GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
INTRODUCTION
Ischaemic heart disease (IHD) is a condition in which the vascular supply to the heart is impeded by atheroma, thrombosis or
spasm of coronary arteries. This may impair the supply of oxygenated blood to cardiac tissue suficiently to cause myocardial
ischaemia which, if severe or prolonged, may cause the death of cardiac muscle cell. Ischaemia occurs when the oxygen
demand exceeds myocardial oxygen supply. The resultant ischaemic myocardium releases adenosine, the main mediator of
chest pain, by stimulating the A1 receptors located on the cardiac nerve endings. Ischaemic heart disease is also described as
Coronary artery disease or Coronary Heart Disease.
EPIDEMIOLOGY
The most up-to-date epidemiological data from the Global Burden of Disease (GBD) dataset were analyzed. GBD collates
data from a large number of sources, including research studies, hospital registries, and government reports. This dataset
includes annual figures from 1990 to 2017 for IHD in all countries and regions. We analyzed the incidence, prevalence, and
disability-adjusted life years (DALY) for IHD. Forecasting for the next two decades was conducted using the Statistical
Package for the Social Sciences (SPSS) Time Series Modeler (IBM Corp., Armonk, NY). Results Our study estimated that
globally, IHD affects around 126 million individuals (1,655 per 100,000), which is approximately 1.72% of the world’s
population. Nine million deaths were caused by IHD globally. Men were more commonly affected than women, and incidence
typically started in the fourth decade and increased with age. The global prevalence of IHD is rising. We estimated that the
current prevalence rate of 1,655 per 100,000 population is expected to exceed 1,845 by the year 2030. Eastern European
countries are sustaining the highest prevalence. Age-standardized rates, which remove the effect of population changes over
time, have decreased in many regions. Conclusions IHD is the number one cause of death, disability, and human suffering
globally. Age-adjusted rates show a promising decrease. However, health systems have to manage an increasing number of
cases due to population aging.
RISK FACTORS
Modifiable
-Increased personal stress
-Cigarette smoking
Non-Modifiable
-Raised serum cholesterol
-Age
-Hypertension
-Sex
-Diabetes
-Family history
-Abdominal obesity
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
1
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
CLINICAL PRESENTATION
Some people who have myocardial ischemia don't have any signs or symptoms (silent ischemia). When they do occur, the
most common is chest pressure or pain, typically on the left side of the body (angina pectoris). -Other signs and symptoms —
which might be experienced more commonly by women, older people and people with diabetes — include:
-Neck or jaw pain
-Shoulder or arm pain
-A fast heartbeat
-Shortness of breath when you are physically active
-Nausea and vomiting
-Sweating
-Fatigue
COMPLICATIONS
Myocardial ischemia can lead to serious complications, including: Heart attack; If a coronary artery becomes completely
blocked, the lack of blood and oxygen can lead to a heart attack that destroys part of the heart muscle. The damage can be
serious and sometimes fatal. Irregular heart rhythm (arrhythmia); An abnormal heart rhythm can weaken your heart and
may be life-threatening. Heart failure; Over time, repeated episodes of ischemia may lead to heart failure.
BRIEF DESCRIPTION OF CORONARY ARTERY

The heart is supplied by 2 coronary arteries

Right coronary artery arising from anterior aortic sinus

Right coronary artery supplies mainly the right atrium and ventricle

Left coronary artery arising from posterior aortic sinus

Left coronary artery supplies mainly the left atrium and ventricle

Anastomosis between the termination of right and left coronary arteries occurs at arteriolar level in the atrioventricular
groove and also between their interventricular and conus branch.
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
2
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
AETIOPATHOGENESIS
The dominant cause of ischemic heart disease syndromes is insufficient coronary perfusion relative to myocardial demand, in
majority of cases this is due to:

Chronic progressive atherosclerotic narrowing of the epicardial coronary arteries

Variable degrees of superimposed acute plaque change

Thrombosis

Vasospasm

Myocardial vessel inflammation

Coronary emboli
PREVENTION OF ISCHAEMIC HEART DISEASE
Ischemic heart disease has a multifactorial aetiology and can be prevented from developing in populations primordially, and
in individuals at high risk by primary prevention.
THE FOUR PRINCIPLES OF PREVENTION

