cardiological disease and treatment

1. CLINICAL PHARMACY INCLINICAL PHARMACY IN
CARDIOLOGYCARDIOLOGY

2. ISCHEMIC HEART DISEASEISCHEMIC HEART DISEASE
There are 35 risk factors for development of IHD
3 most important ones are –
““big triplebig triple””
hypercholesterolaemiahypercholesterolaemia
arterial hypertensionarterial hypertension
smokingsmoking
95 % of patients with IHD are observed to have
aterosclerotic changes in coronary arteries

3. Angina, or angina pectoris, is the medical term used to
describe the temporary chest discomfort that occurs when
the heart is not getting enough blood
 The heart is a muscle (myocardium) and gets its blood supply
from the coronary arteries.
 Blood carries the oxygen and nutrients the heart muscle needs to
keep pumping.
 When the heart does not get enough blood, it can no longer
function at its full capacity.
 When physical exertion, strong emotions, extreme temperatures,
or eating increase the demand on the heart, a person with angina
feels temporary pain, pressure, fullness, or squeezing in the
center of the chest or in the neck, shoulder, jaw, upper arm, or
upper back. This is angina, especially if the discomfort is relieved
by removing the stressor and/or taking sublingual (under the
tongue) nitroglycerin.
 The discomfort of angina is temporary, meaning a few seconds or
minutes, not lasting hours or all day.

4. An episode of angina is not a heart attack. Having angina means the
patient have an increased risk of having a heart attack.
 A heart attack is when the blood supply to part of the heart is cut off
and that part of the muscle dies (infarction).
 Angina can be a helpful warning sign if it makes the patient seek
timely medical help and avoid a heart attack.
 Prolonged or unchecked angina can lead to a heart attack or
increase the risk of having a heart rhythm abnormality. Either of
those could lead to sudden death.

5. Not all chest pain is angina. Pain in the chest can
come from a number of causes, which range from
not serious to very serious
 Chest pain can be caused by:
 acid reflux (gastroesophageal reflux disease, GERD),
 upper respiratory infection,
 asthma, or
 sore muscles and ligaments in the chest (chest wall pain)
 If chest pain is severe and/or recurrent, the patient should see a healthcare
provider.

6. Life-threatning symptoms: chest pain +
 sweating,
 weakness,
 faintness,
 numbness or tingling,
 nausea
 Pain that does not go away after a few minutes
 Pain that is of concern in any way

7. Angina is classified as one of the following two types:
Stable angina
 People with stable angina usually have angina symptoms on a regular
basis. The episodes occur in a pattern and are predictable.
 For most people, angina symptoms occur after short bursts of exertion.
 Stable angina symptoms usually last less than five minutes.
 They are usually relieved by rest or medication, such as nitroglycerin under
the tongue.

8. Unstable angina
 Angina symptoms are unpredictable and often occur at rest.
 This may indicate a worsening of stable angina, but
sometimes the first time a person has angina it is already
unstable.
 The symptoms are worse in unstable angina - the pains
are more frequent, more severe, last longer, occur at
rest, and are not relieved by nitroglycerin under the
tongue.
 Unstable angina is not the same as a heart attack, but it
warrants an immediate visit to the healthcare provider or
a hospital emergency department. The patient may need
to be hospitalized to prevent a heart attack.

9. Most cases of coronary heart disease are caused
by atherosclerosis (hardening of the arteries).
 Atherosclerosis is a condition in which a fatty substance/cholesterol
builds up inside the blood vessels. These buildups are called plaques,
and they can block blood flow through the vessels partially or
completely.
 Multiple risk factors:
 diabetes,
 high blood pressure,
 smoking,
 high cholesterol, and
 genetic predisposition may accelerate this build up.

10. Coronary Artery Spasm
 Another cause of unstable angina is coronary artery spasm.
 Spasm of the muscles surrounding the coronary arteries causes them to
narrow or close off temporarily. This blocks the flow of blood to the heart
muscle for a brief time, causing angina symptoms.
 This is called variant angina or Prinzmetal angina.
 This is not the same as atherosclerosis, although some people have both
conditions.
 The symptoms often come on at rest (or during sleep) and without apparent
cause.
 Cocaine use/abuse can cause significant spasm of the coronary arteries
and lead to a heart attack.

