ANTI ANGINA DAN

INFARK MIOKARD

NURUL HASANAH (1800085)

Lecture Of Study : Novia Sinata, M.Si. Apt

Definition

Classification Of Drugs Anti Angina and Infark Miokard

Mechanisms Of Action

Indication

Contra Indication

Toxicity
ANTI ANGINA
• DEFINITIONS:The name angina pectoris denotes chest pain caused
by accumulation of metabolites resulting from myocardialm ischemia.
• By far the most common cause of angina is atheromatous obstruction
of the large coronary vessels (coronary artery disease,CAD).
Inadequate blood flow in the presence of CAD results in effort
angina , also known as classic angina . However, transient spasm of
localized portions of these vessels, which is usually associated with
underlying atheromas, can also cause significant myocardial ischemia
and pain (vasospastic or variant angina ).
There are two types of angina that
can attack
• 1. stable angina
• 2. unstable angina
• Stable angina is caused by certain triggers such as strenuous exercise,
stress, digestive problems,or other medical conditions that encourage
the heart to work harder. Cold weather can also be one of the triggers
of symptoms of angina.Chest pain will usually improve within 5
minutes after resting or taking medication. Although not dangerous,
stable angina has the potential to cause a heart attack or stroke if not
handled properly.
• Unstable angina represents the chest that was received for no initial
reason and clearly does not improve after taking or consuming the
drug. The pain is longer than angina stable, which is about 30
minutes. This is an emergency and requires immediate medical
attention.
• Symptoms of Angina Pectoris
• 1. Shortness of Breath.
• 2. Feeling sick like symptoms of acid reflux disease (GERD).
• 3. Nausea.
• 4. dizziness
• 5. Easily tired.
• 6. Restless.
• 7. Excessive sweating.
Classification Of Drugs Anti Angina

NITRATES

BETA BLOCKERS

CALCIUM CHANNEL BLOCKERS

MISCELLANEOUS
 ANTI ANGINA
• Mechanism of Actions
• Nitrates
The action of nitrates appears to be mediated indirectly through reduction
of MVO2 secondary to venodilation and arterial-arteriolar dilation, leading
to a reduction in wall stress from reduced ventricular volume and
pressure.
Direct actions on the coronary circulation include dilation of large and
small intramural coronary arteries, collateral dilation, coronary artery
stenosis dilation, abolition of normal tone in narrowed vessels, and relief of
spasm.
 Nitroglycer
in
• Pharmacokinetics:High first-pass effect, so sublingual dose is much
smaller than oral ,high lipid solubility ensures rapid absorption
• Toxicity: Orthostatic hypotension, tachycardia, headache
• Interactions: Synergistic hypotension with phosphodiesterase type 5
inhibitors (sildenafil, etc)
 BETA BLOCKERS

Mechanism of actions:
Nonselective competitive antagonist at β adrenoceptors.
Decreased HR, contractility, and blood pressure reduce MVO2 and
oxygen demand in patients with effort-induced angina.β-Blockers do
not improve oxygen supply and, in certain instances, unopposed α-
adrenergic stimulation may lead to coronary vasoconstriction.
• β-Blockade is effective in chronic exertional angina as monotherapy
and in
• combination with nitrates and/or calcium channel antagonists.
Propranolol
Maximum dose: 320 mg per day
atenolol 50-200mg daily
slow release
metoprolol 50-200mg daily
bisoprolol 5-10 mg daily
Pharmacocinetic: Oral and parenteral,
4–6 h duration of action
Indications: Decreased heart rate, cardiac output,
and blood pressure
• decreases myocardial oxygen demand
Toxicity: Asthma, atrioventricular block,
acute heart failure, sedation
Interactions: Additive with all cardiac
depressants
CALCIUM CHANNEL BLOCKERS
• Mechanism of actions
Nonselective block of L-type calcium channels in vessels and heart
Direct actions include vasodilation of systemic arterioles and coronary
arteries, leading to a reduction of arterial pressure and coronary vascular
resistance as well as depression of myocardial contractility and the
conduction velocity of the sinoatrial and atrioventricular (AV) nodes.
 CALCIUM CHANNEL BLOCKERS
• Verapamil(phenylakilamine),diltiazem(benzotiazepine)
• Indications:Reduced vascular resistance, cardiac rate, and cardiac force
results in decreased oxygen demand
• Pharmacokinetics:Oral, IV, duration 4–8 h
• Toxicity: Atrioventricular block, acute heart failure; constipation, edema
• Interactions: Additive with other cardiac depressants and hypotensive drugs

oral
-Initial dose: 180 mg orally once a day at bedtime; if
adequate response is not obtained with 180 mg, the
dose may be titrated upward.
-Maximum dose: 480 mg/day
 Nifedipine (a dihydropyridine)
• Pharmacokinetics:Oral, duration 4–6 h
• Toxicity: Excessive hypotension, baroreceptor reflex tachycardia
• Interactions: Additive with other vasodilato

Immediate-release capsules:
-Initial dose: 10 mg orally 3 times a day
-Maintenance dose: 10 to 30 mg orally 3 to 4 times a day
-Maximum doe: 180 mg/day

Extended-release tablets:
-Initial dose: 30 to 60 mg orally once a day
-Maintenance dose: 30 to 90 mg orally once a day
-Maximum dose: Up to 120 mg/day
MISCELLANEOUS
• (ranolazine)
• The mechanism of action of ranolazine has not been determined, but it
may be related to reduction in calcium overload in ischemic myocytes
through inhibition of the late sodium current. Its antianginal effects do
not depend on reductions in HR or blood pressure.
Ranolazine is indicated for the treatment of chronic angina.
MISCELLANEOUS
• Ranolazine
• Inhibits late sodium current in heart,also may modify fatty acid
oxidation
• Pharmacokinetics : Oral, duration 6–8 h
• Toxicity: QT interval prolongation, nausea, constipation, dizziness
• Interactions: Inhibitors of CYP3A increase ranolazine concentration
and duration of action
• 500 mg orally twice a day; increase to 1000 mg orally
twice a day as needed

Maximum dose: 1000 mg orally twice a day

 Myocardial infarction
• Definition
• Myocardial infarction is an ischemic necrosis of the myocardium,
caused by occlusion of coronary artery and prolonged myocardial
ischemia.
• MI is an extreme consequence of acute coronary syndromes – the
spectrum of clinical states caused by instability of coronary artery
lumen due to plaque instability and (athero)thrombosis
• MIs can be located in the anterior, septal, lateral, posterior, or inferior
walls of the left ventricle.
• Pathophysiological Principles
• Most patients who sustain an MI have coronary atherosclerosis.
• The thrombus formation occurs most often at the site of an
atherosclerotic lesion, thus obstructing blood flow to the myocardial
tissues.
• Plaque rupture is believed to be the triggering mechanism for the
development of the thrombus in most patients with an MI.
• When the plaques rupture, a thrombus is formed at the site that can
occlude blood flow, thus resulting in an MI.
• The cellular changes associated with an MI can be followed by:
• 1. the development of infarct extension (new myocardial necrosis),
• 2. infarct expansion (a disproportionate thinning and dilation of the
infarct zone), or
• 3. Ventricular remodeling (a disproportionate thinning and dilation of
the ventricle).
• MIs most often result in damage to the left ventricle, leading to an
alteration in left ventricular function.
• Infarctions can also occur in the right ventricle or in both ventricles.
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