Primordial prevention

Primary prevention

Secondary prevention

Tertiary prevention
Primordial prevention of ischemic heart disease
The primordial prevention involved the prevention of the initiation of risk factors, life styles and other socioeconomics factors
that may increase the risk of developing ischemic heart disease. Primordial level of prevention aim is to avoid the emergence
and establishment of social, economic and cultural pattern of living that are known to contribute to the risk of ischemic heart
disease. Note: at this level the risk factors have not exist. The following are some of the measures taken in primordial
prevention:

program to encourage peoples on regular daily physical exercise

Educating peoples about the disease

Educating people not to take diet high in cholesterol, sodium

Avoid smoking

Program on the prevention of hypertension.
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
3
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
Primary prevention of ischemic heart disease
At this level the aim is to stop the risk factors that has already existed in order to avoid development of the diseases such as
smorking, Obesity, and others. This will involve the following measures:

General health promotion

Specific protection

Chemoprophylaxis
GENERAL HEALTH PROMOTION

Dietary modification to reduce overweight and reduction of salt intake for older peoples

Banning of smoking at public places and avoidance of smoking and warning about the danger of smoking

Encouraging overweight people on daily physical exercises for at least 30minuts per day health education
SPECIFIC PROTECTION

Early diagnosis and treatment of medical condition that may contribute to development of the diseases e.g
hypertension, diabetes mellitus

Program on the prevention of hypertension and diabetes mellitus

Regular Early screening of peoples at higher risk
CHEMOPROPHYLAXIS
This involve the use of certain medications to treat disease conditions that could lead to ischemic heart disease.
SECONDARY PREVENTION OF ISCHEMIC HEART DISEASE

Medical therapy and

Surgical procedure to treat the condition in order to manage the patient and to avoid complications
MEDICAL THERAPY

Treatment of patient with hypertension and dyslipidemia.

Treatment of patient atherosclerosis

Treatment/management of myocardial infarction etc.
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
4
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
SURGICAL PROCEDURE
Surgical revascularization by coronary artery bypass grafting is recommended for those with significant left main coronary
artery stenosis, significant stenosis of the proximal left anterior descending artery, multivessel coronary disease, or disabling
angina. Surgical revascularization helps to improve blood supply to affected area on heart.
TERTIARY PREVENTION OF ISCHEMIC HEART DISEASE
This involved rehabilitation for patient who developed complications from the condition, complications may arise from
ischemic heart disease, such as arrhythmias, stroke, and others, in such a case medical rehabilitate is required to the patient.
Examples putting cardiac face marker for patient with arrhythmia.
DIAGNOSIS
The diagnosis of ischemic heart disease is made from the patient clinical history, sign and symptoms, laboratory and
electrocardiographic changes.
BIOMARKERS OF ISCHAEMIC HEART DISEASES.

Cardiospecific troponins

Myoglobin

Cardiac myosin light chain
MARKERS OF INFLAMMATION AND COAGULATION DISORDERS
Although the measurement of total CK is not recommended because of the large skeletal muscle distribution and the lack of
specificity of the enzyme. CK is a cytosolic enzyme involved the transfer of energy in muscle metabolism.
MYOGLOBIN
Myoglobin is an oxygen-binding heme protein that is present in both cardiac and skeletal muscle. Although it lacks specificity.
Its clinical usefulness is in its early release from damaged cardiac or skeletal muscle. Myoglobin rises as early as 1–4 hours
after the onset of symptoms. Myoglobin is not cardiac specific, so care must be taken in its interpretation in patients with renal
failure, trauma, or diseases involving skeletal muscle.
TROPONIN.
The preferred biomarkers for assessment of myocardial necrosis are the cardiac troponins. The troponins have been shown
to have high sensitivity and specificity for myocardial damage. Data indicate that troponins rise 4–10 hours after the onset
of symptoms, peak at 12–48 hours, and remain elevated for 4–10 days. Troponins are not found in the serum of healthy
individuals.
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
5
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
MEASUREMENT OF BIOMARKERS
The European Society of Cardiology and the ACC (ESC/ACC) consensus report recommended samples be collected at
presentation, at 6–9 hours, and again at 12–14 hours if the earlier samples were negative. There has been significant progress
made with regard to the identification and measurement of biomarkers released into circulation from damaged myocytes.
SERUM
Glutamine-oxaloacetic transaminase (SGOT) was replaced by lactate dehydrogenase (LDH) and its isoenzymes and the
classic diagnostic LDH flipped ratio, which was replaced by creatine kinase (CK) and the MB fraction of CK (CK-MB).
Currently, the preferred biomarkers for the detection of myocardial necrosis are cardiac troponins I and T, which are more
specific and sensitive for myocardial necrosis.
LABORATORY TEST PROCEDURE
TROPONIN

Immunoenzymometric assay

No cross reactivity with skeletal muscle troponin

Reference interval

Cardiac troponin T greater than 0.1ng/ml.

