This document discusses various drugs used to treat angina. It outlines different classes of antianginal drugs including organic nitrates like nitroglycerin, beta-blockers, calcium channel blockers like verapamil, and ACE inhibitors. It provides details on the mechanisms and clinical uses of these drug classes and examples of medications within each class. Side effects are also summarized for several individual drugs.

1. ANTIANGINAL DRUGS. DRUGS REGULATINGANTIANGINAL DRUGS. DRUGS REGULATING
CEREBRAL CIRCULATIONCEREBRAL CIRCULATION

2. 22

3. AAntianginalntianginal AAgentsgents
1.Organic Nitrates1.Organic Nitrates
2. β-Blockers2. β-Blockers
3. Ca3. Ca2+2+
Channel BlockersChannel Blockers
4. Angiotensin-Converting Enzyme4. Angiotensin-Converting Enzyme
InhibitorsInhibitors
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4. 1. NITRATES:1. NITRATES:
NitroglycerinNitroglycerin –– Tab. 0.5 mg,Tab. 0.5 mg,
Caps. with 1% oil solution,Caps. with 1% oil solution,
Amp. 1%-2 ml, vial 1%- 5 mlAmp. 1%-2 ml, vial 1%- 5 ml
Nitrong-MiteNitrong-Mite –– Tab.Tab. 2.5 mg2.5 mg
Nitrong-ForteNitrong-Forte –– Tab.Tab. 6.5 mg6.5 mg
Sustac-MiteSustac-Mite –– Tab.Tab. 2.6 mg2.6 mg
Sustac-ForteSustac-Forte –– Tab.Tab. 6.4 mg6.4 mg
Isosorbide DinitrateIsosorbide Dinitrate –– Tab.Tab. 10 and 20 mg10 and 20 mg
Isosorbide MononitrateIsosorbide Mononitrate –– Tab.Tab. 10 and 20 mg10 and 20 mg
44

5. 55

6. NitroglycerinNitroglycerin -- Tab. 0.0005 g (0.5 mg)
Amp. 1%-2 ml, vial 1%- 5 ml
SLSL (or spray form)(or spray form) is considered to be the drug ofis considered to be the drug of
choice to treat Acute Angina.choice to treat Acute Angina.
 Acts withinActs within 1-2 min1-2 min;; peak blood level inpeak blood level in 3-6 min3-6 min
due to direct absorption into systemic circulationdue to direct absorption into systemic circulation
(bypassing liver where ~ 90% is metabolized).(bypassing liver where ~ 90% is metabolized).
The total duration of effect is brief -The total duration of effect is brief - 15–30 min15–30 min..
 The onset of action of forThe onset of action of for Sustained-Release FormSustained-Release Form
is withinis within 20-60 min20-60 min;;
Duration of action forDuration of action for
 Miter-formsMiter-forms –– 3-4 hours3-4 hours
 Forte-formsForte-forms –– 6-8 hours6-8 hours 66

7. 77

8. Clinucal uses of Nitroglycerine:Clinucal uses of Nitroglycerine:
 Prophylaxis and Control of Angina AttackProphylaxis and Control of Angina Attack
 IV Infusion in Myocardial InfarctionIV Infusion in Myocardial Infarction
 Pulmonary Stasis in Cardiac InsufficiencyPulmonary Stasis in Cardiac Insufficiency
Adverse Effects of Nitroglycerine:Adverse Effects of Nitroglycerine:
 Headache (30-60%)Headache (30-60%)
 Hypotension, TachycardiaHypotension, Tachycardia
 Facial FlushingFacial Flushing
 Tinnitus (Ringing in the Ears)Tinnitus (Ringing in the Ears)
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9. 99

10. Overdose With NitroglycerineOverdose With Nitroglycerine::
VASODILATIONVASODILATION andand METHEMOGLOBINEMIA -METHEMOGLOBINEMIA -
 Hypotension, Throbbing Headache, Palpitations,Hypotension, Throbbing Headache, Palpitations,
 Visual disturbances, Flushing of the skin,Visual disturbances, Flushing of the skin,
 Sweating (with skin later becoming cold and cyanotic),Sweating (with skin later becoming cold and cyanotic),
 Nausea and Vomiting, Colic, Bloody Diarrhea,Nausea and Vomiting, Colic, Bloody Diarrhea,
 Initial HyperpnoeaInitial Hyperpnoea (( in the Breathing Rate and/or in thein the Breathing Rate and/or in the
Depth of breathing)Depth of breathing), Dyspnoea,, Dyspnoea,
then Slow Respiratory Rate,then Slow Respiratory Rate,
 Bradycardia, Heart Block,Bradycardia, Heart Block,
  Intracranial Pressure with Confusion, Fever,Intracranial Pressure with Confusion, Fever,
Tissue Hypoxia (fromTissue Hypoxia (from MethemoglobinemiaMethemoglobinemia))
 Cyanosis, and Metabolic Acidosis, Coma, Clonic SeizuresCyanosis, and Metabolic Acidosis, Coma, Clonic Seizures
and Circulatory Collapseand Circulatory Collapse 1010