11. Angina Pectoris Symptoms
 Angina itself is a symptom (or set of symptoms), not a disease. Any of
the following may signal angina:
 An uncomfortable pressure, fullness, squeezing, or pain in the
center of the chest
 It may also feel like tightness, burning, or a heavy weight.
 The pain may spread to the shoulders, neck, or arms.
 It may be located in the upper abdomen, back, or jaw.
 The pain may be of any intensity from mild to severe.

12. Other symptoms may occur with
an angina attack: Shortness of breath
 Lightheadedness
 Fainting
 Anxiety or nervousness
 Sweating or cold, sweaty skin
 Nausea
 Rapid or irregular heart beat
 Pallor (pale skin)
 Feeling of impending doom
These symptoms are identical to the signs of an impending heart attack described by the
American Heart Association. It is not always easy to tell the difference between angina and
a heart attack, except angina only lasts a few minutes and heart attack pain does not go
away.

14. AntianginalAntianginal ((coronary activecoronary active))
drugsdrugs
a group of drugs which using different mechanisms
even out irregularities between myocardium need
in oxygen and it’s blood supply by coronary
arteries
clinically it is manifested by removal or prevention
of angina attacks (improvement of disease current)
and increasing of patients’ tolerance to physical
load

15. ANTIANGINALANTIANGINAL ((CORONARYCORONARY
ACTIVEACTIVE)) DRUGSDRUGS
І.І. Nitrates and sidnonims which are close toNitrates and sidnonims which are close to
the first onesthe first ones
ІІ.ІІ. BetaBeta--blockersblockers
ІІІ.ІІІ. Calcium channel blockers (CCBs):Calcium channel blockers (CCBs):
ІУ.ІУ. Activators of potassium channelsActivators of potassium channels
• Hypercholesterolemia drugs
• Antiplatelets and anticoagulants
• Drugs with metabolic influence on miocardium

16. NITRATESNITRATES
nitroglycerinnitroglycerin
isosorbidisosorbid dinitratedinitrate
isosorbidisosorbid-5--5-mononitratemononitrate

17. MECHANISM OF ACTIONMECHANISM OF ACTION
OF NITRATESOF NITRATES
• Interaction with sulfhydryl (SH-) groups
(nitrate receptors) inside cells of vascular
smooth muscles
• Stimulation of formation of endothelial factor
of relaxation of vessels (ЕRF) – nitrogen
oxide (NO)
• Decreasing of ionized Са2+
contents
• Relaxation, dilation of vessels, including
coronary vessels

18. MECHANISM OF ACTIONMECHANISM OF ACTION
OF NITRATESOF NITRATES
• Decreasing of tone of venules – decreasing of preloading (income
of blood into heart during diastole) – decreasing of work of left
ventricle and heart output
• Decreasing of tone of arterioles – decreasing of afterloading
(decreasing of arterial pressure, end diastolic pressure in left
ventricle and it’s volume, decreasing of tension of myocardium wall
• decreasing of heart need in oxygen
• improvement of blood float in ischemic zone of myocardium –
redistribution of coronary blood circulation with increasing of
perfusion of subendocardial areas
• dilation of large coronary vessels if they are in spasm or narrowed
with aterosclerotic mass
• development of anastomoses between arteries in myocardium (in
case of prolonged administration)

19. NITROGLYCERINENITROGLYCERINE
• TabletsTablets (under the tongue)
• 1 % alcohol or oil solutionsolution (under the tongue)
• aerosolaerosol
Latent period - 2-3 min
Duration of action - 20-30 min
• ampoulesampoules 1 % solution – intravenously dropply
0,01% solution
• prolongedprolonged forms of nitroglycerine: trinitrolong,
sustak, nitrong, ointment, plaster

20. • Nitroglycerin is taken only when the
patient actually has symptoms or expect
to have them. Slow - or long-acting
nitroglycerin can be used as a
preventative treatment for angina but
not until beta blockers are tried first.