Cardiac troponin I, 0.1-3.1ng/mL

Creatine kinase, Colorimetric assay, Serum, Plasma etc.
PRINCIPLE
In the creatine kinase assay protocol, creatine kinase (CK) converts creatine into phosphocreatine and ADP. The
phosphocreatine and ADP then react with the CK enzyme mix to form an intermediate, which reduces a colorless probe to a
colored product with strong absorbance at λ= 450 nm. Range 2nmol/well - 10nmol/well
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
6
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
RECOMMENDED RADIOGRAPHIC IMAGING USED IN ASSESSMENT OF ISCHAEMIC HEART DISEASE (IHD)
Ischemic heart disease is a leading cause of death worldwide. Management of IHD is now best guided by the physiologic
significance of coronary artery stenosis. Multiple noninvasive cardiac imaging modalities can also anatomically delineate or
functionally assess for significant coronary artery stenosis, as well as to detect the presence of myocardial infarction (MI).
Coronary CT angiography can be used to assess the degree of anatomic stenosis, its inability to assess the physiologic
significance of lesions limits its specificity. Radiographic Imaging procedures used in assessment of patients with IHD are: 
Cardiac Ultrasound

Cardiac Computed tomography CT

Conventional Coronary Angiogrpahy (CCA).

Computed Tomography Angiography (CTA)

Magnetic Resonance Angiography (MRA)

Cardiac ultrsound/Echocardiography
Cardiac ultrasound/ Echocardiography: is the most cost-efficient technique, natural competitor and even highly
sophisticated procedure because of its high clinical yield, the ability to assess anatomy, function, contractility, coronary flow
reserve, and heart valve status, all in the same sitting. It uses sound waves to produce images of the heart. This common test
allows to the heart beating and pumping of blood which can be used to identify heart disease. Role of Cardiac
ultrasound/echocardiography in diagnosis of patient with IHD. It provides valuable information regarding cardiac structure
and functions. It allows the visualization of complications such as aneurysm or thrombus formation post-infarction.
Cardiac Computed Tomography: is routinely performed to visualize about the cardiac or coronary anatomy, to detect or
diagnose coronary artery disease (CAD), to evaluate patency of coronary artery bypass grafts or implanted coronary stents or
to evaluate volumetry and cardiac function (including ejection fraction). Role of Cardiac Computed Tomography in diagnosis
of patient with IHD. Cardiac CT is an interesting alternative to Coronary Magnetic Resonance (CMR) for left and right
ventricle assessment in patients unable to undergo a CMR study. The administration of contrast agent should be adapted to
obtain enhancement of the right ventricular cavity if the patient is having an acute myocardial infarction (heart attack).
Screening of asymptomatic patients with low-to-intermediate risk of CAD. Evaluation of coronary artery stents <3 mm.
Contraindication: if the patient is having an acute myocardial infarction (heart attack).
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
7
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
Conventional Cardiac angiography: relies on images produced by X-rays in a two-dimensional plane. Images are taken in
multiple frames for a given time period with a contrast agent flowing to allow visual differentiation from the surrounding
anatomy. The diagnosis of Coronary Artery Disease CAD is made on conventional coronary angiography by impingement
and narrowing of the coronary artery. Significant CAD is considered in the presence of a diameter stenosis of ≥ 70% in a
major vessel or ≥ 50% in the left main vessel. CCA provides valuable information regarding the severity and length of stenosis,
CA occlusions, number of vessels affected, stenosis configuration (smooth, ulcerated), and presence of thrombus, collateral
vessels, CA anatomy and anatomic variants. CCA showing coronary artery stenosis.
Coronary Computed tomography angiography: CT angiography is a type of medical test that combines a CT scan with an
injection of a contrast medium to produce images of blood vessels and tissues in a part of the body. The contrast medium is
injected through an intravenous (IV) line started in the arm or hand. CTA is non-invasive coronary angiography has become
a reality and these techniques are used in daily clinical care in assessment of CAD. A typical clinical examination consists of
an unenhanced CCT for detection and quantification of coronary calcium. A contrast-enhanced CCT for coronary artery
imaging, detection of coronary artery plaques and, to some extent, characterization of the non-calcified plaques. Contrastenhanced CCT is performed following intravenous injection of contrast agent. CTA imaging showing coronary artery
calcifications. Visualization of calcified non-stenotic plaques by CCTA.
Coronary Magnetic resonance angiography (MRA): MRA uses a powerful magnetic field, radio frequency waves and a
computer to evaluate blood vessels and help to identify abnormalities. An MRA exam may or may not use contrast material.
If needed, an injection of a gadolinium-based contrast material may be used. MR angiography (MRA) has been suggested as
a noninvasive method to detect CAD. MRA involves no ionizing radiation, and the lumen of the artery is well depicted on
MRA images, even in the presence of heavy calcification. MRA has a sensitivity and specificity of 93% and 42%, respectively,
for the detection of coronary disease.
PHARMACOLOGICAL TREATMENT

