Cardiology, Acute Coronay Syndrome (ACS), Angina, Myocardial Infarction (MI).

1. AcuteCoronary
Syndrome
DR. VINAYAK R. BHOI.
JR II MD MEDICINE,
Dept. of Medicine,
ACPM Medical College.

2. Ischaemic Heart Disease
 Ischemic heart disease (IHD) represents a group of
pathophysiologically related syndromes resulting from
myocardial ischemia—an imbalance between myocardial supply
(perfusion) and cardiac demand for oxygenated blood.
 In >90% of cases, myocardial ischemia results from reduced
blood flow due to obstructive atherosclerotic lesions in the
epicardial coronary arteries.
 IHD is frequently referred to as coronary artery disease (CAD).

3. IHD can present as one or more of the
following clinical syndromes:-
 Angina pectoris (literally means “chest pain”), where
ischemia is not severe enough to cause infarction, but
the symptoms nevertheless portend infarction risk.
 Myocardial infarction (MI), where ischemia causes
frank cardiac necrosis.
 Chronic IHD with heart failure.
 Sudden cardiac death (SCD).

4. Consequences of Myocardial Ischemia.
 The common feature of the acute coronary syndromes is downstream
myocardial ischemia.
1) Stable Angina:- results from increases in myocardial oxygen demand that
outstrip the ability of stenosed coronary arteries to increase oxygen
delivery; it is usually not associated with plaque disruption.
2) Unstable Angina:- is caused by plaque disruption that results in
thrombosis and vasoconstriction, and leads to severe but transient
reductions in coronary blood flow. In some cases, microinfarcts can occur
distal to disrupted plaques due to thromboemboli.
3) MI:- is often the result of acute plaque change that induces an abrupt
thrombotic occlusion, resulting in myocardial necrosis.
4) SCD:- may be caused by regional myocardial ischemia that induces a
fatal ventricular arrhythmia.

5. Risk Factors
Modifiable Non-Modifiable
 Increasing age
 Gender (male)
 Ethnicity
 Family History
 ? Diabetes
 Smoking
 Obesity
 Diet
 Lack of exercise
 High serum cholesterol
 Hypertension
 ? Diabetes

6. Activities precipitating angina

7. Pathogenesis
 The dominant cause of IHD syndromes is insufficient
coronary perfusion relative to myocardial demand; in
the vast majority of cases, this is due to chronic,
progressive atherosclerotic narrowing of the epicardial
coronary arteries, and variable degrees of
superimposed acute plaque change, thrombosis, and
vasospasm.

8. Coronary artery disease:- pathology

10. What is Acute Coronary Syndrome?
Stable Angina Unstable Angina NSTEMI STEMI

11. Acute Coronary Syndromes (ACS)
 This syndrome includes:-
 unstable angina
 ST elevation MI
 non-ST elevation MI (NSTEMI).
 ACS is a spectrum of disease characterised by either one of the
following:
1) New-onset angina,
2) Angina at rest,
3) Progression of angina of increasing frequency or severity,
4) Angina in response to lower levels of exertion.
 ACS most often represents acute atherosclerotic plaque rupture with
exposure of thrombogenic sub-endothelial matrix. Thrombus formation,
which may be episodic in nature and it is the mechanism by which it
interferes with coronary blood flow.

13. Unstable Angina
 It is due to dynamic obstruction of coronary artery, spasm and or
rupture of plaque.
 It is defined as angina pectoris or equivalent ischaemic discomfort
with either one feature:-
1) It occurs at rest or with minimal exertion usually lasting > 10 min.
2) It is severe and of new onset within the prior 4-6 weeks.
3) It has a crescendo pattern of pain – distinctly severe, prolonged and
more frequent than before.
 Unstable angina is distinguished from by the absence of elevated
serological markers of myocardial necrosis. It is also distinguished
from ST-elevation MI by the absence of persistent ST segment
elevation.

14. Unstable Angina
 The following three patient groups may be said to have unstable
angina pectoris:-
1) Patients with new onset (< 2 months) angina that is severe and/or
frequent (>) 3 episodes/d
2) Patients with accelerating angina, that is, those with chronic
stable angina who develop angina that is distinctly more frequent,
severe, prolonged or precipitated by less exertion than previously.
3) Those with angina at rest.
 When unstable angina is accompanied by objective ECG evidence
of transient myocardial ischaemia, it is associated with critical
stenosis in one or more major epicardial coronary arteries in about
85%.

