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TREATMENT OF ANGINA &
MYOCARDIAL INFARCTION
By: DR: Nida Ayesha
 Spasm/obstruction of coronary arteries
 Myocardial ischemia
 Reduced O2 supply to myocardium
 Chest pain---Angina pectoris
Angina pectoris
Chest pain due to ischemia of heart muscles
Weak relationship between severity of pain and degree
of oxygen supply- there can be severe pain with minimal
disruption of oxygen supply or no pain in severe cases
Four types:
Stable angina
Unstable angina
Microvascular angina
Prinzmetals angina
Stable or Classical
 It occurs due to increase myocardial oxygen
demand during exertion or emotion in a
patient of narrow coronary arteries. It
relieved by rest and nitroglycerine.
. However, when myocardial demand
increases, ischemia results.
N.A.N
Variant or Prinzmetals Angina
 Transient impairment of coronary blood
supply by vasospasm or platelet aggregation
 Majority of patients have an atherosclerotic
plaque
N.A.N
Prinzmetals Angina
 Spasm of a large coronary artery
 Transmural ischemia
 ST-Segment elevation at rest or with
exercise
 More prolonged than in classical angina.
 It occurs more in women under age 50.
N.A.N
Unstable angina:
Also called Crescendo angina
Acute coronary syndrome in which angina worsens
Occurs at rest
Severe and of acute onset
Crescendo pain- pain increases every time
Microvascular angina:
Also called Syndrome X
Cause unknown
Probably due to poor functioning of the small blood
vessels of the heart, arms and legs
No arterial blockage
Difficult to diagnose because it does not have arterial
blockage
Good prognosis
Major risk factors
 Age
 Smoking
 Diabetes Mellitus
 DyslipidemiaHypertension
 Obesity
 Chronic psychological stress
Angina pectoris & mi new
Symptoms
 What is the cause of ischemia ? Inadequate
blood supply and decreased oxygen supply
are directly related to blockade or narrowed
vessels either  oxygen demand or 
oxygen supply
 Aims of therapy
 Prevent disease progression (secondary
prevention)
 Control symptoms
Drugs:
1. For treatment of acute attacks:
Organic nitrates/nitrites
2. For prophylaxis:
Organic nitrates
Beta blockers
Calcium channel blockers
Ranolazine
Relaxation of vascular smooth muscles-
vasodilatation
NO-mediated guanylyl cyclase activation inhibits
platelet aggregation
Relaxation of smooth muscles of bronchi and GIT
Pharmacokinetics:
Orally ineffective because of high first pass metabolism
Administered sublingually to avoid first pass matabolism
Tolerance:
Repeated doses lead to tolerance
Dose spacing is necessary
Reasons for tolerance:
種 Capacity of vascular smooth muscle to convert
nitrates to NO  called true vascular tolerance
ADRs:
Headache- may be severe
May disappear after continued use or,
Decrease dose
Transient episodes of dizziness, weakness, pallor etc-
symptoms of postural hypotension
Rashes
severe hypotension
Uses: Angina pectoris, CHF, MI
Administration of nitrates:
Sublingual
Oral: For prophylaxis, require high doses due to first
pass metabolism, isosorbide dinitrate (20 mg or more)
every 4 h or mononitrate (20 mg or more) OD or BD
Cutaneous:
Ointment (2%) applied to 2.5-5 cm patch of skin
Transdermal nitrogycerine discs impregnated with
nitroglycerine polymer- gradual absorption and 24 h
plasma nitrate concentration
Onset is slow
Peak concentration in 1-2 h
Interrupt therapy for at least 8 h a day to prevent
tolerance
Ca2+ antagonists:
 Ca2+ influx
Negative iono and chronotropic effects
Peripheral vasodilatation
Used in variant angina (spasm), exertional angina,
unstable angina, MI, hypertension, antiarrhythmic
-Blockers:
Effective in reducing severity and frequency of
exertional angina
May worsen vasospastic angina- contraindicated
Reduce myocardial O2 demand by reducing cardiac
work (-ve iono and chrono effects; decrease in BP
during rest and exercise)
All -blockers are equally effective
-Blockers
Protective effect and symptom control
 All patients unless contraindicated
 Asthma (reversible airways obstruction)
 Severe peripheral vascular disease
 Heart block / bradycardia
 Hypotension
 Dose depends on effect (no specific dose)
 Avoid sudden withdrawal if possible
 Monitoring
 Effectiveness
 Heart rate (50-60 bpm if tolerated)
 Blood pressure
 Toxicity
 Side effects (often overemphasised)
 Cold extremities
 Nightmares
 Fatigue (especially on initiation)
 Wheeze
 Impotence
Ranolazine:
 Reserve agent for treatment of chronic, resistant
angina
 Inhibits cardiac late Na+ current
 Effects the Na+ dependent Ca2+ channels and
prevents Ca2+ overload that causes cardiac
ischemia
 Decreases cardiac contractility
 No change in HR, BP
 Prolongs QT interval so it is contraindicated with
drugs that increase QT interval
Myocardial infarction
 MI also known as Heart attack
 When blood flow decreases or stop causing
to a part of the heart, causing demage to the
heart muscle.
