Angina and myocardial infarction are caused by reduced oxygen supply to heart muscles due to coronary artery spasm or obstruction. Angina presents as chest pain and comes in different types based on triggers and severity. It is treated with nitrates, beta blockers, calcium channel blockers, and ranolazine to prevent symptoms and disease progression. Myocardial infarction, also called a heart attack, occurs when blood flow decreases or stops to the heart, damaging the heart muscle. It is diagnosed through cardiac biomarkers and ECG and managed initially with analgesics, anticoagulants, and antiplatelet drugs, followed by lifestyle modifications and secondary prevention medications long-term.
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
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.
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.