Treatment during acute phase

Long term treatment
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
8
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
NON-PHARMACOLOGICAL TREATMENT

Invasive interventions

PTCA: balloon angioplasty, stent replacement.

CABG - coronary artery bypass grafting.

EECP - enhanced external counter pulsation

Lifestyle modifications

Weight management

Smoking cessation

Increased, controlled physical activity (exercise training)
CLASSES OF DRUGS USED IN THE TREATMENT OF ISCHAEMIC HEART DISEASE

Thrombolytic agents: Streptokinase, Anistreplase

Antiplatelets: Aspirin, Clopidogrel

Anticoagulant: Heparin, Warfarin, Agatroban

Beta Blockers: Atenolol, Metoprolol etc

Vasodilators
 Calcium channel blocker e.g Amlodipine
 Angiotensin converting enzymes inhibitors e.g Lisinopril, Ramipril etc
 Nitrates: Nitroglycerine

Others
 Statins
 Analgesics
 Oxygen
 Antiarrhythmic Drugs
Thrombolytic drugs: cause lysis of formed clots in both arteries and veins and reestablish tissue perfusion. First Generation:
Streptokinase (Streptase, Kabikinase), Urokinase (Abbokinase). Second Generation: Anistreplase (Eminase),Anistreplase
(Eminase),Reteplase (Retavase). General mechanism of action: Break up the thrombus or clot and restore the patency of the
coronary artery, thereby limiting the infarct size and irreversible damage to the myocardium. General pharmacokinetics:
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
9
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
They are given intravenously. Streptokinase has two half-lives.The faster one (11 to13 minutes) is due to drug distribution
and inhibition by circulating antibodies, and the slower one (23 to 29 minutes) is due to loss of enzyme activity. The plasma
half-life of urokinase is approximately 10 to 20 minutes. Alteplase is rapidly cleared from the blood (half-life is 5 to 10
minutes). Anistreplase It has a long catalytic half-life (90 minutes).
ANTIPLATELETS AND ANTICOAGULANTS
Antiplatelets: Drugs that inhibit platelet function are administered for the relatively specific prophylaxis of arterial thrombosis
and for the prophylaxis and therapeutic management of myocardial infarction and stroke. e.g Aspirin and Clopidogrel.
Anticoagulants: Anticoagulant drugs inhibit the development and enlargement of clots by actions on the coagulation phase.
They do not lyse clots or affect the fibrinolytic pathways.e.g Heparin (LMWH & Unfractionated Heparin), Warfarin,
Agatroban.
Antiplatelets mechanism of action: Aspirin inhibits platelet aggregation and prolongs bleeding time.It acetylates and
irreversibly inhibits cyclooxygenase (primarilycyclooxygenase-1)both in platelets, preventing the formation of TxA2, and in
endothelial cells, inhibiting the synthesis of PGI2. Clopidogrel is structurally related drugs that irreversibly inhibit platelet
activation by blocking specific purinergic receptors for Adenine 5 Diphosphate (ADP) on the platelet membrane. This action
inhibits ADP-induced expression of platelet membrane GPIIb/IIIa and fibrinogen binding to activated platelets.
Pharmacokinetics: They are well absorbed orally. They are highly metabolised by the liver and excreted by the kidney. They
highly bound to plasma protein.
Anticoagulants MOA: Heparin binds to antithrombin III and induces a conformational changes that accelerates the interaction
of antithrombin III with the coagulation factors. Heparin also catalyzes the inhibition of thrombin by heparin cofactor II, a
circulating inhibitor. Other Anticoagulants e.g warfarin. They are vitamin K antagonists. Vitamin K is required to catalyze
the conversion of the precursors of vitamin K–dependent clotting factors II,VII, IX, and X. Pharmacokinetics: HEPARIN is
given IV, SC and orally. Heparin’s action is terminated by uptake and metabolism by the reticuloendothelial system and liver
and by renal excretion of the unchanged drug and its depolymerized and desulfated metabolite. Heparin is not bound to plasma
proteins or secreted into breast milk, and it does not cross the placenta. WARFARIN is bound extensively (95%) to plasma
proteins. It does not cross BBB but crosses the placenta to cause teratogenic toxicity. It metabolised by the hepatic enzyme
P450. Hepatic disease may potentiate anticoagulant response.
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
10
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
BETA-BLOCKERS