15. NSTEMI & ST Elevated MI
 NSTEMI Includes
 Unstable Angina +
 Evidence of Myocardial Necrosis(Cardiac Biomarkers)+/-
 Non-specific ECG changes (ST depression / T
inversion/normal)
 STEMI:
 Sustained chest pain s/o AMI
 ECG changes s/o Acute ST elevation or new LBBB.

16. Cascade of Atheromatous
Plaque, Thrombus
Formation & Myocardial
Ischaemia

17. Epithelial Injury
Migration of monocytes/macrophages
LDL lipids consumed  foam cells
Growth factors  smooth muscle, collagen, proteoglycans
Atheromatous plaque forms
Chronic plaque occluding the vessel lumen

18. Rupture, fissuring, ulceration, haemorrhage or sudden disruption of plaque
Platelets adhere, aggregate, become activated
Release of various mediators & activation of coagulation cascade
Vasospasm & Thrombus Formation
Incomplete or complete occlusion of vascular lumen

19. Insufficient coronary perfusion relative to myocardial demand
ISCHAEMIC HEART DISEASE

20. Coronary Artery
Calibre Changes In
Classical & Varient
Angina

21. Sub-endocardial Crunch In Angina

22. Cascade of mechanism & manifestation of
ischaemia

23. Distinguishing features
 UA:
platelet
adhesion
 NSTEMI:
platelet
aggregation
 STEMI:
complete
occlusion
 SA:
plaque
formation
 At rest or minimal exertion
 Lasts >20 minutes
 Often accompanied by other s/s
 Poor GTN relief
 Precipitated by stress or
exertion
 Lasts <20 minutes
 Relieved by GTN / resting

24. Factors influencing myocardial oxygen supply and
demand

25.  Clinical features:- Symptoms
 Dyspnoea
 Palpitations
 Chest pain
 Nausea
 Acute confusion
 Sweating
 Vomiting
 Syncope
 Anxiety or fear of
impending death

26.  Signs
 Impaired myocardial function:-
 Hypotension, oligouria, cold peripheries
  JVP, narrow pulse pressure
 S3, Heart murmurs
 Sympathetic activation:-
 Pallor,
 Sweating,
 Tachycardia
 Vagal activation:-
 Bradycardia
 Vometing
 Asymptomatic/silent
 Tissue damage:- Fever
 Complications:- Arrythmia,
MR, Pericarditis

27. Angina Pectoris (Chest Pain)
 A discomfort in the chest and adjacent area due to
myocardial ischaemia.
 It is due to a discrepancy between myocardial oxygen
demand and supply.

28. Characteristics of
Anginal Pain

29. Site Substernal or Retrosternal
Nature
Pressing, squeezing, strangling,
constricting, ‘a band across the chest’,
‘a weight in the centre of the chest’.
The patient cannot pinpoint the site of
pain.
Radiation
To both the shoulders, epigastrium,
back, neck, jaw, teeth. Anginal pain
can radiate in all directions, as
mentioned above, but more commonly
radiates to the left shoulder and ulnar
aspect of the left arm.
Duration 5 to 15 minutes
Aggravating Factors
Exertion, emotion, after a heavy meal,
or exposure to cold
Relieving Factors Rest, nitrates.

30. Differential Diagnosis
Cardiac
• MI
• Angina
• Pericarditis
• Aortic dissection
Respiratory
• Pulmonary embolism
• Pneumothorax
• Pneumonia
GI
• Oesophageal spasm
• GERD
• Pancreatitis
Musculoskeletal
• Costochondriasis
• Trauma
Chest pain

31. Anginal Equivalent
Anginal equivalents are symptoms of
myocardial ischaemia other than angina such as
dyspnoea, faintness, fatigue and eructations.
They are precipitated by exertion and relieved
by rest and nitrates.

32.  In 1959 Prinzmetal et al. described a syndrome of severe
ischemic pain that usually occurs at rest and is usually associated
with transient ST-segment elevation or depression.
 Prinzmetal’s variant angina (PVA) is caused by focal spasm of an
epicardial coronary artery, leading to severe transient myocardial
ischemia and occasionally infarction. The cause of the spasm is
not well defined, but it may be related to hypercontractility of
vascular smooth muscle due to adrenergic vasoconstrictors,
leukotrienes, or serotonin.
Prinzmetal Angina

33. Nocturnal Angina
Angina occurs during sleep at night due to
coronary ostial stenosis, as seen in
cardiovascular syphilis.

34. Second Wind Angina
 It occurs on initial exertion, but then subsides without
the patient resting only to sometimes recur with
continuing exertion. It is not uncommon and may
cause diagnostic confusion.
 Levine Test:-
Relief of anginal pain by carotid sinus massage.