21. NitroglycerineNitroglycerine
Unique transdermal system in a form of plaster

22. SIDE EFFECTS OFSIDE EFFECTS OF
NITROGLYCERINENITROGLYCERINE
burstingbursting,, pulsating headachepulsating headache
decreasing of arterial pressuredecreasing of arterial pressure
((heartbeatheartbeat,, dizzinessdizziness,, collapsecollapse))
skin rednessskin redness,, feeling of feverfeeling of fever

23. Contraindications forContraindications for
nitroglycerine usenitroglycerine use
• Close-angled form of glaucoma
• increasing of intracranial pressure,
stroke
• acute myocardium infarction (in case of
presence of hypotension and collapse)

24. PROLONGED FORMS OFPROLONGED FORMS OF
NITROGLYCERINENITROGLYCERINE
• Trinitrolong – polymer films (0,001 g or 0,002 g of
nitroglycerine) action develops immediately, lasts for 3-5
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

25. Other nitratesOther 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

26. Iso Mak Retard 20mg
Iso Mak Retard 40mg
Isomak Retard 60mg
(isosorbid dinitrate)

27. IsoketIsoket
Isosorbid dinitrateIsosorbid dinitrate

28. SYDNONIMINSSYDNONIMINS
MolsidomineMolsidomine –– corvatoncorvaton --
sydnopharmsydnopharm
is metabolized in liver forming a substance – SIN-1a which contains free
NО group (doesn’t need previous interaction with SH-groups)
• nitrogen oxide stimulates guanilatecyclase that activates synthesis of cGMP
• cGMP causes dilation of vessels
2 mg of molsidomine= 0,5 mg of nitroglycerine

29. MolsidomineMolsidomine
• latent period - 20 min (5-10 min – if administered
sublingually), action duration - 6 hours.
• can be used for prophylaxis and releasing angina
attacks in patients with glaucoma (doesn’t
increase intraocular 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 drugs containing
SH- groups)
• absence of withdrawal syndrome

30. BETA-BLOCKERSBETA-BLOCKERS
Using in AnginaUsing in Angina
• blockade of β1
-adrenoreceptors of heart: decreasing of power
and frequency of heart contractions and as follows cardiac need
in oxygen
• decreasing of thrombocyte aggregation and prevention of clotts
formation
• increasing of diastole duration – improvement of coronary
vessels saturation with blood – improvement of perfusion of
ischemic areas of myocardium
• Decreasing of calcium ions accumulation – releasing of cardiac
muscle tension, improvement of metabolic processes, increasing
of ATP synthesis
• in case of acute myocardium infarction – increasing of blood
supply of ischemic areas of heart, decreasing of size of
infarction seat, prevention of development of cardiac
arrhythmias

31. AnaprilinAnaprilin
β1- β 2 adrenoblocker

32. VasocardinVasocardin 100100 mgmg
Methoprolol tartrateMethoprolol tartrate

33. NebivololNebivolol
beta-blocker that also causes vasodilation by stimulating the releasebeta-blocker that also causes vasodilation by stimulating the release
of nitric oxideof nitric oxide

34. • Beta blockers are taken every day,
regardless of whether the patient is
having symptoms, because they are
proven to prevent heart attacks and
sudden death.

35. Calcium channel blockers
1. Derivatives of difenilalkilamin (verapamil)
2. Derivatives of benzothiazepine
(dylthiazem)
3. Derivatives of dyhydropyridine (nifedipin,
amlodipin, nimodipin)
Drugs of 1 and 2 groups dominantly influence on heart
(depress automatism of sinus node, conductivity through
conductive heart system), show antiarrhythmic, antianginal
and hypotensive action.
Derivatives of dyhydropyridine (group of nifedipin) –
decrease blood pressure and cause dilation of coronary
vessels, cause reflective tachycardia

