Heart disease is a leading cause of death worldwide. A heart attack occurs when blood flow to the heart is blocked, killing heart muscle tissue. In India, there are an estimated 30 million people with coronary artery disease and 3 million die each year from heart attacks. Kerala has 40,000-50,000 cardiac deaths annually, most under age 40, and 82% occur in those with low incomes. Thiruvananthapuram has the highest rate of heart disease in Kerala.

2. Heart Attack
 It account for almost 30% of all death in a year
 16 million people die due to CVD world wide
 In India there are a projected 3o million people
with CAD & 3 million die every year due to MI
 A Heart attack is essentially the death of the
Heart

3. കേരളത്തില്....
• പ്രതിവര്ഷം 40000-50000 മരണം
• 30%- 40yrs താഴെ.
• 10% േുെഞ്ഞുവീണു മരണം.
• 82% േുറഞ്ഞ വരുമാനക്കാരില്.
• തിരുവനന്തരുരമാണ്
ഴോകറാണറിഹൃകപ്രാഗത്തി
ന്ഴറ തലസ്ഥാനം

4. ISCHEMIC HEART

6. IHD
 IHD implies
that Coronary
blood supply
to the
myocardium is
inadequate as
compared to
its demand.

7. ISCHEMIC HEART DISEASE
 DEFINITION :-
• IHD is defined as myocardial impairment due to
imbalance between coronary blood flow &
myocardial requirement.
• Imbalance between oxygen supply & Demand

8. Aethiology
• 1. Atherosclerosis
• 2.Arteritis
• 3.Embolism
• 4.Coronory mural thickening
• 5.Congenital
• 6.coronary artery spasm with out
sclerosis
• 7.vegetations of B E
• 8.LVH

9. Risk Factors
Modifiable &
Non Modifiable

10. Modifiable Risk Factors
• Hyper Lipidemia
• Diet
• Hypertension
• Smoking
• Obesity
• Physical inactivity
• Diabetes
• stress

11. Non Modifiable Factors
• Hereditary- F/H
• Age> 35
• Sex-M>45, F>55

12. Coronary Risk Factors
• DM
• Hyper lipidemia
• HPTN
• Smoking
• Obesity
• Low veg . food
• Alcoholism
• BMI <23-25
• ↑CRP , Homocysteine
In KERALA
87 lakhs-HPTN
34 lakhs- DM
Hyper lipid- (M)52%
- (F)61%

13. Pathogenesis
• Occlusion of coronary arteries
• as a result of lipid deposition within the
intima of the coronary arteries  narrowing
of lumen of the arteries & diminution of
blood supply to the myocardium

14. Grading of occlusion
• Gr.1- Mild Occlusion- (50-60 %)- Sub clinical
• Gr.2- Moderate Occlusion (>70%)-Angina
on effort (SA)
• Gr.3- Threatening (90%)- unstable Angina
• Gr.4- Total occlusion (100%)- Infarction.

16. ? Presentation
• AP (90%)
• A M I
• Sudden Death
• CCF / LVF
• Arrhythmias
• Conduction Defects
• Autonomic Disturbances-N,V,S etc……

17. Keep in mind
• Only 10-20% Patient admitted in CCU with
chest pain might be due to Heart attack.
• The development of symptoms may not
closely related to the pathology of the
Atherosclerotic plaques ??

18. ANGINA
PECTORIS
‘ Angina ‘ = Strangulation
Pectoris= Pectoral
muscles

19. ANGINA PECTORIS
• It’s a clinical syndrome
characterized by sudden attack
of chest pain, of short duration,
precipitated by physical
exertion & relieved by rest / by
Sublingual Nitrates.

20. CAUSES OF ANGINA
• Reduced Myocardial Oxygen supply
• * Coronary Artery Disease
• * Severe Anemia
• * Increased Myocardial Oxygen demand
• * Left Ventricular Hypertrophy-
• Hypertension
• AS /AR
Hypertrophic Cardio myopathy
• Rapid Tachy arrhythmias

21. Precipitating factors
• Physical exertion
• Drugs
• Stress
• Tachycardia
• Heavy meals
• Exposure to cold

22. ??PAIN

23. Sensation as if…
• Dull /aching
• Strangling / Choking /
• Squeezing / Sharp cutting
• Lump in Chest
• Pressure/ Tightness / Heaviness /shortness of
breath
• Difficult to express the
• discomfort, as if a weight had lay down over
the chest

24. In Arms and
Wrists as…
-- Numbness
Sensationas if

25. ? LOCATION
• Retro / Sub sternal
• --- Trans- sternal
• --- Neck, jaw, Throat
• --- Back, Shoulder,
• --- inter scapular,
• --- Arm , fingers
• --- Abdomen ( Anginal equivalent)

26. Radiation of Anginal Pain
• Usually Retro sternal & commonly radiates
along either shoulders…
• To the ulnar aspect of the Arm ( More
commonly on the left side) , up to fingers
• Sometimes to the Neck& back ie.
Infra scapular region
• Occasionally at sites like epigastria , molar
teeth & the jaw

27. Radiation of Anginal Pain
• ??? Intensity and duration ???
•
• Variable in
• ischemia and
• Infarction ??

28. Duration Of Angina ??
• It usually lasts for 1 to 3 minutes (10-
30 mts /even hours)
• < 30 mts.
• It subsides either spontaneously with
rest or after administration of Nitrates
• < by emotion, sexual intercourse ,
heavy meal, cold weather, at night

29. Physical signs- concomitant
• In most cases there are no abnormal
physical signs
• During or in between the episodes
of angina, in some cases there may
be pallor, sweating, & hypotension .