Non-selective: Propranolol, nadolol, timolol, pindolol, labetolol

Cardioselective: Metoprolol, atenolol, esmolol, betaxolol.

Mixed (ß and α) adrenergic receptor blockers: Labetolol and carvedilol.
Mechanism of action: They bind to beta-1 receptors of the heart causing decrease in cardiac contractility and decrease in
oxygen demand. Pharmacokinetics: Atenolol is given orally. About 50% of a dose is absorbed after oral doses. Peak plasma
concentrations are reached in 2 to 4 hours. The plasma half-life is about 6 to 7 hours. Atenolol undergoes little or no hepatic
metabolism and is excreted mainly in the urine. Metoprolol is readily and completely absorbed from the gastrointestinal tract
but is subject to considerable first-pass metabolism, with a bioavailability of about 50%. Peak plasma concentrations vary
widely and occur about 1.5 to 2 hours after a single oral dose. It is extensively metabolized in the liver, mainly by the
cytochrome P450 isoenzyme CYP2D6. The half-life is about up to 7 hours. The metabolites are excreted in the urine together
with only small amounts of unchanged metoprolol.
VASODILATORS

ACEIs

Nitrates

CCBs
General MOA: Reduce oxygen demand and myocardial wall stress by reducing afterload and/or preload and can halt the
remodeling process. Some vasodilators (nitrates & CCBs) may increase the blood supply to the myocardium by enhancing
coronary vasodilatation. ACEIs; Captopril, lisinopril, enalapril, ramipril and fosinopril. Nitrates; Nitroglycerine, isosorbide
dinitrate, isosorbide mononitrate. They decrease venous return to the heart and therefore decrease the work load on the heart.
They promotes coronary vasodilatation even in the presence of atherosclerosis.
Pharmacokinetics: They given SL, IV, topical and as transdermal patch. Duration of action depends on the route of
administration. SL - 10-30min. Translingual spray - 10-30min. IV - 3-5min. Topical ointment - 4-8hr. Transdermal patch - 48hr. Nifedipine: 45-56% bioavailable; metabolized - intestine/liver, highly plasma bound (≈ 90%). Amlodipine (Norvasc):
Peak plasma level, 6-9 hours; half-life, 30-50 hours. Nimodipine (Nimotop): Peak plasma level, less than 1 hour; half-life, 12 hours.
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
11
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
OTHERS

STATINS: Artovastatin and Simvastatin.

ANALGESICS: Ibuprofen, Acetamenophen, Diclofenac.

ANTIARRYTHMIC DRUGS: Lidocaine, Procainamide, Amiodarone, Ibutilide.
THE RATIONALE OR PRINCIPLES OF USING THE ABOVE MENTIONED DRUGS IN THE MANAGEMENT
OF ISCHEMIC HEART DISEASE
In general, the management of IHD using chemotherapy can in grouped as follows:

Pre-Hospital management

Hospital management upon admission and

Long term management
PRE-HOSPITAL MANAGEMENT
This involved the use of medications and other supportive measure to arrest the onset of infarct attack. Drugs used for such
regards include:
Aspirin 300-600mg PO
Morphine 2.5mg when necessary
Streptokinase 1.5million unit by intravenous injection
RATIONALE
Aspirin: Aspirin was believe to inhibit the prostaglandins formation as well as thromboxane. Thereby relieving pain as well
as increasing blood flood by inhibiting the formation of thrombus. The higher the dose of Aspirin, the high the onset of
therapeutic effect, that is why it was recommended 300-600mg for ischemic heart disease
Morphine: Morphine can be prescribed based on the severity of the chest pain, as described by individual patient. A dose of
2.5mg is initiated and later titrated depending on patient's need, due to its potential addiction.
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
12
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
Streptokinase: Streptokinase 1.5million unit IV over 30-60minutes reduces the mortality due to ischemic heart disease by
25%, when used for 2days, will reduces mortality by 50% after 5-7days, reduction in mortality rate is 80-95%.
Tissue Plasminogen activator: This is administer due to adverse effect of streptokinase. Reduction in mortality rate is 95%
at a dose of 15mg bolus followed by 0.75mg/kg over 30minutes without exceeding 50mg and maintenance dose of 0.6mg/kg
HOSPITAL MANAGEMENT
Upon hospital admission, beta-blockers and ACE inhibitors are added. They are added to reduce the incidence of arrythmia,
infarct size, and mortality.
RATIONALE
Atenolol: Atenolol and Timolol 5mg over 5minutes by IV route is given to avoid crashing of BP which can lead to
hypotension.
ACE inhibitors: Captopril 6.5mg or equivalent can be administer if there is other compelling indication such as pregnancy.
LONG TERM MANAGEMENT
Beta blockers: Oral Atenolol or Timolol 50mg is given for long term management of IHD
Others: ACE inhibitors, IV. Nitroglycerin 5microgram per minute, low dose Aspirin, and statins are given, follow by regular
and controlled exercise.
POSSIBLE DRUGS ADVERSE EFFECTS OF BETA BLOCKERS
Beta-Blockers: Beta-blockers are relatively effective, safe, and affordable. As a result, they’re often the first line of treatment
in heart conditions. However, the most common side effects of beta-blockers are: Fatigue and dizziness, Poor circulation,
Gastrointestinal symptoms, Sexual dysfunction, Weight gain, Difficulty breathing, Hyperglycemia, Depression, insomnia,
and nightmares. NOTE: The above side effects differ from patient to patient and also from drug to drug.
POSSIBLE MANAGEMENT/PREVENTIVE MEASURES OF BETA BLOKERS ADVERSE EFFECTS
Take Beta-Blockers with food to help relieve stomach symptoms. Patients are advised to inform their doctors or pharmacists of drugs
they have been taking to avoid drug interactions especially medications that lower blood pressure. Patients are also advised to inform
their doctors or pharmacists of their underlying medical conditions especially lung diseases, diabetes, hypotension, bradycardia, metabolic
acidosis, serious blood circulation conditions, and other heart diseases. Patients should seek medical attention when they experience any
of the side effects. It’s dangerous to stop taking beta-blockers suddenly, even if patients are experiencing side effects. The body gets used
to the heart’s slower speed when one takes Beta-Blockers. When withdrawn suddenly, there's a risk of a serious heart problem, such as
a heart attack. The dose needs to be tapered slowly before switching the patient to another drug.
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
13
GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
ADVERSE EFFECTS OF CALCIUM CHANNEL BLOCKERS (CCBs)
Though differs from patient to patient, side effects of CCBs include: Dizziness, Headache, Constipation, Heartburn, Nausea,
Askin rash or flushing, which is redness of the face, Swelling in the lower extremities, Fatigue. Certain CCBs can also lower
blood glucose levels in some people.
POSSIBLE MANAGEMENT/PREVENTIVE MEASURES CCBs ADVERSE EFFECTS
Patients should seek immediate medical attention if they experience any side effects. Dose of the drug may be adjusted or the
drug may be switched to another if the side effects don’t go away, are uncomfortable, or pose a threat to the patient's health.
Age of the patient should be considered before prescribing CCBs.
SIDE EFFECTS OF ACE INHIBITORS