36. Calcium channel blockers
classification

37. NifedipinNifedipin -- corinfarcorinfar -- fenigidinfenigidin --
adalateadalate
Doesn’t depress conductivity in myocardium,
has a weak antiarrhythmic action
Maximal concentration of the drug in blood
occurs after 45-60 min after administration
orally and after 2-3 min – if administered
sublingually
Effect lasts for 4-6 hours

38. Antagonists of calcium ionsAntagonists of calcium ions – derivatives of
dyhydropyridine of ІІІІ generationgeneration
(amlodipinamlodipin, isradipin, nicardipin)
• almost don’t cause tachycardiaalmost don’t cause tachycardia
• areare indicated for prolonged treatment ofindicated for prolonged treatment of
patients with stable anginapatients with stable angina
• aren’t indicatedaren’t indicated in case of non stable anginain case of non stable angina
((long lasting latent periodlong lasting latent period))

39. Indications

40. Nifedipin
(Са2+
ions antagonist of dyhydropyrydine series)

41. Nifedipin
(

42. • Calcium channel blockers are used
primarily when beta blockers cannot be
used and/or the patient is still having
angina with beta blockers. Calcium
channel blockers also lower blood
pressure and certain ones slow heart
rate. Calcium channel blockers have to
be taken every day.

43. Common side effects of
calcium channel blockers
include:
• headache,
• constipation,
• rash,
• nausea,
• flushing,
• edema (fluid accumulation in tissues),
• drowsiness,
• low blood pressure, and
• dizziness.
• Sexual dysfunction, overgrowth of gums, and liver dysfunction also have
been associated with calcium channel blockers. Verapamil (Covera-HS,
Verelan PM, Calan) and diltiazem (Cardizem LA, Tiazac) worsen heart
failure because they reduce the ability of the heart to contract and pump
blood.

44. POTASSIUM-CHANNELPOTASSIUM-CHANNEL
ACTIVATORACTIVATORSS
NICORANDILNICORANDIL IkorelIkorel
• activates Са2+
-depending potassium channels
• causes relaxation of smooth muscles of vessels –
coronary, arteriolar and venous vasodilation
• improvement of blood supply of myocardium,
decreasing of pre- and afterloads of heart, decreasing
of myocardial need in oxygen, separation of ischemic
damage zone

45. Antiplatelet agents
Commonly prescribed include:
• Aspirin
• Ticlopidine
• Clopidogrel
• Dipyridamole

46. Acetylsalicylic acidAcetylsalicylic acid
• 80-100 mg per day – as antiplatelet drug,
decreases risk of development of acute myocardial
infarction and decreases mortality of patients with
IHD
• Helps prevent clotting in patients who have had a
heart attack, unstable angina, ischemic strokes,
TIA (transient ischemic attacks, or "little strokes")
and other forms of cardiovascular disease.
• Usually prescribed preventively when plaque
buildup is evident but there is not yet a large
obstruction in the artery.

47. Common types of cholesterol-
lowering drugs include:
• statins
• resins
• nicotinic acid (niacin)
• gemfibrozil
• clofibrate
• Various medications can lower blood cholesterol levels. They
may be prescribed individually or in combination with other
drugs. They work in the body in different ways. Some
affect the liver, some work in the intestines and some
interrupt the formation of cholesterol from circulating in
the blood.
Reason for Medication
• Used to lower LDL ("bad") cholesterol, raise HDL ("good")
cholesterol and lower triglyceride levels

48. Choose good nutrition
Reduce blood cholesterol
Lower high blood pressure
Be physically active every day
Aim for a healthy weight
Manage diabetes
Reduce stress
Limit alcohol
Stop smoking

49. ACUTE MYOCARDIALACUTE MYOCARDIAL
INFARCTIONINFARCTION
• one of the main reasons of disablement and mortality of
people of employed age in many world countries,
including Ukraine
• men suffer from MI almost 5 times more often than
women
• Mortality of patients with MI during first two hours
starting from the beginning of the process makes around
50 % of all mortal cases connected with MI
• the most often death causes – acute cardiac-vascular
insufficiency (angina pectoris, lung edema, cardiogenic
shock), heart rupture, heavy cardiac arrhythmia
• other complications of MI – thrombosis and emboli, acute
and chronic heart aneurisms, Dresler’s syndrome, chronic
cardiac insufficiency