35. Evaluation of Pts
With Known or
Suspected IHD

36. Investigations
Bedside Observation, ECG, BP Monitoring
Blood
CBC, Urine, RFT, LFT, Lipids, Cardiac enzymes,
Amylase, CRP
Imaging CXR
Special
2D-Echo, Angiography, Stress Test, Myocardial
Perfusion Scan
* ST elevation is >1mm in limb leads and >2mm in chest leads

37. Troponin & ECG Changes in IHD
UA NSTEMI STEMI
Normal troponin Raised troponin Raised troponin
* ECG normal
* Possible ST
depression
* ST depression
* Can be normal
* Possible T wave
inversion
* ST elevation
* Hyperacute T
waves
* New LBBB
* T inversion (hours)
* Q waves (days)

38. Important ECG findings

39. Cardiac Biomarkers

40. Cardiac Biomarkers

41. Forms of exercise-induced ST depression(Stress Test)
A) Planar ST depression is usually indicative of myocardial ischaemia.
B) Downsloping depression also usually indicates myocardial ischaemia.
C) Up-sloping depression may be a normal finding.
STRESS TEST

42. The resting 12-lead ECG shows
some minor T-wave changes in
the inferolateral leads but is
otherwise normal. After 3
minutes’ exercise on a treadmill,
there is marked planar ST
depression in leads V4 and V5
(right offset). Subsequent
coronary angiography revealed
critical three-vessel coronary
artery disease.
A positive Exercise(Stress) Test (chest leads)

43. A myocardial perfusion scan
showing reversible anterior myocardial
ischaemia. The images are cross-sectional
tomograms of the LV. The resting scans
(left) show even uptake of the
99technetium-labelled tetrofosmin and
look like doughnuts. During stress (e.g. a
dobutamine infusion), there is reduced
uptake of technetium, particularly along
the anterior wall (arrows), and the scans
look like crescents (right).

44. Algorithm For Evaluation & Management of Pts With
Suspected ACS

45. Algorithm For
Management of
the Pt with IHD

46. Risk Stratification in ACS : The GRACE Score

47. Scoring systems
GRACE scoring
 Predicts 6/12 mortality in
NSTEMI patients
 Age
 HR and systolic BP
 Killip class (CCF,
pulmonary oedema, shock)
 Cardiac arrest on
admission
 Elevated cardiac markers
 ST segment change
TIMI
 Risk of cardiac events in
next 30 days
 Age >65
 Known coronary artery
disease
 Aspirin in last 7/7
 Severe angina (>2 in
24hr)
 ST deviation >1mm
 Elevated troponins
 > CAD risk factors

48. Risk stratification in stable
angina

49. Treatment of Acute Coronary Syndrome

51. Common ACS management
 Morphine (2 - 5mg slow IV injection),
 Oxygen (titrate SpO2 94-98%),
 Nitrates - GTN spray (400mcg = 1 spray) or tablet
(1mg),
 Aspirin (300mg chewed),
 Plus an antiemetic i.e.
Metoclopramide 10mg IV,
 Supportive Care.

52. Unstable angina & NSTEMI
 LMWH i.e. Enoxaparin 1mg/kg BD or Fondaparinux
2.5mg OD
 Clopidogrel 300mg loading dose
 Beta blocker - atenolol 5mg
 Nitrates – usually IV
 Consider coronary angiography within 72 hr

53. Advice to patients with stable
angina

54. Antianginal Drugs(Anti Ischaemic ℞)
1) Nitrates:-
a) Short acting:- Glyceryl trinitrate (GTN, Nitroglycerine)
b) Long acting:- Isosorbide dinitrate (short acting by sublingual route),
Isosorbide mononitrate, Erythrityl tetranitrate, Pentaerythritol tetranitrate
2) β Blockers:- Propranolol, Metoprolol, Atenolol and others.
3) Calcium channel blockers:-
a) Phenyl alkylamine:- Verapamil
b) Benzothiazepine:- Diltiazem
c) Dihydropyridines:- Nifedipine, Felodipine, Amlodipine, Nitrendipine,
Nimodipine, Lacidipine, Lercanidipine, Benidipine
4) Potassium channel opener:- Nicorandil
5) Others Dipyridamole, Trimetazidine, Ranolazine, Ivabradine, Oxyphedrine