11. TreatmentTreatment of Overdose with NITROGLYCERINEof Overdose with NITROGLYCERINE::
 Gastric Lavage; Activated CharcoalGastric Lavage; Activated Charcoal
 Oxygen therapy (Hyperbaric Oxygenation)Oxygen therapy (Hyperbaric Oxygenation)
ANTIDOTESANTIDOTES::
 Ascorbic acidAscorbic acid 5%-10-15 ml5%-10-15 ml
++GlucoseGlucose 5% 500-8005% 500-800 ml IV infusionml IV infusion
 Methylene BlueMethylene Blue ((Methylenum ceruleumMethylenum ceruleum ) -) -
1% - 7-10 ml1% - 7-10 ml oror
 ChromosmonChromosmon --
1%1% Methylene blueMethylene blue in 25%in 25% GlucoseGlucose - 7-10 ml- 7-10 ml
SYMPTOMATIC TREATMENT:SYMPTOMATIC TREATMENT:
 Sodium hydrocarbonateSodium hydrocarbonate oror TrisamineTrisamine,,
 SulfocamphocaineSulfocamphocaine (10% 3-4 ml),(10% 3-4 ml), Mesaton,Mesaton,
 Noradrenaline hydrotartrateNoradrenaline hydrotartrate 0.2%-1 ml0.2%-1 ml
in Sol.in Sol.GlucoseGlucose 5%-500 ml IV infusion in collapse.5%-500 ml IV infusion in collapse.1111

12. β-Blockers:β-Blockers:
PropranololPropranolol (Anaprilin)(Anaprilin) (β(β11, β, β22) – tab. 10 and 40 mg) – tab. 10 and 40 mg
TimololTimolol (β(β11, β, β22) – tab. 0.01) – tab. 0.01;;0.020.02; eye drops; eye drops 0.5%-5 ml0.5%-5 ml
OxprenololOxprenolol (Trasicor) (β(Trasicor) (β11, β, β22) – tab. 20 and 80 mg) – tab. 20 and 80 mg
AtenololAtenolol (β(β11 ) –) – tab. 50 and 100 mgtab. 50 and 100 mg
MetoprololMetoprolol (β(β11 ) –) – tab. 50 and 100 mgtab. 50 and 100 mg
NadololNadolol (Corgard)(Corgard) (β(β11 ) –) – tab. 20; 40; 80 mgtab. 20; 40; 80 mg
LabetalolLabetalol (β(β11 , α, α11 ) -) - tab.tab. 0.10.1; 0,2;; 0,2; amp 1%-5 mlamp 1%-5 ml
CarvediolCarvediol (β(β11 , α, α11 ) –) – tab.tab. 12.5 and 25 mg12.5 and 25 mg
1212

13. CaCa2+2+
Channel BlockersChannel Blockers
I. DiphenylalkylaminesI. Diphenylalkylamines::
VerapamilVerapamil
II. DihydropyridinesII. Dihydropyridines::
1st
Generation:
Nifedipine (Adalat, Procardia)
2nd
Generation:
Amlodipine, Isradipine, Nicardipine
III. BenzothiazepinesIII. Benzothiazepines::
DiltiazemDiltiazem
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14. 1414

15. 1515

16. 1616

17. VerapamilVerapamil appears to have antianginal, antihypertensiveappears to have antianginal, antihypertensive
and antiarrhythmic action.and antiarrhythmic action.
It manages unstable and chronic stable angina by:It manages unstable and chronic stable angina by:

