2. ➢Ischaemic heart disease (IHD) is defined as an
acute or chronic form of cardiac disability
arising from an imbalance between the
myocardial supply and demand for oxygenated
blood.
3. • Etiology
• IHD is invariably caused by disease affecting the coronary arteries, the
most prevalent being atherosclerosis accounting for more than 90% of
cases, while other causes are responsible for less than 10% of cases of
IHD. Therefore, it is convenient to consider the etiology of IHD under
three broad headings:
• i) coronary atherosclerosis;
• ii) superadded changes in coronary atherosclerosis; and
• iii) non-atherosclerotic causes.
4. ANGINA
• Angina is chest pain or discomfort you
feel when there is not enough blood
flow to your heart muscle.
• Angina pectoris is the result of
myocardial ischemia caused by an
imbalance between myocardial blood
supply and oxygen demand
5. Types:
There are three types of angina:
• Stable angina is the most common type.
• It happens when the heart is working harder than usual — for instance,
during exercise.
• Stable angina has a regular pattern. Rest or medicines relieve the symptoms.
• Unstable angina is the most dangerous.
• It does not follow a regular pattern and can happen without physical
exertion.
• It does not go away with rest or medicine alone.
• It mostly results from atherosclerosis, which involves a blockage preventing
blood from reaching the heart.
• Unstable angina can indicate the risk of a heart attack.
6. • Variant or Prinzmetal angina is rare.
• It can develop when the body is at rest, often around midnight or the
early morning.
• It happens when a spasm occurs in the coronary arteries. It is a chronic
condition, but medication can help manage it.
• Microvascular angina: Microvascular angina can occur with coronary
microvascular disease.
• This affects the smallest coronary arteries.
• Microvascular angina tends to be more persistent than stable angina.
• It often lasts longer than 10 minutes and sometimes longer than 30
minutes.
7. CLASS Characteristic
ClassI No angina with ordinary activity.Angina with
strenuousactivity
ClassII Angina during ordinary activity, e.g. walking up hills, walking rapidly
upstairs, with mild limitationof activities
ClassIII Angina with low levels of activity, e.g. walking 50– 100 yards on the
flat, walking up one flight of stairs, with markedrestrictionof activities
ClassIV Angina at restor with any level of exercise
Classification
8.
9. Causes
• Angina usually results from underlying coronary artery disease.
• The coronary arteries supply the heart with oxygen-rich blood. When
cholesterol collects on the wall of an artery and forms hard plaques,
this effectively narrows the arteries.
• Other factors, including damage to the arteries and smoking, increase
the risk of plaque buildup.
• When the arteries narrow, it becomes harder for oxygen-rich blood to
reach the heart. Also, plaques may break off and form clots that
block the arteries.
• If blood cannot carry oxygen to the heart, the heart muscle cannot work
properly. This causes angina.
10. Risk factors
Angina can develop as a result of:
• Stress
• An overuse of alcohol
• Smoking
• Exposure to particle pollution, for example, at work
• Low physical activity
• An unhealthful diet
• High cholesterol levels
• Overweight or obesity
• Genetic factors
• Conditions such as heart disease, diabetes, low blood pressure,
metabolic syndrome, and anaemia
• An age of over 45 for males, or 55 for females
11. Symptoms
• Chest pain is the primary symptom of angina. Angina-related chest pain
makes you feel tight and heavy in the chest. The pain is felt in the left
portion of the body from the back, neck, and jaw and extends up to
the left arm.
• Feeling of breathlessness
• Indigestion-like discomfort in the lower portion of the chest and belly
• Feeling of nausea
• Experiencing severe tiredness from time to time
12. Pathophysiology of angina
• Angina pectoris is the most common clinical manifestation of myocardial
ischemia.
• Myocardial ischemia is caused by chemical and mechanical stimulation
of sensory afferent nerve endings in the coronary vessels and
myocardium.
• Increases in the heart rate and myocardial contraction result in
increased myocardial oxygen demand.
• Myocardial ischemia can result from a reduction of coronary blood
flow, abnormal constriction of coronary microcirculation, or reduced
oxygen-carrying capacity of the blood.
13. • Increases in both afterload and preload increase myocardial wall
tension and, therefore, increase myocardial oxygen demand.
• Oxygen supply to any organ system is determined by blood flow. The
ability of the coronary arteries to increase blood flow in response
to increased cardiac metabolic demand is referred to as coronary
flow reserve (CFR).
• Fixed atherosclerotic lesions of at least 90% almost completely
abolish the flow reserve; patients with these lesions may experience
angina at rest or unstable angina.
14. • Patients with a fixed coronary atherosclerotic lesion of at least 50%
show myocardial ischemia during increased myocardial metabolic
demand, resulting in stable angina.
• These patients are not able to increase their coronary blood flow
during stress to match the increased myocardial demand, thus they
experience angina.