Dry cough, increased potassium levels in the blood (hyperkalemia), Fatigue, Dizziness from blood pressure going too low,
Headaches, Loss of taste.
POSSIBLE MANAGEMENT/PREVENTIVE MEASURES ACEI ADVERSE EFFECTS
Patients with diabetes and kidney disease are at increased risk of hyperkalemia so ACE inhibitors must be used with caution
in these patients. Patients experiencing angioedema while using an ACE inhibitor must discontinue the medication and avoid
all ACE inhibitors in the future. Concomitant use of ACE inhibitors with a diuretic or non-steroidal anti-inflammatory drugs
(NSAIDs) is discouraged, as these combinations increase the risk of kidney injury. Patients should seek immediate medical
attention if they experience any of the side effects.
ADVERSE EFFECTS OF NITRATES
Common side-effects include: A throbbing headache, A flushed face, Dizziness, Lightheadedness (from the nitrate causing
low blood pressure), Feeling slightly nauseous, With the spray under the tongue: a slight burning or tingling sensation under
the tongue.
POSSIBLE MANAGEMENT/PREVENTIVE MEASURES OF NITRATES ADVERSE EFFECTS
Thankfully these side-effects are unpleasant but not serious. Often they get better once the patient have been using the
medicine for a few weeks.
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
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GHF – PRESENTATION: MANAGEMENT OF ISCHEMIC HEART DISEASE
Presenters: Pharm. S. Bawa, Sci. Haruna, Sci. Hassan, Sci. SAS, Rad. Abdul, Pharm. Joseph, Pharm. Nasir, Pharm. Maryam
From: 6th March, 2022
To: 8th March, 2022
ADVERSE EFFECTS OF ANTIPLATELETS
Antiplatelets can cause: Bleeding, Abdominal pain, Flatulence (intestinal gas), Headache, Lethargy, Dizziness, Fever, Nausea,
Upset stomach, Stomach pain, Diarrhea, Rash, Itching, Difficulty swallowing.
POSSIBLE MANAGEMENT/PREVENTIVE MEASURES OF ANTIPLATELETS ADVERSE EFFECTS
Patients should talk to their doctor/pharmacist if they have underlying medical condition such as peptic ulcer, bleeding
disorder, liver or kidney problem. Age should also be considered before antiplatelet is prescribed. To ease nausea and stomach
upset, the drug should be taken with meal. Patients should seek medical attention if the side effects are severe or don't go
away. Patients should avoid taking NSAIDs when taking this drugs except if the benefits outweighs the risks.
ADVERSE EFFECTS OF ANTICOAGULANTS
Common side effects include: Bleeding, Abdominal pain, Flatulence, Headache, Lethargy, Dizziness, Fever, Local injection
site reactions, Nausea, Anemia, Bruises caused by trauma (ecchymosis), Diarrhea, Hair loss (alopecia), Rash, Itching
(pruritus), Changes is sense of taste, Fainting (syncope), Shortness of breath, Low blood pressure (hypotension), Chest pain
POSSIBLE MANAGEMENT/PREVENTIVE MEASURES OF ANTIPLATELETS ADVERSE EFFECTS
Patients should talk to their doctor/pharmacist if they have underlying medical condition such as peptic ulcer, bleeding disorder, liver or
kidney problem. Age should also be considered before antiplatelet is prescribed. To ease nausea and stomach upset, the drug should be
taken with meal. Patients should seek medical attention if the side effects are severe or don't go away. Patients should avoid taking
NSAIDs when taking this drugs except if the benefits outweighs the risks.
ADVERSE EFFECTS OF THROMBOLYTICS
The side effects associated with thrombolytics include: Major bleeding in the brain, Kidney damage in patients with kidney disease,
Severe hypertension (high blood pressure), Severe blood loss or internal bleeding, Bruising or bleeding at the site of thrombolysis,
Damage to the blood vessels, Fragments of the clot may migrate to other vessels and cause obstruction, Increased risk of bleeding in
pregnant woman, elderly people, and people with bleeding disorders Increased risk for infection, Allergic reactions.
POSSIBLE MANAGEMENT/PREVENTIVE MEASURES OF THROMBOLYTICS ADVERSE EFFECTS
Patients should check with their doctor or pharmacist to make sure these drugs do not cause any harm when they take them along with
other medicines. Patients should never stop taking their medication and never change their dose or frequency without consulting their
doctor or pharmacist. Patients should seek immediate medical attention if the side effects are severe or don't go away. Above all, patients
with ischemic heart diseases are advised to take their medications as prescribed and report any side effects immediately it is noticed.
SAY NO TO SELF MEDICATION, YOUR HEALTH IS OUR CONCERN. THANK YOU…!!!
COMPILED BY: A. A. NASEER (MGHF – UDUS_PHARMACY)
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