 AfterloadAfterload, thereby -, thereby -  OO22 ConsumptionConsumption..
It alsoIt also  myocardialmyocardial OO22 demand and cardiac work by:demand and cardiac work by:
 ExertingExerting Negative Inotropic EffectNegative Inotropic Effect --  Heart Rate:Heart Rate:
the drugthe drug slows Cardiac Conduction directlyslows Cardiac Conduction directly
 Relieving coronary artery spasmRelieving coronary artery spasm
 Dilating peripheral vesselsDilating peripheral vessels..
In patients withIn patients with Prinzmetal’s Variant AnginaPrinzmetal’s Variant Angina,,
VerapamilVerapamil inhibits coronary artery spasm, resulting ininhibits coronary artery spasm, resulting in
increased myocardial oxygen delivery.increased myocardial oxygen delivery.
Adverse EffectsAdverse Effects::
Myocardial Depression, includingMyocardial Depression, including Cardiac ArrestCardiac Arrest,,
Bradycardia, AV block, Hypotension, Heart Failure,Bradycardia, AV block, Hypotension, Heart Failure,
Constipation, Peripheral Edema.Constipation, Peripheral Edema.
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18. 1818

19. NifedipineNifedipine – functions mainly as an– functions mainly as an arteriolar vasodilatorarteriolar vasodilator..
It dilates systemic arteries, resulting in:It dilates systemic arteries, resulting in:
Total Peripheral ResistanceTotal Peripheral Resistance
 Systemic APSystemic AP with slightlywith slightly Increased Heart RateIncreased Heart Rate,,
 AfterloadAfterload,, and increased cardiac index.and increased cardiac index.
 The vasodilation effect ofThe vasodilation effect of NifidipinNifidipinee is useful in theis useful in the
treatment oftreatment of Variant AnginaVariant Angina caused by spontaneouscaused by spontaneous
coronary spasm.coronary spasm.
 InIn Prinzmetal’s anginaPrinzmetal’s angina,, NifedipineNifedipine inhibits coronary arteryinhibits coronary artery
spasm, increasing myocardialspasm, increasing myocardial Oxygen Delivery.Oxygen Delivery.
and peripheral edema as side effects of itsand peripheral edema as side effects of its vasodilationvasodilation
activityactivity..
Adverse effectsAdverse effects:: Flushing, Headache, Tachycardia,Flushing, Headache, Tachycardia,
Hypotension , Dizziness, Nausea,Hypotension , Dizziness, Nausea,
Constipation, Peripheral EdemaConstipation, Peripheral Edema
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20. AmlodipineAmlodipine is ais a DihydropyridineDihydropyridine compoundcompound ––
the 2the 2ndnd
GenerationGeneration long-acting Calong-acting Ca2+2+
antagonistantagonist..
It blocks the Inward Movement of CaIt blocks the Inward Movement of Ca2+2+
by binding toby binding to L-typeL-type
CaCa2+2+
channelschannels in the Heart and in Smooth Muscle ofin the Heart and in Smooth Muscle of
the Coronary and Peripheral Vasculaturethe Coronary and Peripheral Vasculature =>=>
=>=> Vascular Smooth Muscle RelaxationVascular Smooth Muscle Relaxation
Dilating MainlyDilating Mainly ARTERIOLESARTERIOLES..
The drug has anThe drug has an Intrinsic Natriuretic EffectIntrinsic Natriuretic Effect..
It hasIt has Antianginal,Antianginal, Hypotensive, VasodilativeHypotensive, Vasodilative andand
SpasmolyticSpasmolytic ActionAction
Clinical Use:Clinical Use:
 Arterial Hypertension,Arterial Hypertension,
 Stable and Unstable angina,Stable and Unstable angina,
 Prinzmetal’s or Variant Angina PectorisPrinzmetal’s or Variant Angina Pectoris..
Peak effects occur within 1-2 hours and persist for 24 hours.Peak effects occur within 1-2 hours and persist for 24 hours.
Adverse effectsAdverse effects:: headache, peripheral edema.headache, peripheral edema.
CaCa2+2+
channel blockerschannel blockers are useful in the treatment of patientsare useful in the treatment of patients
who also hawho also haveve ASTHMA, HYPERTENSION, DIABETESASTHMA, HYPERTENSION, DIABETES,,
andand/or/or PERIPHERAL VASCULAR DISEASEPERIPHERAL VASCULAR DISEASE.. 2020

