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Transcript
Drug therapy of
cardiovascular diseases
Angina pectoris
Angina pectoris is a clinical syndrome
characterized by episodes of chest pain. It occurs
when there is a deficit in myocardial oxygen supply
(myocardial ischemia) in relation to myocardial oxygen
demand. It is most often caused by atherosclerotic
plaque in the coronary arteries but may also be
caused by coronary vasospasm. The development
and progression of atherosclerotic plaque is called
coronary artery disease.
Risk factors for coronary artery disease
Smoking
Hypertension
Hyperlipidaemia
Diabetes mellitus
Antianginal (coronary
active) drugs
a group of drugs that relieve anginal pain by
reducing myocardial oxygen demand or
increasing blood supply to the myocardium.
Clinically it is manifested by removal or
prevention
of
stenocardia
attacks
(improvement of disease current) and
increasing of patients’ tolerance to physical
load
ANTIANGINAL (CORONARY
ACTIVE) DRUGS
І. Nitrates and sidnonims
ІІ. Beta-adrenoblockers
ІІІ. Calcium channel blockers
ІУ. Activators of potassium channels
NITRATES
Glyceryl trinitrate
isosorbid dinitrate
isosorbid-5-mononitrate
INDICATIONS
Treatment and prevention of angina.
Treatment of acute left ventricular
failure.
NITRATES
1. Nitrates are first-line treatments for the symptoms of
angina but do not affect the course of the underlying
disease.
2. They cause vasodilatation; this can be hazardous in
some patients:
Patients who are hypovolaemic (severe
hypotension).
Patients with cardiac disease such as hypertrophic
cardiomyopathy or mitral stenosis.
Patients with bleeding (e.g. following head trauma or
cerebral haemorrhage).
No dosage adjustment is usually required in renal or
hepatic insufficiency.
Avoid these drugs during pregnancy; the effects on
blood pressure can affect placental blood flow.
NITROGLYCERINE
Tablets (under the tongue)
1 % alcohol or oil solution (under the tongue)
aerosol
Latent period - 2-3 min
Duration of action - 20-30 min
ampoules 1 % solution – intravenously
dropply 0,01% solution
prolonged forms of nitroglycerine:
trinitrolong, sustak, nitrong, ointment, plaster
Contraindications for
nitroglycerine use
Close-angled form of glaucoma
Increasing of intracranial pressure,
insult
Acute myocardium infarction (in case
of presence of hypotension and
collapse)
PROLONGED FORMS OF
NITROGLYCERINE
Trinitrolong – polymer films (0,001 g or 0,002 g of
nitroglycerine) action develops immediately, lasts for 35 hours
Sustac
Sustaс-mite (contains 0,0026 g of
nitroglycerine) and Sustac-forte (0,0064 g of
nitroglycerine)
beginning of action – after 10 min,
maximal action – after 1 hour,
duration of action – 4-5 hours
Nitrong – microcapsule form of nitroglycerine of
prolonged action
latent period – 30-60 min,
maximal effect - after 3-4 hours,
action duration - 6-8 hours
Other nitrates
Nitrosorbid – isosorbid dinitrate
latent period 30-50 min,
duration of action – 4-6 hours and more
With sublingual administration of the drug latent period grows
short to 3-5 min
buccal form (Dinitrolslrbilong)
tablets of prolonged action (Isoket-retard)
ointment
aerosol
drugs for intravenous introduction
Isosorbid-5-mononitrate
- pharmacologically active metabolite of isosorbid dinitrate
duration of action - from 6 till 24 hours
The adverse effects of nitrates are related to
their vasodilator properties
The most common is a throbbing headache;
this may improve with time.
Other common adverse effects include
dizziness, postural hypotension, and
tachycardia.
Hypotension is the most serious adverse
effect; take care to titrate the dose to minimize
the risk of falls.
Prolonged intravenous administration can
cause methaemoglobinaemia; this is rare.
Avoid prolonged intravenous administration;
the patient will become tolerant to the effects of
the drug.
SYDNONIMS
Molsydomin – corvaton sydnopharm
2 mg of molsydomin = 0,5 mg of
nitroglycerine
Molsydomin
latent period - 20 min (5-10 min – if
administered sublingually), action duration 6 hours.
can be used for prophylaxis and releasing
stenocardia attacks in patients with
glaucoma
(doesn’t increase
intraoccular pressure)
indicated for patients who make breaks in
using nitrates to decrease tolerance towards
them
doesn’t lead to development of tolerance
(doesn’t need previous combining with
sulfhydryl groups)
Treatment of angina
Glyceryl trinitrate is given as sublingual tablets or spray for the
symptomatic relief of angina. It acts within a few minutes and
lasts for 20-30 minutes.