30. O/ A, during the attack
• Apical systolic murmur due to papillary
muscle dysfunction may be heard
• Evidence of LVH , secondary to HPTN ,
valvular disease etc may be present.
• With Pain BP may be high
• 3rd/4th HS.

32. • Mainly 3 Anginal Syndromes are recognized
• each associated with characteristic coronary
pathology
• Stable Angina
• Unstable Angina
• Variant Angina
• Silent Angina/Ischemia
• (p/c :- vertigo/nausea/dyspnoa / PUD like,
sweating, vomiting, weakness=Anginal equlence

33. 1. STABLE ANGINA
CAUSES:-
• Commonest – Coronary Atheroma
( Atherosclerosis)
Others –
•Aortic stenosis
•Aortic incompetence
•Syphilitic Aortitis
•Polycythemia vera
•Rapidly developing anaemia

34. STABLE ANGINA
CLINICAL FEATURES
• Characterized by Retro-sternal ,constricting
Discomfort , which may radiate to either arms ,
throat or jaw
• Associated with shortness of breath
• Precipitated by exertion or other forms of stress
• Promptly relieved by rest
CAB↓50-60%=SC
CAB= > 70%-> s/s

35. PHYSICAL EXAMINATION
• Frequently Negative
• During attacks of pain-
• - Elevation of BP
• - 3 rd / 4 th heart sounds
• - Evidence of Mitral Incompetence due to
papillary muscle dysfunction may be seen

36. DIAGNOSIS
• By taking History
• Resting ECG may be normal
• Most common ECG change
are- Non specific ST-T wave
changes with or without
abnormal Q waves
• Depression or elevation of S-
T segment– Diagnostic of
Angina
S-T Depression
S-T Elevation

37. 2. UNSTABLE ANGINA
• It is a clinical syndrome characterized by new
onset or rapidly worsening Angina on minimal
exertion, or angina at rest
• This condition shares common patho
physiology mechanisms with Acute MI
• The term ‘ Acute Coronary Syndrome ‘ used
to describe these collectively CAB= > 90%

38. Common cause of USA
• Sub occlusive
coronary
thrombosis
• Rupture of
atheromatous
plaque
embolism
• (recurrent &
prolonged angina)

39. Mode of presentation
• Not related to physical exertion
• More severe & longer duration & does not
show any satisfactory response to rest/drugs.
• It is associated with more severe degree of
atherosclerosis

40. CLINICAL & LAB FINDINGS
• Abrupt & progressive reduction in the Threshold
of physical activity required to provoke angina….
Considered as the warning for the onset of
Unstable Angina
• Rest angina / Nocturnal Angina
• Radiation of pain to additional site
• Onset of associated symptoms such as Nausea,
Vomiting, Sweating, Palpitation, & Dyspnea are
taken as suggestive symptoms

41. Physical Examination
• Transient 3 rd & 4 th heart sounds
• Dyskinetic apical impulse
suggesting Left Ventricular
Dysfunction
•Transient Murmur of Mitral
Regurgitation
•There may be Hypotension during
the episodes of pain adverse
prognosis

42. ELECTROCARDIOGRAM
• ST segment depression &
T wave changes
• New ST segment
deviation of only 0.05mV,
is specific & important
measure of Ischemia &
prognosis
• T wave changes –
sensitive , but non-specific
of acute Ischemia
• Transient inverted ‘U’
waves
ST segment
Depression
ST segment
Elevation

43. ST DEPRESSION
Normal ECG

44. 3.PRINZMETALS ANGINA / VARIANT ANGINA
• First described by Prinzmetals in 1959
• An unusual syndrome of severe cardiac
pain secondary to MI , that occurs
exclusively at rest , usually at the same
time of the day/night, with normal
exercise capacity
• not precipitated by physical exertion or
emotional stress

45. PRINZMETALS ANGINA/ VARIANTANGINA
• Associated with ST segment elevation in
ECG, which disappears on cessation of pain
• May be associated with acute MI, severe
cardiac arrhythmia (including ventricular
tachycardia & fibrillation) and sudden death

46. Pathogenesis
1. Hyper contractility of arterial wall ,
associated with atherosclerotic
process itself
2. Endothelial injury
Risk factors :-
• cigarette smoking
• Use of cocaine
• Hyper insulinaemia
• Insulin resistance