21. The Angiotensin-Converting Enzyme (ACE) Inhibitors:The Angiotensin-Converting Enzyme (ACE) Inhibitors:
Captopril, Lisinopril, EnalaprilCaptopril, Lisinopril, Enalapril
block the ACEblock the ACE that cleavesthat cleaves Angiotensin IAngiotensin I to formto form
Angiotensin IIAngiotensin II – a potent vasoconstrictor.– a potent vasoconstrictor.
They alsoThey also  the rate ofthe rate of BRADYKININBRADYKININ inactivation.inactivation.
 Vasodilation occurs as a result of the combined effects ofVasodilation occurs as a result of the combined effects of
diminished levels ofdiminished levels of ANGIOTENSIN IIANGIOTENSIN II andand
the potent vasodilating effect of increasedthe potent vasodilating effect of increased BRADYKININ.BRADYKININ.
By reducing circulating angiotensin II levels, ACEI:By reducing circulating angiotensin II levels, ACEI:
 Aldesterone SecretionAldesterone Secretion, resulting in decreased Na+ and, resulting in decreased Na+ and
water retention.water retention.
 Unlike β-blockers, ACEIs are effective in the managementUnlike β-blockers, ACEIs are effective in the management
of patients with chronic CHF.of patients with chronic CHF.
 ACE inhibitors are now a standard in the care of a patientACE inhibitors are now a standard in the care of a patient
following a Myocardial Infarction.following a Myocardial Infarction.
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22. ANTIPLATELET DRUGSANTIPLATELET DRUGS
AspirinAspirin - 0.075 – 0.325 g daily- 0.075 – 0.325 g daily
 blocks formation of PGblocks formation of PG Thromboxan AThromboxan A22 (TXA(TXA22))
that causes platelets to change shape,that causes platelets to change shape,
to release their granules, and to aggregate.to release their granules, and to aggregate.
DipyridamoleDipyridamole is a coronary dilator,is a coronary dilator,
increases total coronary flow.increases total coronary flow.
 prevens uptake and degradation ofprevens uptake and degradation of
ADENOSINEADENOSINE which is a local mediatorwhich is a local mediator
involved in autoregulation of coronaryinvolved in autoregulation of coronary
flow in response to ischemia.flow in response to ischemia. 2222

23. CORONARY STEAL PHENOMENONCORONARY STEAL PHENOMENON
occurs when two branches fromoccurs when two branches from
the main coronary vessel havethe main coronary vessel have
different degrees of obstructiondifferent degrees of obstruction..
One branch may be relatively NORMALOne branch may be relatively NORMAL andand
capable of DILATINGcapable of DILATING in response to changes in Oin response to changes in O22
demand, while the OTHER BRANCHdemand, while the OTHER BRANCH IS UNABLEIS UNABLE..
If aIf a powerful arteriolar dilatorpowerful arteriolar dilator ((Acetylcholine, Adenosine,Acetylcholine, Adenosine,
Dipyridamole, HydralazineDipyridamole, Hydralazine) is administered,) is administered,
the arterioles in the unobstructed vessel will be forcedthe arterioles in the unobstructed vessel will be forced
to dilate =>to dilate =>  Resistance in the Normal BranchResistance in the Normal Branch andand
 Flow through the Adequately Perfused TissueFlow through the Adequately Perfused Tissue..
=>=> Perfusion PressurePerfusion Pressure in thein the main vesselmain vessel ,,
 flow through the obstructed brunchflow through the obstructed brunch
andand ANGINAANGINA maymay WORSENWORSEN.. 2323

24. Drugs for the Treatment ofDrugs for the Treatment of
Acute Myocardial InfarctionAcute Myocardial Infarction
The major principles treatment of AMIThe major principles treatment of AMI::
 Pain syndrome eliminationPain syndrome elimination
 Removal of Disparity between EnergeticRemoval of Disparity between Energetic
Demands of Myocardium and Blood SupplyDemands of Myocardium and Blood Supply
 Struggle with ThrombogenesisStruggle with Thrombogenesis
 Electrolytes and ACID-BASE EquilibriumElectrolytes and ACID-BASE Equilibrium
Correction.Correction.
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25.  NeuroleptanalgesiaNeuroleptanalgesia withwith
FentanylFentanyl 0.005% 2-4 ml0.005% 2-4 ml
DroperidolDroperidol 0.25%-1-4 ml0.25%-1-4 ml
- is a base of all schemes of anesthesia- is a base of all schemes of anesthesia
at Acute Coronary Syndrome.at Acute Coronary Syndrome.
 TheThe antiplatelet agent –antiplatelet agent – AspirinAspirin -- isis
administered at the first suspected signs ofadministered at the first suspected signs of
infarction.infarction.
AspirinAspirin prevents platelet aggregation and hasprevents platelet aggregation and has
an additional beneficial effect on thrombolysis.an additional beneficial effect on thrombolysis.
2525

