular tachyarrhythmia.
Differential Diagnosis

• Consider other cause of chest pain like

• Pleurisy
• Pneumonia
• Pericarditis
• Ischemia associated with AS or HCMP
• Aortic Dissection
• Biliary Colic
• Cholecystitis
• Panic disorder
• Pulmonary embolism
• Varicella zoster virus
Treatment
• Therapy for angina should be directed either
• reducing myocardial oxygen demand, or
• to compensate for impaired flow through
diseased coronary arteries or
• at increasing myocardial oxygen supply (i.e.
blood flow)
• General measures
• Lifestyle Measures
• Counsel patients about cessation of smoking
• Diet (‘healthy’ diet like low fat and low
caloric diet with increased habit of eating
fruits and vegetables)
• Regular exercise
• Weight reduction
Medical therapy
• a) Nitrates
• produce venodilation and to lesser extent
arteriolar dilation
• short-acting nitrates (e.g., 0.4 mg sublingual
nitroglycerin) for acute attacks
• Consider long-acting nitrates in patients who
have refractory chest pain despite maximal
tolerated beta-blocker therapy
• b) β-blockers:
• reduce heart rate and myocardial contractility.
• reduce cardiac oxygen demand.
• Propranolol: 20 -80 mg PO BID to QID
• Metoprolol: 25-200 mg Po BID
• Atenolol: 50 -150 mg PO daily
• Contraindicated in patients with asthma and
severe form of CHF
• C) Calcium channel blockers:
• decrease the tone of the smooth muscle of
coronary arteries.
• These drugs are especially effective in
preventing coronary spasm that cause variant
angina.
• Nifedipine XL: 30 mg PO O daily
• Verapamil: 180-240 mg daily
• Amlodipine: 5-10 mg daily
• Consider calcium channel blockers when
beta-blockers are contraindicated or are
not tolerated.
• Consider using combination therapy
cautiously (e.g., a beta-blocker and
calcium antagonist or nitrate) for patients
who fail to respond adequately to
monotherapy
• D) Anti-platelet agents :
• Aspirin: to prevent the occurrence of MI.
• Dose: 75 – 150 mg PO daily.
• E) Lipid lowering drugs :
• prescribe a lipid-lowering medication (statins) and a
low-fat, low-cholesterol diet for patients with CAD
and elevated LDL
• Goal= LDL level of < 100 mg/dl
• ACE inhibitor : may be beneficial in all
patients
• with significant CAD or
• in those with previous MI who also have
DM and/or LV systolic dysfunction
• Revascularization: Considered
when optimal medical therapy proves
inadequate.
• • Percutaneous coronary intervention
(PCI): a balloon is infl ated inside the
• stenosed vessel, opening the lumen. A
stent is usually inserted to reduce the
risk of re-stenosis.
• Dual antiplatelet therapy (DAPT; usually
aspirin and clopidogel) is
• recommended for at least 12 months
after stent insertion to reduce the risk of
in _stent thrombosis.
• CABG: compared to PCI, patients undergoing
CABG are less likely to need repeat
revascularization and those with multivessel
disease can expect better outcomes .
However, CABG is open heart surgery and so
recovery is slower and the
• patient is left with two large wounds (sternal
and vein harvesting).
Prognosis
• Important prognostic indicators in patients
with angina pectoris include LV function,
severity and location of atherosclerotic
lesions, and response of symptoms to medical
treatment.
• LV function is the strongest predictor of long-
term survival. Elevated LV end-diastolic
pressure and volume along with reduced LV
ejection fraction ( (< 40%) are poor prognostic
signs.
Prognosis
• Critical lesions of left main and
proximal left anterior descending
coronary arteries are associated with
a greater risk. Mortality rates are also
directly associated with the number
of epicardial arteries involved.
Prognosis
• Patients who continue to smoke after an
MI have a 22-47% increased risk of
reinfarction and death.
• These share a common underlying pathology
—plaque rupture, thrombosis, and infl
ammation . However, ACS may rarely be due
to emboli, coronary spasm, or vasculitis in
normal coronary arteries. Myocardial
infarction means there is myocardial cell
death, releasing troponin. Ischaemia means a
lack of blood supply, ±cell death. MIS have
troponin rises, unstable angina does not
Risk factors
• Non-modifi able: age, gender, family
history of IHD (MI in 1st-degree relative
<55yrs). Modifi able: smoking,
hypertension, DM, hyperlipid aemia,
obesity, sedentary lifestyle, cocaine use.
Controversial risk factors include: stress,
type Apersonality, LVH, ⬆️fibrinogen,
hyperinsulinaemia, ⬆️homocysteine levels,
• The severity and duration of the
imbalance between myocardial oxygen
supply and demand determine whether
the damage is reversible ( ≤20 min for
total occlusion in the absence of
collaterals) or whether it is permanent,
with subsequent myocardial necrosis (>20
min).
Clinical presentation
• Acute central chest pain, lasting >20min, often
associated with nausea, sweating , dyspnoea,
palpitations. ACS without chest pain is called
‘silent’; mostly seen in elderly and diabetic
patients. Silent MIs may present with:
syncope, pulmonary oedema, epigastric pain
and vomiting, post-operative hypotension
acute confusional state, stroke, and diabetic
hyperglycaemic states.
Sign s
• Distress, anxiety, pallor, sweatiness,
pulse⬆️or ⬇️, BP ⬆️or ⬇️, 4th heart
sound.
• There may be signs of heart failure
(⬆️JVP, 3rd heart sound, basal
crepitations) or a pansystolic murmur
(papillary muscle dysfunction/rupture,
VSD)
• ECG(ST- elevation or depression),Q-
wave T waves inversion
• CXR :Look for cardiomegaly, pulmonary
oedema, Don’t routinely delay treatment
whilst waiting for it.
• Cardiac enzymes:CK-MB, troponin
• Blood: FBC, U&E, glucose, lipids
• Echo
Treatment
• Emergency management :
• Management of patients should start before they
reach the hospital emergency room
• 1. General measures
• Reassure and make the patient comfortable
• Supply O2 by mask
• Secure IV line
• Give Aspirin 160-325 mg tablets –helps to
prevent further platelet aggregation
Treatment
• immediate referral to hospitals with
intensive care unit (ICU) facility is
mandatory
• Early(cotrol the pain,treat hypoxemia,
• Symptom control manage chest pain with
PRN GTN and opiates. If this proves insuffi
cient, consider a GTN infusion (monitor BP,
Manage symptomatic heart failure
Treatment
• Antiplatelets: aspirin (75mg OD) and a
second antiplatelet agent (eg clopidogrel)
• for at least 12 months to ⬇️vascular events
(eg MI, stroke). Consider adding a PPI (eg
lansoprazole) for gastric protection.
• • Anticoagulate, eg with heparin until
discharge
Treatment
• βblockade reduces myocardial oxygen
demand. Start low and increase slowly,
• monitoring pulse and BP. If
contraindicated, consider verapamil or
diltiazem.
• ACE-i in patients with LV dysfunction,
hypertension, or diabetes unless not
tolerated (consider ARB). Titrate up slowly,
monitoring renal function.
Treatment
• • High-dose statin, eg atorvastatin 80mg
Limitation of infarct
size
• through reperfusion or revascularization
• Thrombolysis/Fibrinolysis
• Direct percutanous transluminal
coronary angioplasty PCI
Complications of AMI

