1) Ischaemic heart disease (IHD), also called coronary artery disease, is caused by reduced blood flow and oxygen delivery to the heart muscle. The two main manifestations of IHD are angina and myocardial infarction (MI). 2) Angina is characterized by chest pain or discomfort that occurs when the heart muscle doesn't get enough oxygen. MI occurs when an area of the heart is damaged or dies due to complete blockage of blood supply. 3) Risk factors for IHD include smoking, high blood pressure, high cholesterol, diabetes, obesity, lack of exercise, and family history. Treatment involves lifestyle changes, medications, procedures like angioplasty and bypass surgery.

1. ISCHEAMIC
HEART
DISEASE
By Dr.Akshay Rane

2. ISCHAEMIC HEART DISEASE
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1.INTRODUCTION TO IHD
2.ETHIOPATHOGENESIS OF
3.ANGINA PECRORIS
4.MYOCARDIAL INFARCTION
5.7 STEPS TO A HEALTHIER HEART

3. Ischaemic Heart Disease :
DEFINATION:
It is defined as acute or chronic form of cardiac disability
arising from imbalance between the myocardial supply
and demand for oxygenated blood.
 It is also called as CORONARY ARTERY DISEASE.

4. PHYSIOLOGY
• Pumping oxygenated blood to
• the other body organs.
• Pumping nutrients and other vital
• substances to different organs.
• Receives deoxygenated blood and
• pumps it to the lungs for oxygenation.
• Maintaining blood pressure

5. HEART
• Hollow muscular organ that pumps blood throughout the circulatory system.
• About 10 cm long ,weight about 225g in females, and 310g in males.
• LOCATION: In thoracic cavity in mediastinum.
ANATOMY
Histologically; Heart has 3 layer i.e.
• Outer – Pericardium
• Middle – Myocardium
• Inner – Endocardium
• 4 chambers
• 2 atrium
• 2 ventricles
4 valves
• mitral
• Aortic
• Tricuspid
• Pulmonary

6. Etiopathogenesis of
IHD
Coronary
atherosclerosis
Superadded changes
in coronary
atherosclerotic plaque
Non- atherosclerotic
causes
• Acute changes in
plaque
• Coronary artery
thrombosis
• Local platelet
aggregation
• Vasospasm
• Stenosis of coronary ostia
• Arteritis
• Embolism
• Thrombotic disease
• Trauma
• Aneurysms
• Compression

7. EFFECTS OF IHD
1.ANGINA PECTORIS
 DEFINATION:
Angina pectoris is a clinical syndrome of IHD resulting from transient myocardial ischemia.
o It is characterized by paroxysmal pain in substernal or precardial region of the chest which is
aggravated by an increase in the demand of the heart and relived by a decrease in the work of
the heart.

8. ETIOLOGY
1.Coronary Artery Disease CAD (Development of Atherosclerosis)
2.Smoking
3.High blood pressure
4.High cholesterol
5.Diabetes mellitus
6.Sedentary lifestyle
RISK FACTORS
MODIFIABLE RISK FACTORS NON-MODIFIABLE RISK FACTORS
1.Tobacco use 1.Family history of heart disease
2. High blood cholesterol or Triglyceride levels 2. Older age
3.Lake of Exercise 3.Diabetes
4.Obesity 4. High blood pressure
5.Stress

9. PATHOPHYSIOLOGY
Atherosclerosis Arterial spasm Atherosclerosis +Thrombolysis
gradual obstruction sudden reversible obstruction occlusion
ISCHEAMIA
HYPOXIA
Reduced oxygen demand – Angina
Thrombolysis – Unstable Angina

10. CLASSIFICATION OR TYPES OF ANGINA
 STABLE OR TYPICAL
ANGINA
 Most common
 Physical or Emotional
 Excitement
 Chronic stenosing
 Coronary Atherosclerosis
 Decrease oxygen to
myocardium
Workload on heart disease
 ECGC depression of ST
segment
 Relived by rest
(No reversible myocardial
injury)
 PRINZMETALS
VARIENT ANGINA
Occurs in rest
sudden coronary
vasospasm
OR
Coronary Trunk
ECG-ST Segment
change Elevation
Changes in coronary in each
angina picture form
 UNSTALE OR
CRESEENDO ANGINA
Also called as pre-infarction
angina
Most serious, more frequent,
onset of pain of prolonged
duration may led to MI
Occurs due to coronary
atherosclerosis , superimposed
thrombosis , hemmorhage
ulceration of coronary plaques

11. TYPES OF ANGINA

12. CLINICAL FEATURES : Nausea
Sweating
Breathlessness
Fatigue
Anxiety
Dizziness
Chest pain
Discomfort and pain in back, neck and shoulders.
 INVESTIGATIONS:
1. Physical examination
2. History collection
3. ECG
4. Chest X-ray
5. Stress test
6. Blood tests
7. Echocardiogram
8. CT scan (Cardiac Computerized Tomography)
9. Cardiac magnetic resonance imaging MRI
10. Coronary angiography

