▪ Coronary artery disease (CAD) is the leading cause
of ischemic heart disease.
▪ Ischemic heart disease (IHD) is defined as lack
of oxygen and decreased or no blood flow to the
myocardium resulting from coronary artery
narrowing or obstruction.
▪ IHD present as:
▪ Acute coronary syndrome (ACS): includes unstable angina,
non-ST-segment myocardial infarction (MI), or ST-segment
▪ Stable ischemic heart disease or Angina
▪ Angina pectoris: a discomfort in the chest and/or an
adjacent area resulting from myocardial ischemia (1).
▪ Stable angina: is defined as a predictable occurrence
of chest discomfort with physical exertion (2) and is
predictably resolved with rest or administration of
sublingual nitroglycerin (3).
▪ Prinzmetal angina: Angina caused by spasm of the
coronary arteries (4).
Diagnosis depends principally upon the history:
1. Circumstances that precipitate and relieve angina:
Angina occurs most commonly during activity and is
relieved by resting.
2. Characteristics of the discomfort: Patients often do not
refer to angina as “pain” but as a sensation of tightness, ,
burning, or pressing.
3. Location and radiation: In most cases, the discomfort is
felt behind or slightly to the left of the mid sternum. It
radiates most often to the left shoulder and upper arm,
frequently moving down the arm. It may also radiate to the
right shoulder or arm, the neck, or even the back.
4. Duration of attacks: Duration of attack is usually 0.5–30
minutes. Relief of pain occurring within 45 seconds to 5
minutes of taking Nitroglycerin
CP & Diagnosis:
▪ The resting ECG is normal in about one
half of patients with angina who are not
experiencing an acute attack (8).
▪ Stress ECG Testing (9).
▪ Coronary angiography: Coronary
angiography is regarded as the definitive
test as it demonstrates the presence of
occlusions, their position and their
Annual influenza vaccinations are
Smoking Obesity Sedentary Life
Risk factors Modification
Goal of Therapy & the GDMT
▪ Goals of Treatment: A primary goal of therapy is complete (or
nearly complete) elimination of anginal chest pain and return to
▪ Long-term goals are to slow progression of atherosclerosis and
prevent complications such as MI, heart failure, stroke, and death.
▪ Guideline-directed medical therapy (GDMT) reduces the rates of
death and MI similar to revascularization therapy
▪ The current national guidelines recommend that all patients be given the
following unless contraindications exist :
▪ (1)-Sublingual nitroglycerin for immediate relief of angina.
▪ (2)- Antiplatelet (Aspirin or Clopidogrel in patients with aspirin hypersensitivity
or intolerance. DAPT preserved for high risk specific group).
▪ (3)-β- blockers.
▪ (4)-Calcium antagonists (N-DHP) or long-acting nitrates [isosorbide
dinitrate(ISDN) or isosorbide mononitrate (ISMN) ]for reduction of symptoms
when β-blockers are contraindicated (or they may be used in combination with
β-blockers when initial treatment with β-blockers is not successful).
▪ (5)-LDL-lowering therapy: moderate- or high-dose statin therapy Addition
of ezetimibe (first) or a PCSK9 inhibitor (second) is reasonable for patients
who do not tolerate statins or do not attain a 50% decrease in LDL .
▪ Aspirin therapy: (75–162 mg daily) should
be prescribed for all patients with angina.
Clopidogrel, 75 mg daily is a good
alternative in aspirin-intolerant patients.
▪ Dual antiplatelet therapy (DAPT) with
aspirin plus a P2Y12 inhibitor (clopidogrel,
prasugrel, ticagrelor) is beneficial after PCI
with coronary stent placement and after
treatment for ACS. Its benefits in other
situations are less clear. The combination
of aspirin (75–162 mg daily) and
clopidogrel 75 mg daily may be reasonable
in certain high-risk patients. Clinical Pharmacology of Antiplatelet Drugs for Neurointerventionalists.
β-Adrenergic Blocking Agents:
▪ They reduce heart rate and force of
contraction, allowing greater time
for perfusion and decreased
demand for oxygen.