• Prinzmetal angina is defined as resting angina caused by coronary artery
spasm.
• Prinzmetal angina may be due to a deficiency of nitric oxide
production, hyperinsulinemia, low intracellular magnesium levels,
smoking cigarettes, and using cocaine.
16. Complications:
Complications of angina include:
• Arrhythmias (irregular heartbeats): Arrhythmias are caused by
an abnormality in the conduction of nerve signals (impulses)
within the heart muscle that affects the way the heart beats.
• Heart attack (myocardial infarction): A heart attack, or
myocardial infarction, happens when the heart tissue does not
receive enough oxygen.
• Heart damage
18. Nitrate
Ex. Glyceryl trinitrate, Isosorbide dinitrate
• Act directly on vascularsmooth muscleto produce venous and arteriolar
dilatation
• Reduction in myocardial oxygen demand
• Increase in myocardial oxygen supply
• Pprophylactically 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
• Nocturnalangina:Long-acting nitrates can be given at the end of the day
19. • β-blockers:
• lower myocardial oxygen demand by
reducing heart rate, BP and myocardial
contractility
• Calciumantagonists
• 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
20. Potassiumchannelactivators
• Nicorandil(10–30mg12-hourlyorally)- only drug in this class currently
available for clinical use
• If channel antagonist
• Ivabradineis the first of this class of drug
• Induces bradycardiaby modulating ion channels in the sinusnode
• Comparatively, does not have other cardiovascular effects
• Safe to use in patients with heart failure
21. • Passing a fine guidewire across a coronarystenosisunder radiographic
control
• Ballonis placed and then inflated to dilate the stenosis
• Then a coronarystentis 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
Percutaneous Coronary Intervention (PCI)
23. • Stenosed artery is by-passed with
– internal mammaryarteries
– radialarteries
– reversedsegmentsof the patient’s saphenousvein
• Major surgery under cardiopulmonarybypass,
• 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 comorbidities, 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.
Coronary artery bypass grafting
24.
25. MYOCARDIAL INFARCTION
• MI is defined as a diseased condition that is caused by reduced blood
flow in a coronary artery due to atherosclerosis & occlusion of an
artery by an embolus or thrombus.
• MI or heart attack is the irreversible damage of myocardial tissue
caused by prolonged ischemia and hypoxia.
26. • Etiology
• Tobacco, smoking
• Hypertension
• Drug abuse
• Obesity
• Stress
• Alcohol
• Age
• Gender
• Diabetes
• Hyperlipoproteinaemia
• Family history of Ischaemic
Heart Disease
• Hyperhomocysteinemia
• Chronic kidney disease
28. • Symptoms of MI include
• Chest pain, which travels from left arm to neck,
• Shortness of breath,
• Sweating,
• Nausea,
• Vomiting,
• Abnormal heart beating,
• Anxiety,
• Fatigue,
• Weakness,
• Stress, depression, and other factors.
30. Complications:
Complications of angina include:
• Arrhythmias (irregular heartbeats): Arrhythmias are caused by
an abnormality in the conduction of nerve signals (impulses)
within the heart muscle that affects the way the heart beats.
• Heart attack (myocardial infarction): A heart attack, or
myocardial infarction, happens when the heart tissue does not
receive enough oxygen.
• Heart damage
32. Nitrate
• Act directly on vascularsmooth muscleto 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
• Nocturnalangina:Long-acting nitrates can be given at the end of the day
33. • β-blockers:
• lower myocardial oxygen demand by
reducing heart rate, BP and myocardial
contractility
• Calciumantagonists
• 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
34. Potassiumchannelactivators
• Nicorandil(10–30mg12-hourlyorally)- only drug in this class currently
available for clinical use
• If channel antagonist
• Ivabradineis the first of this class of drug
• Induces bradycardiaby modulating ion channels in the sinusnode
• Comparatively, does not have other cardiovascular effects
• Safe to use in patients with heart failure
35. • Passing a fine guidewire across a coronarystenosisunder radiographic
control
• Ballonis placed and then inflated to dilate the stenosis
• Then a coronarystentis 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
Percutaneous Coronary Intervention (PCI)
37. • Stenosed artery is by-passed with
– internal mammaryarteries
– radialarteries
– reversedsegmentsof the patient’s saphenousvein
• Operative mortality is approximately 1.5% but risks are higher
– elderly patients,
– with poor left ventricular function
– those with significant comorbidities, 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.
Coronary artery bypass grafting
38.
39. • 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)
• IVAntiemetics:initially metoclopramide 10mg
• Intramuscular injections should be avoided
Analgesics
40. Antiplatelet therapy
• Aspirin: oral dose of 300mg first tablet within the first 12 hours, 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 (Tirofiban
and eptifibatide) reduce the combined endpoint of death or MI and are used
in the context of PCI
Antithrombotic Therapy
41. 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
revascularization
Antithrombotic Therapy
42. Reperfusion Therapy
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