CRITERIA FOR ACUTE MI
 It should be used when there is evidence of
myocardial necrosis in a clinical settings
along with acute ischemia
 Detection of rise and fall of cardiac
biomarkers values
 Symptoms
 Significant st segments
CLINICAL FEATURES
 Chest pain
 Breathlessness
 Vomiting
 Collapse/ Syncope
 Anxiety
Diagnosis
 Biochemical marker of cardiac demage such
as Trop I &T
 ECG is the gold standard method
(Misleading when new bundle branch block or
previous MI)
 X-Ray chest shows pulmonary
edema/cardiomegaly
DIAGNOSIS
 CK more sensitive
 Start to rise at 4-6 hours,peak up to 12 hours
 Present in skeletal muscle
 Trop T & I are released within 4-6 hours &
remain elevated for up to 2 weeks
 leucocytosis peak on 1st day
 C-reactive & ESR are raised
MANAGEMENT
 Immediate manage the patient 1st 12 hours
 Pt should be admited urgently to the
hospital
 Analgesia- IV opiates, Morphine sulphate
 Anti emetic  Metoclopramide
 Anti thrombolitic therapy
Antithrombolitic therapy
 Antiplatelet & anticoagulants
 oralAspirin 75 -325mg daily,1st 12 hours
If any side effect seen combo of Aspirin with
Clopidogrel for 1 week.
ANTICOAGULANTS
 Reduce risk of thromboembolic
complications
 Prevent reinfections
 Aspirin LMW Heparin S/C BD
 Warfarin- persistant atrial fibrillation or
Echo show mobile mural thrombus.
COMPLICATIONS
 Transmural MI
 Arythmias
 Ventricular fibrillations
 Atrial fibrillations
 Bradycardia
 Embolism
 Acute circulatory failure
Late Management
 Life style modifications
 Diet (weight control)
 Stop smoking
 Regular excersise
SECONDARY PREVENTION
 Antiplatelet
 Beta blockersa
 Statin
 ACE inhibitors
 Control Diabetes /Hypertension
 Rehabilitation
 Devices: implantable cardiac debrillator
(high risk patient)
PROGNOSIS
 One quarter of all the case death occour
within few minutes without medical care
 Half of the patient death occour within 24
hour
 Prognosis is better who survive to reach
hospital is much better.

More Related Content

Angina pectoris & mi new

  • 1. TREATMENT OF ANGINA & MYOCARDIAL INFARCTION By: DR: Nida Ayesha
  • 2. Spasm/obstruction of coronary arteries Myocardial ischemia Reduced O2 supply to myocardium Chest pain---Angina pectoris Angina pectoris Chest pain due to ischemia of heart muscles
  • 3. Weak relationship between severity of pain and degree of oxygen supply- there can be severe pain with minimal disruption of oxygen supply or no pain in severe cases Four types: Stable angina Unstable angina Microvascular angina Prinzmetals angina
  • 4. Stable or Classical It occurs due to increase myocardial oxygen demand during exertion or emotion in a patient of narrow coronary arteries. It relieved by rest and nitroglycerine. . However, when myocardial demand increases, ischemia results. N.A.N
  • 5. Variant or Prinzmetals Angina Transient impairment of coronary blood supply by vasospasm or platelet aggregation Majority of patients have an atherosclerotic plaque N.A.N
  • 6. Prinzmetals Angina Spasm of a large coronary artery Transmural ischemia ST-Segment elevation at rest or with exercise More prolonged than in classical angina. It occurs more in women under age 50. N.A.N
  • 7. Unstable angina: Also called Crescendo angina Acute coronary syndrome in which angina worsens Occurs at rest Severe and of acute onset Crescendo pain- pain increases every time
  • 8. Microvascular angina: Also called Syndrome X Cause unknown Probably due to poor functioning of the small blood vessels of the heart, arms and legs No arterial blockage Difficult to diagnose because it does not have arterial blockage Good prognosis
  • 9. Major risk factors Age Smoking Diabetes Mellitus DyslipidemiaHypertension Obesity Chronic psychological stress
  • 11. Symptoms What is the cause of ischemia ? Inadequate blood supply and decreased oxygen supply are directly related to blockade or narrowed vessels either oxygen demand or oxygen supply
  • 12. Aims of therapy Prevent disease progression (secondary prevention) Control symptoms
  • 13. Drugs: 1. For treatment of acute attacks: Organic nitrates/nitrites 2. For prophylaxis: Organic nitrates Beta blockers Calcium channel blockers Ranolazine
  • 14. Relaxation of vascular smooth muscles- vasodilatation NO-mediated guanylyl cyclase activation inhibits platelet aggregation Relaxation of smooth muscles of bronchi and GIT