If the patient has predictable angina on exertion, they can
take the glyceryl trinitrate beforehand to prevent angina.
If the first dose of glyceryl trinitrate does not relive the angina,
advise the patient to take a second dose after 5 minutes. If this
does not relieve their symptoms, they should seek urgent
medical attention.
Glyceryl trinitrate can relieve symptoms of angina at rest or on
minimal exertion, but these are symptoms of unstable disease;
advise the patient to seek urgent medical attention.
Glyceryl trinitrate is most useful for intermittent symptoms.
Glyceryl trinitrate is relatively unstable; the sublingual tablets
have a limited shelf-life. Advise the patient to dispose of any
unused tablets after 3 months, and obtain a fresh supply. The
spray formulation lasts longer.
Treatment of angina (cont’d)




If the patient has frequent symptoms, a modified-release
formulation that acts over a longer period may be suitable.
Remember that nitrates do not affect the disease process;
ensure that the patient has been adequately investigated.
If nitrates are given repeatedly, patients rapidly become tolerant
to their effects (within 24 hours). It is important to have a nitratefree period of at least 4-8 hours during the day.
Immediate-release formulations should usually be given at
08.00 and 14.00, to give a nitrate-free period overnight. The
timing of the doses can be altered to coincide with the patient's
symptoms, but they should not be given 12 hours apart.
Modified-release formulations are usually formulated to provide
relief over an 18-hour period.
Remove nitrate patches to provide a nitrate-free period(usually
overnight).
Avoid giving intravenous glyceryl trinitrate for long periods.
Treatment of angina (cont’d)
Nitrates by intravenous infusion are used
in the treatment of acute coronary
syndromes for symptomatic relief and
because they lower blood pressure.
Intravenous nitrates are sometimes given
to control severe hypertension before
thrombolysis.
Treatment of angina (cont’d)
Angina is the symptom experienced when the myocardium is
ischaemic, usually as a result of coronary artery disease.
Classically, angina is a dull, tight, central chest pain that may
radiate to the neck and left arm. Some patients do not have
classical symptoms, but recognize other symptoms as angina.
The first-line treatment for angina is a beta-blocker given
regularly, and a nitrate given as required to relieve the pain.
Coronary artery disease is usually the cause of angina; patients
need to be advised how to adjust their lifestyle to modify their
risk factors (e.g. smoking, diet, exercise). Patients with angina
should also be given an antiplatelet drug (e.g. aspirin) and a
cholesterol-lowering drug (e.g. a statin).
Once a diagnosis of angina has been made, the patient should
have their risk of myocardial infarction assessed. This is usually
by means of an exercise tolerance test with electrocardiographic
monitoring. An alterative is a cardiac nuclear perfusion scan.
Treatment of angina (cont’d)
Those at high risk should be assessed for coronary
angiography, with a view to percutaneous intervention or bypass
grafting. Some patients are at low risk, and others do not have
lesions amenable to intervention. For these patients optimization
of pharmacotherapy, in combination with lifestyle changes, is
indicated.
Many patients are adequately treated with a beta-blocker and
nitrate alone. Beta-blockers are recommended as they have
beneficial effects on vascular growth and function.
Some patients are unable to take a beta-blocker, or their
symptoms are inadequately controlled. Consider a calcium
channel blocker for these patients. The most commonly
prescribed are the dihydropyridines (e.g. amlodipine, nifedipine).
Verapamil and diltiazem lower heart rate; this may be beneficial
if tachycardia is a feature. Verapamil should not be given to
patients taking beta-blockers (risk of severe hypotension and
asystole).
ANTIARRHYTMIC DRUGS
Antiarrhythmic agents are a group of
pharmaceuticals that are used to suppress
abnormal rhythms of the heart (cardiac
arrhythmias), such as atrial
fibrillation, atrial flutter, ventricular
tachycardia, and ventricular fibrillation.
These drugs were classified into various
groups by SINGH VAUGHAN WILLIAMS
as follows:
CLASSIFICATION OF ANTI-ARRHYTHMIC
DRUGS
Na+ channel blockers (membrane
stabilizing group).
II. Beta- adrenergic blockers
III. K+ channel blockers (prolong
repolarisation and action potential)
IV. Ca2+ channel blockers L-type
I.
