Angina Pectoris

DR. SUBASINI
UTHIRAPATHY

Angina Pectoris

Symptoms of patient with ischemic heart

disease
Manifested by sudden, severe, pressing
sub-sternal pain that often radiates to
the left shoulder, along the flexor surface
of the left arm.
Usually precipitated by exercise,
excitement or a heavy meal

symptoms - patient with angina

Central chest tightness or heaviness,

which may be brought on by exertion or
relieved by rest.
It may radiate to one or both arms, the
neck, jaw or teeth.
Other associated symptoms include:
dyspnoea (shortness of breath), nausea,
sweatiness and faintness

Modifiable risk factors

hyperlipidaemia
smoking
hypertension
lack of exercise
poor diet
personality
obesity
heavy alcohol consumption
contraceptive pill
stress.

Non-modifiable risk
factors

age
gender
positive family history
diabetes mellitus
ethnicity
Age
Indian origin
Sedentary job/possible lack of exercise
Smoking
Gender men are at increased risk.

Types of Angina

Classical Angina (Typical angina) or

stable angina
Pain is commonly induced by exercise,
excitement or a heavy meal
Secondary to advanced atherosclerosis
of the coronary vessels.
Associated with ST segment
depression on ECG

Classical angina (stable angina)

Obstruction is stable
Patients symptoms also stable
Always ppted exertional/emotional or
walking or exercise
Angina pain starts,
patients take rest, - demand will be able
to meet oxygen supply
Sublingual nitrates within 2-3 mts angina
will disappear

Variant Angina(Prinzmetal angina)

Pain is induced while at rest.

Associated with ST-segment elevation
on ECG
Secondary to vasospasm of the
coronary vessels.
Not related with exertion or tachycardia
Patients taking rest it may produced
(vasospasicity)

Unstable Angina

May involve coronary spasm and may

also have the component of
atherosclerosis
The duration of manifestation is longer
than other first two and has the
manifestation of MI

Unstable angina

Unstable coronary plug

Atheromatic plug surface may be platelet
aggregation with irregular fibrin deposition or
it rupture the outer surface or ulceration
thrombus formation
It is produced severe ischemic, deeper sub
endothelial myocardium vessel may undergo
occlude completely.
Lost more than 30 mts undergo MI

Etiology
Decreased oxygen supply
Increased oxygen demand
Determinant of Myocardial oxygen supply
Determinant of oxygen demand
wall stress
- Intraventricular pressure
- Ventricular volume
- Wall thickness
Heart rate
Contractility
Vascular tone

Treatment Plan

Decrease the risk factor like

atherosclerosis, hypertension, smoking
Increase oxygen supply
Decrease oxygen demand

Anti-Anginal drugs

Agents which decrease o2 demand and

increase o2 supply

Nitrates GTN and Isosorbide dinitrate

Calcium Channel Blockers
Verapamil, diltiazem, nifedipine,
amlodipine, niodipine etc
Agents which decrease o2 demand

Beta Blockers Propanolol,

metoprolol,atenolol etc.

Nitrates and Nitrites

Classification Nitrates
1. rapidly acting nitrates used to terminate
acute attack of angina
Eg. Nitroglycerine and Amyl nitrate
Route: sublingually (3-5 mts)
2. Long acting Nitrates
eg. Erythrytyl tetranitrate
Isosorbide dinitrate
Penta erythrytyl tetranitrate
Route: orally or topically

MOA (Nitrates)

At therapeutic doses the main effect of

nitrates is to act on vascular smooth muscle
to dilate the veins, thus reducing central
venous pressure (preload) and ventricular
end-diastolic volume.
The overall effect is to lower myocardial
contraction, wall stress and oxygen demand,
thereby relieving the angina.
Nitrates also promote vasodilation of the
coronary blood vessels.