  • 15. Pharmacokinetics: Orally ineffective because of high first pass metabolism Administered sublingually to avoid first pass matabolism Tolerance: Repeated doses lead to tolerance Dose spacing is necessary Reasons for tolerance: 種 Capacity of vascular smooth muscle to convert nitrates to NO called true vascular tolerance
  • 16. ADRs: Headache- may be severe May disappear after continued use or, Decrease dose Transient episodes of dizziness, weakness, pallor etc- symptoms of postural hypotension Rashes severe hypotension Uses: Angina pectoris, CHF, MI
  • 17. Administration of nitrates: Sublingual Oral: For prophylaxis, require high doses due to first pass metabolism, isosorbide dinitrate (20 mg or more) every 4 h or mononitrate (20 mg or more) OD or BD Cutaneous: Ointment (2%) applied to 2.5-5 cm patch of skin
  • 18. Transdermal nitrogycerine discs impregnated with nitroglycerine polymer- gradual absorption and 24 h plasma nitrate concentration Onset is slow Peak concentration in 1-2 h Interrupt therapy for at least 8 h a day to prevent tolerance
  • 19. Ca2+ antagonists: Ca2+ influx Negative iono and chronotropic effects Peripheral vasodilatation Used in variant angina (spasm), exertional angina, unstable angina, MI, hypertension, antiarrhythmic
  • 20. -Blockers: Effective in reducing severity and frequency of exertional angina May worsen vasospastic angina- contraindicated Reduce myocardial O2 demand by reducing cardiac work (-ve iono and chrono effects; decrease in BP during rest and exercise) All -blockers are equally effective
  • 21. -Blockers Protective effect and symptom control All patients unless contraindicated Asthma (reversible airways obstruction) Severe peripheral vascular disease Heart block / bradycardia Hypotension
  • 22. Dose depends on effect (no specific dose) Avoid sudden withdrawal if possible Monitoring Effectiveness Heart rate (50-60 bpm if tolerated) Blood pressure Toxicity Side effects (often overemphasised) Cold extremities Nightmares Fatigue (especially on initiation) Wheeze Impotence
  • 23. Ranolazine: Reserve agent for treatment of chronic, resistant angina Inhibits cardiac late Na+ current Effects the Na+ dependent Ca2+ channels and prevents Ca2+ overload that causes cardiac ischemia Decreases cardiac contractility No change in HR, BP Prolongs QT interval so it is contraindicated with drugs that increase QT interval
  • 24. Myocardial infarction MI also known as Heart attack When blood flow decreases or stop causing to a part of the heart, causing demage to the heart muscle.
  • 25. CRITERIA FOR ACUTE MI It should be used when there is evidence of myocardial necrosis in a clinical settings along with acute ischemia Detection of rise and fall of cardiac biomarkers values Symptoms Significant st segments
  • 26. CLINICAL FEATURES Chest pain Breathlessness Vomiting Collapse/ Syncope Anxiety
  • 27. Diagnosis Biochemical marker of cardiac demage such as Trop I &T ECG is the gold standard method (Misleading when new bundle branch block or previous MI) X-Ray chest shows pulmonary edema/cardiomegaly
  • 28. DIAGNOSIS CK more sensitive Start to rise at 4-6 hours,peak up to 12 hours Present in skeletal muscle Trop T & I are released within 4-6 hours & remain elevated for up to 2 weeks leucocytosis peak on 1st day C-reactive & ESR are raised
  • 29. MANAGEMENT Immediate manage the patient 1st 12 hours Pt should be admited urgently to the hospital Analgesia- IV opiates, Morphine sulphate Anti emetic Metoclopramide Anti thrombolitic therapy
  • 30. Antithrombolitic therapy Antiplatelet & anticoagulants oralAspirin 75 -325mg daily,1st 12 hours If any side effect seen combo of Aspirin with Clopidogrel for 1 week.
  • 31. ANTICOAGULANTS Reduce risk of thromboembolic complications Prevent reinfections Aspirin LMW Heparin S/C BD Warfarin- persistant atrial fibrillation or Echo show mobile mural thrombus.
  • 32. COMPLICATIONS Transmural MI Arythmias Ventricular fibrillations Atrial fibrillations Bradycardia Embolism Acute circulatory failure
  • 33. Late Management Life style modifications Diet (weight control) Stop smoking Regular excersise
  • 34. SECONDARY PREVENTION Antiplatelet Beta blockersa Statin ACE inhibitors Control Diabetes /Hypertension Rehabilitation Devices: implantable cardiac debrillator (high risk patient)
  • 35. PROGNOSIS One quarter of all the case death occour within few minutes without medical care Half of the patient death occour within 24 hour Prognosis is better who survive to reach hospital is much better.