Angina pectoris is the medical term for chest pain or discomfort due to coronary heart disease. It occurs when the heart muscle doesn't get as much blood as it needs. This usually happens because one or more of the heart's arteries is narrowed or blocked, also called ischemia.
2. Angina
Angina is a type of chest pain that results from reduced blood flow to the heart. The pain is
often triggered by physical activity or emotional stress.It occurs when an area of the heart
muscle receives less blood oxygen than usual.
Angina is not a disease but a symptom. It usually happens due to ischemia, when one or more of
the coronary arteries becomes narrow or blocked. It is often a symptom of coronary heart
disease (CHD). Alone, angina is not life threatening, but it can resemble the symptoms of a heart
attack, and it is a sign of heart disease.
Myocardial cells
3. Types of Angina
Variant Angina
Variant (Prinzmetal's) angina
results from coronary
vasospasm, which temporarily
reduces coronary blood flow.
Thereby decreasing the oxygen
supply/demand ratio.
Stable Angina
predictable & consistent pain
that occurs on exertion and
relieved by rest.
Stable angina occurs when the
heart is working harder than usual
for instance, during exercise. It
usually lasts around 5 minutes.
It has a regular pattern, and a
person may experience it for
months or years.
Unstable angina
Unstable angina is a condition in
which your heart doesn't get
enough blood flow and oxygen.
It may lead to a heart
attack. Due to spasm and partial
obstruction of coronaries
All three forms are associated with a reduction in the oxygen supply/demand ratio
4. Etiology and pathogenesis
Symptoms are results of myocardial ischemia due to insufficient
blood flow through atherosclerotically changed coronary vessels
5. Clinical symptoms
• Patient history is a˝golden standard˝
• Retrosternal pain
• Dyspnea
• Nausea
• Arrhythmia
• Restlessness
• Pain eased after taking nitrates
7. Diagnosis of angina
• Electrocardiogram (ECG)
• Stress test
• Echocardiogram
• Chest X-ray
• Coronary angiography
• Cardiac computerized tomography (CT) scan
• Cardiac MRI
• C-reactive protein ( CRP) is a marker for
inflammation of vascular endothelium which
caused by CAD.
8. Treatment of Angina Pectoris
Drugs used in angina exploit two main strategies:
Drugs that reduce myocardial oxygen demand are commonly used to prevent and treat episodes
of ischemic pain associated with fixed stenotic lesions (i.e., chronic stable angina). Some of
these drugs reduce oxygen demand by decreasing heart rate (decreased chronotropy) and
contractility (decreased inotropy), while other drugs reduce afterload and or preload on the
heart. Afterload and preload reducing drugs act by dilating peripheral arteries and veins.
Reduction of
oxygen
demand
12. Nitrates & Nitrates
• Nitroglycerin, which has been used since the 19th century, is commonly used
in the treatment of angina because it is very fast acting (within 2 to 5
minutes) when administered sublingually.
• Its effects usually wear off within 30 minutes. Therefore, nitroglycerin is
particularly useful for preventing or terminating an acute anginal attack.
• Longer-acting preparations of nitroglycerin (e.g., transdermal patches) have a
longer onset of action (30 to 60 minutes), but are effective for 12 to 24
hours.
• Intravenous nitroglycerin is used in the hospital setting for unstable angina
and acute heart failure.
14. Side Effects
• Headache
• Dizziness
• Lightheadedness
• Nausea
• Flushing
• Burning and tingling under the tongue
• Low blood pressure
•Nitrates can slow down metabolism of cabergoline and ergonovine, resulting in an increase in
systolic blood pressure and an increased likelihood of angina symptoms.
•Sildenafil, tadalafil and vardenafil increase the blood pressure lowering effects of nitrates
and may cause excessive blood pressure reduction. Men taking nitrates should not
take sildenafil, tadalafil, or vardenafil.