50. TREATMENT OF MYOCARDIAL
INFARCTION
threethree stagesstages
• Immediate treatment – decreasing pain and treatment of
heart beats arrest
• Early treatment – separation of zone of infarction seat and
prevention of early life threatening complications (cardiac
arrhythmias, acute cardiac insufficiency)
• Further treatment – prevention and therapy of late
complications of MI, prophylaxis of recurrent MI and
death of the patients

51. TREATMENT OF ACUTE MYOCARDIALTREATMENT OF ACUTE MYOCARDIAL
INFARCTIONINFARCTION
Releasing of pain andReleasing of pain and
cardiogenic shock prophylaxiscardiogenic shock prophylaxis
• nitroglycerin (1 tablet under the tongue every 7-10 min.)
• Neuroleptanalgesia (fentanil with droperidol), morphine,
omnopon, promedol (in combination with atropine, dimedrol,
aminasine)
• nitrous oxide in combination with neuroleptics
• in case of remaining pain – non narcotic analgesics in
combination with antihistamine and neuroleptic drugs
• to increase arterial pressure during cardiogenic shock –
intravenously dropply dopamine (drugs of choice), noradrenalin,
mesaton
• sometimes glucocorticosteroids are used

52. TREATMENT OF ACUTE MIOCARDIAL
INFARCTION (cont’d)
Size limitationSize limitation
of infarction seatof infarction seat
• Intravenous dropply introduction of
0,01 % nitroglycerin solution
• Administration of β-blockers

53. TREATMENT OF ACUTE MYOCARDIALTREATMENT OF ACUTE MYOCARDIAL
INFARCTION (cont’d)INFARCTION (cont’d)
Treatment and prophylaxis of heartTreatment and prophylaxis of heart
arrhythmiasarrhythmias
Treatment of ventricular arrhythmias – i.v. slowly 0,2 %
solution of xycain, novocainamid intramuscularly
• Prophylaxis of ventricular extrasystole and tachycardia –
magnesium sulfate (intravenous dropping introduction of 4-
5 % solution),
β-adrenoblockers
• Arrhythmias of atrial origin – heart glycosides, antagonists
of calcium channels
• Bradycardia - isadrin, atropine sulfate, alupent (i.v.)

54. TREATMENT OF ACUTE MYOCARDIAL
INFARCTION (cont’d)
CORRECTION OF BLOOD CLOTTINGCORRECTION OF BLOOD CLOTTING
• thrombolytic drugsthrombolytic drugs
streptokinase (1,5 mln OD), urokinase (2 mln OD),
aktilise – recombinant tissue activator of plasminogen
(100 mg) intravenous
• after performing of thrombolytic therapy – intravenous
introduction of heparin, at first 10 000 OD, after 1000 OD
per hour during 24-48 hours
• anticoagulants of indirect actionanticoagulants of indirect action
• acetylsalicylic acidacetylsalicylic acid
(80-100-300 mg per day)

55. Treatment of heart insufficiencyTreatment of heart insufficiency
• i.v. furosemid (40-120 mg); i.v. dropply nitroglycerine (12-20 hours),
morphine
• i.v. dropply dopamin and dobutamin
• heart glycosides – in tachysystolic form of scintillating arrhythmia or
fluttering of atria with moderate left-ventricular insufficiency
General measuresGeneral measures
• oxygen inhalation
• correction of acid-base balance

58. ANTIARRHYTHMIC DRUGS
CLASS Mechanism of Action Drug name
IA Na+
Channel blocker Disopyramide, procainamide, quinidine
IB Na+
Channel blocker Lidocaine, mexiletine, tocainide
IC Na+
Channel blocker Flecainide, propafenone
II β Adrenoreceptor blocker Esmolol, metoprolol, pindolol,
propranolol
III K+
Channel blocker Amiodarone, bretylium, sotalol
IV Ca++
Channel blocker Diltiazem, verapamil
Other antiarrhythmic drugs Adenosine, digoxin