MOA (Nitrates)

Coronary artery dilatation

Relieved coronary vasospasm

Increased coronary blood flow

Increased oxygen supply

MOA ( Nitrates)

Reduction of Peripheral resistance

Decrease blood flow

Decrease after load

Decrease work load

Decrease oxygen consumption

MOA(molecular level)
Organic nitrates

No
Guanalyl Cyclase

cGMP

cGMP dependent proteinkinase dephosphorylation of MLCK

Intracellular Ca++
Vascular SM relaxation

Route of administration

Sublingual route: Rational and effective for the

treatment of acute attack of angina
Oral route: to provide convenient and prolonged
prophylaxis against attack of angina
IV route: useful in the treatment of coronary
vasospasm and Ischemic syndrome
Topical route: used to provide gradual absorption
of the drug for prolonged prophylactic purpose
Eg. Buccal mucosa 3-6 mts
Transdermal 8-10 hrs.

Adverse effects

Throbbing headache
Flushing of the face
Dizziness especially at the beginning of
treatment (palpitation weakness, fainting)
Postural hypotension (due to pooling of blood
below portion of the body)
Less commonly nausea, vomiting, heartburn,
flushing.
Methmoglobinemia
`Reflex Tachycardia

Clinical Indications

Stable angina
Coronary vasospasm
LVF accompanying MI
Hypertension during cardiac surgery
0.5 mg SL
0.4 -0.8 mg SL spray
IV begin with 5mcg/ mints

Contraindications

Renal ischemia
Acute Myocardial infarction
Patients receiving other antihypertensive
agent

Beta Blockers

Hemodynamic effects
1. decrease Heart rate
2. decrease pressure and cardiac
contractility
3. decrease cardiac output

Beta Blockers (BB)

Atenolol (Tenormin)
Metoprolol (Lopressor)
Propranolol (Inderal)
Nadolol (corgard)

MOA (Beta blockers)

Decrease heart rate

Duration of diastole

&

Contractility
decrease
workload

coronary blood flow

oxygen supply
o2 supply

Contraindications

Congestive heart failure

Asthma (COPD)
Complete heart block
Diabetic mellitus
Depression

Side effects

1. CVS: bradycardia, hypotension

2 or 3 degree heart block
heart failure
2. Metabolic: Altered glucose and lipid
metabolic
3. CNS: dizziness, fatigue, mental
depression, lethargy, drowsiness
4. Others: Impotence, wheezing,
dysponea

Reflex Tachycardia- nitrates+BetaB

Calcium Channel Blockers

Three types Ca+ channels in smooth muscles Voltage

sensitive, receptor operated and leak channel
Voltage sensitive are again 3 types L-Type, T-Type and N-Type
Normally, L-Type of channels admit Ca+ and causes
depolarization excitation-contraction coupling through
phosphorylation of myosin light chain contraction of vascular
smooth muscle elevation of BP
CCBs block L-Type channel:
Smooth Muscle relaxation
Negative chronotropic, ionotropic and dromotropic effects in
heart
DHPs have highest smooth muscle relaxation and vasodilator
action followed by verapamil and diltiazem
Other actions: DHPs have diuretic action

Classification

Ca++ Channel Blockers

Coronary artery dilatation

Reduction of peripheral resistance
( decrease after load)
Commonly used CCB
Nifedipine
Verapamil
Diltiazam
Nicardifine
Felodipine

Calcium Channel Blockers (CCB):

Calcium Channel Blockers (CCB):

Verapamil, diltiazem, nifedipine,
felodipine, amlodipine, nimodipine etc.
MOA: Blocks influx of Ca++ in smooth
muscle cells relaxation of SMCs
decrease BP

Unwanted effect

Nausea, vomiting
Dizzyness
Flushing of the face
Tachycardia due to hypotension

Contraindications

Cardiogenic shock
Recent MI
Heart failure
Atrio ventricular block

Combination Therapy

Nitrates and BB = EDV

CCA and BB
= BP
CCA and Nitrates = preload & afterload
afterload

Triple drugs therapy

Nitrates + CCB + BB
Nitrates - preload
Nifedipine afterload
BB
- Heart rate &
contraictility

Newer group of drugs

Trimetazidine (modify myocardial
metabolism)

Ranolazine

Clinically reduces the frequency of

angina attacks in persons with stable
angina.
Both drugs reduces ischemic symptoms
in angina pts by preventing myocardial
sodium and calcium overload.

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