Drugs interact with nitrates
15. Special Condition
To abort or terminate anginal
attack:
Nitroglycerin(sublingually)
Isosorbide dinitrate(sublingually)
For chronic prophylaxsis:
Nitrates, β-blockers, CCBs,
potassium channel openers &
others drugs
16. β Blockers
β-adrenoceptors
Blockers
Activation of β1 adrenoreceptor on
the heart
Cardiac Output
Decrease blood Pressure
Β-Blockers blocks the action of substances, such as adrenaline, on nerve cells and causes blood vessels to
relax and dilate (widen). This allows blood to flow more easily and lowers blood pressure and the heart rate.
Beta-blockers are used to treat high blood pressure, chest pain (angina).
17. Side effects of B Blockers
Fatigue and dizziness-
Beta-blockers slow down your heart rate. This can trigger symptoms associated with low blood
pressure(hypotension).
Poor circulation-
Heart beats more slowly when you take beta-blockers. This makes it more difficult for blood to reach your
extremities. might experience coldness or tingling in your hands and feet.
Gastrointestinal symptoms-
These include upset stomach, nausea, and diarrhea or constipation. Taking beta-blockers with food may help
relieve stomach symptoms.
Sexual dysfunction-
Some people report erectile dysfunction when taking beta-blockers. This is a common side effect with
medications that lower blood pressure.
Weight gain-
This is a side effect of some older, nonselective beta-blockers. Doctors aren’t sure why it happens, but it
may be related to how beta-blockers affect your metabolism.
Beta blockers are the only anti-anginal drugs that decrease mortality in patients with CAD
(Post-MI) &
contra-indicated in variant angina
18. calcium-channel blockers
• Currently approved calcium-channel blockers (CCBs) bind to L-type calcium
channels located on the vascular smooth muscle, cardiac myocytes, and cardiac
nodal tissue (sinoatrial and atrioventricular nodes).
• These channels are responsible for regulating the influx of calcium into muscle
cells, which in turn stimulates smooth muscle contraction and cardiac myocyte
contraction.
• In cardiac nodal tissue, L-type calcium channels play an important role
in pacemaker currents and in phase 0 of the action potentials. Therefore, by
blocking calcium entry into the cell, CCBs cause vascular smooth muscle
relaxation (vasodilation), decreased myocardial force generation (negative
inotropy), decreased heart rate (negative chronotropy), and decreased
conduction velocity within the heart (negative dromotropy), particularly at
the atrioventricular node.
19. Calcium channel blockers
CCB’s
binds to α1 subunit of L- type Ca2+channels &
block their activity
decrease in transmembrane calcium current smooth muscle
relaxation, decreased
contractility in cardiac muscle, decrease in pacemaker
activity & conduction velocity
Calcium channel blockers lower your blood pressure by preventing calcium from
entering the cells of your heart and arteries. Calcium causes the heart and
arteries to contract more strongly. By blocking calcium, calcium channel blockers
allow blood vessels to relax and open
20. Side effects of CCB
• Constipation
• Dizziness
• Fast heartbeat (palpitations)
• Fatigue
• Flushing
• Headache
• Nausea
• Rash
• Swelling in the feet and lower legs
Avoid grapefruit products while taking certain calcium channel blockers. Grapefruit
juice interacts with the drug and can affect heart rate and blood pressure
21. POTASSIUM CHANNEL OPENERS
• Nicorandil
• Nicorandil is the agent that causes coronary dilation by activating myocardial ATP sensitive
K+ channels. In addition it possesses Nitric Oxide releasing property; to which tolerance does not develop
22. PARTIAL FATTY ACID OXIDATION INHIBITORS
• Trimetazidine is a drug which act in angina by this new strategy. Heart normally
utilizes fatty acids as fuel (not very efficient fuel).
• Heart starts utilizing glucose (very efficient fuel) as a fuel, if oxidation of
fatty acids is inhibited by these drugs
• Further by inhibiting the lipid peroxidation,
these drugs reduce the generation of free
radicals and protect the myocardium from
harmful effects of ischemia. Thus, it can
provide beneficial effects in angina
nonhemodynamic mechanisms