47. Clinical Features
• Anginal discomfort is
Extremely severe.
Arrhythmias
It may be accompanied by
syncope & Sudden Death
• Occasionally Angina
accompanied by other vaso
spastic disorders like
migraine & Raynaud’s
disease

48. ECG
• Elevation of ST segment
during pain
• Conduction disturbances
& Ventricular
Arrhythmias may occur
during the anginal attacks
Elevation of ST
segment

49. Prognosis
• Long term survival is good
• Survival at 5 years = 89-97%
• The extent & activity of coronary artery
disease have adverse influence on
prognosis for long term survival &
freedom from M I.
• Patients with Variant Angina are at
higher risk of Sudden Cardiac
Death

50. Management
• In Prinzmetal Angina –
Nitrates are beneficial ;
action being exclusively
direct vasodialating effect
of spastic coronaries
• Calcium Antagonists –
very effective in preventing
the coronary artery spasm
of variant angina & used in
maximally tolerated doses

51. Management
Of Angina Pectoris
General Measures
• Reassurance of the patient
• Modifiable risk factors- avoided
• Control of exacerbating conditions

52. prevention
• Primordial prevention- childhood onwards-
obesity, smoking, exercise, dhyan, yoga
• Primary prevention-life style modification= DM,
HPTN, LIPIDS, obesity, sedentary life style ,
smoking, stress ,
• Secondary prevention- AFTER FIRST ATTACK
• TIME IS MUSCLE-1st hr= Golden hr.
• CPR= 60times/mts.
• Pace maker- HB↓20/m.

53. prevention
• Keep BMI↓ 23
• LDL =↓100
• HDL=↑50 (Exercise)
• TGL=↓150 (TGL/HDL= >3.5=↑Small
denseLP(Transfat, ↑carbohydrates, DM,
↑TGL,&↓HDL, X-Syndrme increases the rate
of SDLPL.
• BP =↓130/85mmHg.
• (pulse pressure↑10 =CAD↑12%, HF↑14%)

54. Regular check up
• Age>3oPSC
• HbA1c↓ 7%
• Bp=↓130/80
• Sc=↓180 (↓150)

55. • Regular exercise
• Restrict saturated fat ,Carbohydrates,
• Use olive oil,(coconut oil contain97% S.FA &
65% in Palm oil )
• veg.food
• Abstinence of Smoking

56. HOMOEOPATHIC
Management
-- Digitalis
-- Cactus
-- Crataegus
Strophanthus
-- Naja
--lactrodectus
Laurocerasus
-- Aconite

57. ISCHAEMIC
CARDIOMYOPATHY
• Multiple small infarcts & extensive diffuse
fibrosis of the myocardium
• It presents a picture of Cardiomegaly &
Congestive Cardiomyopathy
•Accompanying Mitral Incompetence may be
there
•End stage Ischemic Cardiomyopathy –
indication for Cardiac transplantation

58. ASYMPTOMATIC CORONARY ARTERY
DISEASE
•Not Uncommon
• Routine stress testing may bring out the abnormality
• Such cases may develop Acute MI or die suddenly as a
result of Ventricular Fibrillation / Cardiac Arrest
• Significant abnormalities in the treadmill test are the
indication for Coronary Arteriography

59. PREVENTION
Of Coronary Artery Disease
Primary Prevention By
1. Proper dietary manipulation to avoid high
intake of saturated fats & Over nutrition
2. Avoidance of Smoking
3. Regular exercise=40mts=3.5km.
4. Regular Medical Check- Up
5. Reduce Stress & Emotional tension

60. Common D/D
• Costochondritis
• Hiatus hernia
• Spasm of cardiac sphincter
• Cardiomyopathy
• Cervical spondylitis
• Pericarditis
• COPD

61. ADVERSE PROGNOSTIC FACTORS
• Older Age
• Diabetes Mellitus
• Continuing rest pain despite medical therapy
• Ischemia detected by Holter Monitoring
• Significant ST – T wave changes on ECG
• Troponin positive cases
• Levels of markers of inflammation- C reactive
protein, serum amyloid, fibrinogen↑↑
• Multi vessel disease, presence of thrombus or
complex coronary morphology at coronary
angiography

62. MANAGEMENT
• Control of Hypertension
• Control of Diabetes
• Treatment of Thyrotoxicosis /
Hypothyroidism &
Anemia
• Avoidance of Smoking & Caffeine

63. Maximum predicted heart rate
• 220-age/mts.(M)
• 200-age/mts( F)

64. n
• DR.P.N. Karam Chand,MD (Hom.)
HOD of Medicine
D P M H M C,
Chottanikkara
Kochi- Kearala
Mob: 944 710 99 18
• DR.P.N. Karam Chand, MD (Hom.)
HOD of Medicine
D P M H M C,
Chottanikkara
Kochi- Kearala
Mob: 944 710 99 18