Malignant arrhythmias
conduction disturbances
Heart failure
Cardiogenic shock
Pericarditis
Mitral regurgitation& VSD
Dressler’s syndrome
Death
Left ventricular aneurysm
• Dressler’s syndrome ;Recurrent pericarditis,
pleural eff usions, fever, anaemia , and⬆️ESR
1–3wks post-MI.
• Treatment: consider NSAIDS; steroids if severe.
• Left ventricular aneurysm This occurs late (4–
6wks post-MI), and presents with LVF, angina,
recurrent VT, or systemic embolism. ECG:
persistent ST-segment elevation.
• Treatment: anticoagulate, consider excision.
General advice
• Driving: drivers with group 1 licences (car and
motorcycle) can resume driving 1wk after
successful angioplasty, or 4wk after ACS
without successful angioplasty, if their ejection
fraction is >40%
• . Group 2 licence holders must inform the
DVLA of their ACS and stop driving; depending
on the results of functional tests, they may be
able to restart after 6wk.
• Work: how soon a patient can return to work
will depend on their clinical progress and the
nature of their work. They should be
encouraged to discuss speed of return
• ± changes in duties (eg to lighter work if
manual labour) with their employer. Some
occupations cannot be restarted post-MI: eg
airline pilots & air traffi c controllers.
Thank you