Class I drugs are divided into three
subgroups:
Subgroup I A
Subgroup I B
Subgroup I C
SINUS TACHYCARDIA
Sinus tachycardia (also colloquially known
as sinus tach or sinus tachy) is a heart
rhythm with elevated rate of impulses
originating from the sinoatrial node, defined
as a rate greater than 100 beats/min (bpm) in
an average adult. The normal heart rate in
the average adult ranges from 60–100
beats/min. Note that the normal heart rate
varies with age, with infants having normal
heart rate of 110–150 bpm to the elderly, who
have slower normals.
SINUS TACHYCARDIA IS USUALLY A RESPONSE TO NORMAL
PHYSIOLOGICAL SITUATIONS, SUCH AS EXERCISE AND AN
INCREASED SYMPATHETIC TONE WITH
INCREASED CATECHOLAMINE RELEASE—STRESS, FRIGHT, FLIGHT, ANGER.
OTHER CAUSES INCLUDE:
Pain
Fever
Anxiety
Dehydration
Malignant hyperthermia
Hypovolemia with hypotension and shock
Anemia
Heart failure
Hyperthyroidism
Mercury poisoning
Kawasaki disease
Pheochromocytoma
SYMPTOMS
1. Palpitations, or sweating, dizziness,
vertigo, fatigue, or the performance of
primary disease.
2. Can be induced by other arrhythmia or
angina.
3. Heart rate for 100 to 150 times / min,
heart sounds are mostly strong, or signs of
primary heart disease.
ECG CHARACTERISTICS
Rate: Greater than or equal to 100.
Rhythm: Regular.
P waves: Upright, consistent, and normal
in morphology (if no atrial disease)
P–R interval: Between 0.12–0.20 seconds
and shortens with increasing heart rate
QRS complex: Less than 0.12 seconds,
consistent, and normal in morphology.
DIAGNOSIS
Usually apparent on the EKG, but if heart rate is
above 140 bpm the P wave may be difficult to
distinguish from the previous T wave and one
may confuse it with a paroxysmal
supraventricular tachycardia or atrial flutter with
a 2:1 block. Ways to distinguish the three are:
Vagal maneuvers (such as carotid sinus
massage or Valsalva's maneuver) to slow the
rate and identification of P waves
administer AV blockers
(e.g., adenosine, verapamil) to identify atrial
flutter with 2:1 block
TREATMENT
Not required for physiologic sinus tachycardia. Underlying causes are
treated if present.
Acute myocardial infarction. Sinus tachycardia can present in more
than a third of the patients with AMI but this usually decreases over time.
Patients with sustained sinus tachycardia reflects a larger infarct that are
more anterior with prominent left ventricular dysfunction, associated with
high mortality and morbidity. Tachycardia in the presence of AMI can
reduce coronary blood flow and increase myocardial oxygen demand,
aggravating the situation. Beta blockers can be used to slow the rate,
but most patients are usually already treated with beta blockers as a
routine regimen for AMI.
Practically, many studies showed that there is no need for any treatment.
Inappropriate sinus tachycardia and Postural tachycardia
syndrome. Beta blockers are useful if the cause is sympathetic
overactivity. If the cause is due to decreased vagal activity, it is usually
hard to treat and one may consider radiofrequency catheter ablation.
ATRIAL FLUTTER
Atrial flutter is an abnormality of the heart
rhythm, resulting in a rapid and sometimes
irregular heartbeat. Such abnormalities,
whether in the rate or regularity of the
heartbeat, are known as arrhythmias.
ATRIAL FLUTTER CAUSES
Atrial flutter may be caused by abnormalities
of the heart, by diseases of the heart, or by
diseases elsewhere in the body that affect
the heart. Atrial flutter may also be caused
by consuming substances that change the
way electrical impulses are transmitted
through the heart. Atrial flutter can occur
after open heart surgery. In a few people, no
underlying cause is ever found.
Heart diseases or abnormalities that can cause atrial
flutter include the following:
Decreased blood flow to the heart (ischemia) due to
coronary heart disease, hardening of the
arteries (atherosclerosis), and/or a heart attack
High blood pressure (hypertension)
Disease of the heart muscle (cardiomyopathy),
especially associated with congestive heart failure
Abnormalities of the heart valves, especially the mitral
valve
An abnormally enlarged chamber of the heart
(hypertrophy)
ATRIAL FLUTTER SYMPTOMS
Some people have no symptoms with
atrial flutter. Others describe the following
symptoms:
Palpitations (a rapid heartbeat or a
pounding sensation in the chest)
A fluttering feeling in the chest
Shortness of breath
Anxiety
Weakness
ATRIAL FLUTTER SYMPTOMS
People with underlying heart or lung
disease who experience atrial flutter may
have these symptoms as well as the
following more significant symptoms:
Angina pectoris (chest or heart pains)
Feeling faint or light headed
Fainting (syncope)