26. THROMBOLYTIC THERAPY:THROMBOLYTIC THERAPY:
AlteplaseAlteplase oror StreptokinaseStreptokinase to dissolve theto dissolve the
thrombus pharmacologicallythrombus pharmacologically
HeparinHeparin is given to prevent a possibleis given to prevent a possible
vascular reocclusionvascular reocclusion
Treatment of life-threatening ventricularTreatment of life-threatening ventricular
arrhythmias calls for an antiarrhythmic ofarrhythmias calls for an antiarrhythmic of
the I class ofthe I class of NaNa++
channel blockerschannel blockers,,
e.g.,e.g., LidocaineLidocaine..
aa ββ-blocker-blocker and anand an ACE inhibitorACE inhibitor --
to improve long-term prognosis –to improve long-term prognosis –
prevention of ventricular enlargement afterprevention of ventricular enlargement after
myocardial infarctionmyocardial infarction 2626

27. 27
Agents Regulating Cerebral Circulation
I. Agents affecting the platelet aggregation and
coagulation
1. Antiaggregants (Antitplatelet Drugs):
Aspirin, Ticlopidine
2. Anticoagulants: Heparin
Low-molecular-weight Heparins:
Enoxaparine, Dalteparine
II. Agents Increasing Cerebral Circulation:
1. Derivatives of purine alkaloids -
methylxanthine derivatives:
Pentoxifylline
Xantinol nicotinate
Instenon

28. 28
2. Derivatives of Vinca alkaloids - derived from
the lesser periwinkle plant Vinca minor:
Vinpocetin (Cavinton)
3.Derivatives of Ergot alkaloids: ("Rye Ergot Fungus")
Nicergoline (Sermion)
4. Opioid alkaloid of isoquinoline range:
Papaverine hydrochloride
5. Ca2+
channel blockers:
Nimodipin, Cinnarisin, Flunarisine
6. GABA and its compounds:
Aminalone, Picamilone

29. 29
Pentoxiphylline - Tab. 0.1 g, amp 2%-5 ml -
a Methylxanthine derivative.
Mechanism of Action:
1). Inhibition of the enzyme PDE => accumulation of cAMP and
intracellular level of Ca2+
2). Blockade of Adenosine receptors
Pharmacological effects: dilation of cerebral vessels,
prevention the development of edema of the cerebral tissue.
● Inhibits aggregation of thrombocytes and improves
microcirculation in the zone of ischemia.
● Antianginal effect (O2 delivery to heart) is due to coronary
arteries dilatation.
● Improves blood oxygenation and prevents storage of
cholesterol and atherogenic lipoproteins in vessels wall,
improves rheological properties of blood.
Clinical uses: all types of hyperlipidemias,
disorders of cerebral and peripheral blood circulation of spastic

30. 30
Instenon is combined agents for the treatment of
Ischemic Cerebrovascular Diseases.
It contains: Methylxanthine Ethophylline,
Analeptic Etamivan
Spasmolytic Hexobendine.
The drug improves cerebral circulation, stimulates the CNS,
activates metabolism.
The important role in the mechanism of action of Instenon plays
inhibiting action of Ethophylline on PDE and as a result
accumulation cAMP in tissues that induces slowdown of
actomyosin complex and reduction of smooth muscle
contractility.

31. 31
Vinpocetin (Cavinton)
Tab. 5 mg, Amp 0.5%-2 ml
is an alkaloid derivative from
Periwinkle (Vinca minor).
● has spasmolytic properties and acts mainly on cerebral
vessels.
● possesses antiplatelet properties and decreases
pathologically high blood viscosity.
As a result the microcirculation improves.

32. 32
Nicergolin (Sermion) – Tab. 5 mg, 10 mg;
Vial 4 mg IM
combines the structures of
Ergot alkaloids and Nicotinic acid.
It has α-adrenoblocker and spasmolytic activities.
The drug dilates cerebral and peripheral vessels.
Adverse effects: hypotension, dizziness,
reddening of skin, pruritus,
dyspeptic disorders.

33. 33
Nimodipine (Nimotop)-
a Ca2+
channel blocker with mainly
influence on cerebral circulation.
It inhibits Ca2+
ion influx across cardiac and
smooth muscle cells, thus decreasing myocardial contractility
and oxygen demand, and dilates coronary, cerebral and
peripheral arteries and arterioles.
The drug dilates the small cerebral resistance vessels and
increases collateral circulation.

34. Thank you for attentionThank you for attention!!
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