▪ Cardioselective beta-blockers, such
as atenolol and metoprolol, are
preferred. Only the β-blockers
carvedilol, metoprolol succinate, and
bisoprolol should be used in patients
with HFrEF, starting with low doses
and titrating upward slowly.
▪ Note: β-Blockers have little or no role
in the management of variant
angina as they may induce coronary
vasoconstriction and prolong
▪ Nitrate therapy may be used to terminate an
acute anginal attack, to prevent effort- or stress-
induced attacks, or for long-term prophylaxis.
▪ Sublingual, buccal, or spray nitroglycerin
products are preferred for alleviation of
anginal attacks because of rapid absorption.
▪ If the pain persists or is unimproved in 5
minutes after the first dose of NTG, contact
physician & take a maximum of two more
tablets each 5 minutes apart (3 tablet in 15 min
totally). The patient should contact their
physician or be transported to an emergency
room as they may be experiencing an MI.
▪ Chewable, buccal, oral, and
transdermal products are acceptable for
long-term prophylaxis of angina.
▪ The main limitation to long-term
nitrate therapy is tolerance, which can
be limited by using a regimen that
includes a minimum 8- to 10-hour
period per day without nitrates
(nitrate-free interval) (**Balance
with B blockers if used in
Calcium Channel Blockers
▪ Good candidates for calcium channel
antagonists include patients with
contraindications or intolerance to β-blockers,
Prinzmetal's angina, and peripheral vascular
▪ Because calcium channel antagonists may be
more effective, some authorities consider them
the agents of choice for variant angina. A
patient unresponsive to calcium channel
antagonists alone may have nitrates added.
▪ CCBs modulate calcium entry into the
myocardium, vascular smooth muscle, and
other tissues, which reduces the cytosolic
concentration of calcium responsible for
activation of the actin–myosin complex and
contraction of vascular smooth muscle and
▪ All CCBs reduce MVO2 by reducing wall
tension via lowering arterial BP and (to a
minor extent) depressing contractility.
▪ CCBs also provide some increase in supply
by inducing coronary vasodilation and
Others antianginal agents: add-on therapy mostly
▪ Ranolazine reduces ischemic
episodes by selective inhibition of
late sodium current (INa), which
reduces intracellular sodium
concentration and improves
myocardial function and
▪ Monotherapy used only if patients
cannot tolerate traditional agents
due to hemodynamic or other
▪ Adverse effects include:
constipation, nausea, dizziness, and
headache. Ranolazine can prolong
the QTc interval and should be used
with caution in patients receiving
▪ It can be combined with a β-
blocker when initial treatment
with β-blockers alone is
▪ Assess for symptom improvement by number of angina
episodes, weekly SL NTG use, and increased exercise
capacity or duration of exertion needed to induce angina.
▪ Use statins for dyslipidemia, strive to achieve BP and A1C
goals, and implement the lifestyle modifications of dietary
modification, smoking cessation, weight loss, and regular
▪ Once patients have been optimized on medical therapy,
symptoms should improve over 2–4 weeks and remain
stable until the disease progresses. Patients may require
evaluation every 1–2 months until target endpoints are
achieved; follow-up every 6–12 months thereafter is
▪ The Seattle Angina Questionnaire, Specific Activity Scale, and
Canadian Cardiovascular Society classification system can be
used to improve reproducibility of symptom assessment.
▪ If the patient is doing well, no other assessment may be
necessary. Although follow-up exercise tolerance testing with
or without cardiac imaging can be performed to objectively
assess control of ischemic episodes, this is rarely done if
patients are doing well because of the expense involved.
▪ Monitor for adverse drug effects such as headache and
dizziness with nitrates; fatigue and lassitude with β-blockers;
and peripheral edema, constipation, and dizziness with CCBs.
Psychological interventions (eg, screening and treatment for depression if appropriate), limitation of alcohol intake, and avoiding exposure to air pollution.
Statin therapy has also antithrombotic and anti-inflammatory properties