55. Nitrates
 Administer Sublingually, if symptoms persists consider IV
 C/I :-
• Hypotension,
• Pt on PDE-5 Inhibitors
 Topical, oral, or buccal nitrates are acceptable alternatives
for patients without ongoing or refractory symptoms.
 5–10 μg/min by continuous infusion titrated up to 75–100
μg/min until relief of symptoms or limiting side effects
(headache or hypotension with a systolic blood pressure <90
mmHg or more than 30% below starting mean arterial
pressure levels if significant hypertension is present)

56. Nitrate Therapy in Pts with IHD

57. β Blockers
 Clinical Condition:- Unstable angina
 C/I :-
 PR interval (ECG) <0.24 sec
 2° or 3° AV Block
 HR <60 beats/min
 Systolic Pressure < 90 mmhg
 LVF
 Shock
 Severe Reactive Airway Disease
 Dose:-
 Metoprolol 25–50 mg by mouth every 6 h
 If needed, and no heart failure, 5-mg increments by slow (over 1–2
min) IV administration.

58. Calcium channel blockers
 Patients whose symptoms are not relieved by
adequate doses of nitrates and beta blockers, or in
patients unable to tolerate adequate doses of one or
both of these agents, or in patients with variant
angina.
 C/I :-
 Pulmonary Edema
 LV Dysfunction (Diltiazem, Verapamil)
 Dose:- Depends on specific agent.

59. Morphine sulfate
 Patients whose symptoms are not relieved after three
serial sublingual nitroglycerin tablets or whose
symptoms recur with adequate anti-ischemic therapy.
 C/I :-
 Hypotension,
 Respiratory Depression,
 Confusion,
 Obtundation.
 Dose:- 2 – 5 mg IV
 May be repeated every 5–30 min as needed to relieve
symptoms and maintain patient comfort.

60. Antithrombotic Therapy
Antiplatelets
Anticoagulants

61. Oral Antiplatelet Therapy
 Aspirin:- COX - Inhibitor
 Initial dose of 325 mg nonenteric formulation followed by
75–100 mg/d of an enteric or a nonenteric formulation
 Clopidogrel:- P2Y12 Inhibitor
 Loading dose of 300–600 mg followed by 75 mg/d
 Prasugrel:- P2Y12 Inhibitor
 Pre-PCI: Loading dose 60 mg followed by 10 mg/d
 Ticagrelor:- Reversible P2Y12 Inhibitor
 Loading dose of 180 mg followed by 90 mg twice daily

62. Intravenous Antiplatelet Therapy
GPIIb/IIIa Inhibitors
 Abciximab:-
 0.25 mg/kg bolus followed by infusion of 0.125 μg/kg
per min (maximum 10 μg/min) for 12–24 h
 Eptifibatide:-
 180 μg/kg bolus followed 10 min later by second
bolus of 180 μg with infusion of 2.0 μg/kg per min for
72–96 h following first bolus
 Tirofiban:-
 25 μg/kg per min followed by infusion of 0.15 μg/kg
per min for 48–96 h

63. Anticoagulants:- Heparins
 Unfractionated heparin(UFH):-
 Bolus 70–100 U/kg (maximum 5000 U) IV followed by
infusion of 12–15 U/kg/h (initial maximum 1000 U/h)
titrated to ACT 250–300 s
 Enoxaparin:- LMWH
 1 mg/kg SC every 12 h; the first dose may be preceded
by a 30-mg IV bolus; renal adjustment to 1 mg/kg OD
if creatine clearance <30 cc/min

64. Anticoagulants
Fondaparinux:- Indirect Factor Xa Inhibitor
2.5 mg SC qd
Bivalirudin:- Direct Thrombin Inhibitor
Initial IV bolus of 0.75 mg/kg and an
infusion of 1.75 mg/kg per/h

65. Invasive Interventions
PCI
Following treatment with anti-ischemic and
anti-thrombotic agents, coronary arteriography
is carried out within ∼48 h of presentation,
followed by coronary revascularization (PCI or
coronary artery bypass grafting), depending on
the coronary anatomy.

66. Long-term management
 Continuous ECG monitoring as inpatient/ CCU
 Aspirin 75mg OD (lifelong)
 Clopidogrel 75mg (1 year)
 Beta blocker (1 year - lifelong)
 ACE inhibitor/ ARB’s
 Statins
 Modification of risk factors

67. Complications
Early <72hr
 Death
 Cardiogenic shock
 Heart failure
 Ventricular arrhythmia
 Myocardial rupture
 Thromboembolism
Late
 Ventricular wall rupture
 Valvular regurgitation
 Ventricular aneurysms
 Cardiac tamponade
 Dresslers syndrome
 Thromboembolism

68. THANK YOU