13. TREATMENTS
ALLOPATHIC AYURVEDIC HOMOEOPATHIC
• Nitrates * Arjuna ( Terminal arjuna) * Mag phos
• P- Blockers * Punarnava (Boerhavia diffusa) * Lachesis
• Calcium channel blockers * Pipal tvak (ficus religiosa) * Naja
• Aspirin * Shankpushpi (convovulus * Aconite
• Statins pluricaulis) * Arsenic album
* Cimicifuga
* Spigelia
 Surgical- Angioplasty with stenting
 Procedures – Open heart surgery (Coronary artery bypass surgery)

14. Auxiliary line of Treatments / Lifestyle /
Home remedies
• Avoid smoking and exposure to second hand smoke.
• Exercise and manage weights.
• Eats & Healthy diets.
• Manage other health conditions – Diabetes, high blood pressure, high
blood cholesterol.
• Avoid or limit alcohol.
• Practice stress relief.

15. 2.MYOCARDIAL INFRACTION (MI)
 Myocardial infraction refers to the process by which myocardial tissues are
permanently destroyed in the region of the heart that are deprived of an adequate
supply of blood (myocardial ischemia ) because of a reduced coronary blood flow,
subsequently necrosis or death of myocardial tissue occurs.

16. ETIOPATHOGENESIS OF MI
 MYOCARDIAL ROLE OF ACUTE PLAQUE NON ATEROSCEL- ISCHAEMIA
PLATELETS RUPTURE ROTIC CAUSES
 DIMINISHED Rupture of atherosclerotic Superimposed 10% MI
 Blood flow plaque coronary thrombosis
 Increase myocardial Exposure of sub- Intramural plaque * Coronary vasospasm
demand endothelial collagen
 To platelets hemorrhage
Arteritis
 Platelets get * Embolism activated * Trauma blood flow
Formation of clots of .
Platelets * Coronary ostial stenosis
 Initiate thrombosis

17. ETIOPATHOGENESIS OF MI
Myocardial
ischaemia
Acute plaque
rupture
Non
arterioclsclerotic
cause
Role of
platelets
Diminished
blood flow
Increased
myocardial
demand
Hypertrophy of heart
without simultaneous
increase of coronary of
coronary blood flow
Rupture of
atherosclerotic
plaque
Exposure to
endothelial
collagen to
platelets
Platelets gets
activated
Formation of
clots of platelets
Initiate
thrombosis
Superimposed
coronary
thrombosis
Intramural
plaque
haemorrhage
10% MI
o Coronary
vasospasm
o Arteritis
o Embolism
o Trauma
o Coronary ostial
stenosis

18. TYPES OF INFARCTS
 According to anatomic region of left ventricle involved:
Anterior
Posterior
Lateral
Septal
Circumferential
Combinations – Anterolateral, Posterolateral, Anteroseptal
 According to degree of thickness of ventricular wall involved:
*Transmural (full thickness)
*Laminar (subendocardial )
 According to age of infarcts:
*Newly formed (acute, recent, fresh)
*Advanced infarcts (old, healed, organized)

19. LOCATION OF INFARCTS
 1. Stenosis of the left anterior descending coronary artery is the most
common (40-50%). The region of infarction is the anterior part of the left
ventricle including the apex and the anterior part of the left ventricle
including the apex and the anterior two-thirds of the interventricular
septum.
 2. Stenosis of the right coronary artery is the next most frequent (30-
40%). It involves the posterior part of the left ventricle and the posterior
one-third of the interventricular septum.
 3. Stenosis of the left circumflex coronary artery is seen least frequently
(15-20%). Its area of involvement is the lateral wall of the left ventricle.

20. CHANGES IN EARLY INFARCTS
Electron microscopic Chemical and histochemical
changes changes
 1. Disappearance of perinuclear glycogen 1.Glycogen depletion in myocardial
granules within 5 minutes of Ischaemia. Fibers within 30 to 60 minutes of
. . infarction.
 2.Swelling of mitochondria in 20 to 30 2. Increase in lactic acid in the
minutes myocardial fibers.
3.Disruption of sarcolemma. 3.Loss of K+ from the ischaemic fibers.
4.Nuclear alterations like peripheral 4.Increase of Na+ in the ischaemic
cells. clumping of nuclear chromatin.
5. Influx of Ca+ into the cells causing .
. irreversible cell injury

21. DIAGNOSIS
Clinical features ECG changes Serum cardiac biomarkers
 Pain ST segment elevation Creatine
phosphokinase & Indigestion (STEMI)
CK-MB I so enzyme Apprehension T wave inversion
Lactate dehydrogenase from Shock Deep Q waves
cardiac muscle (LDH). Oliguria
Cardiac- specific troponins Low grade fever
Myoglobin Acute pulmonary oedema.

22. Complications
10-20% cases 80-90% cases
no sever complications sever complications
 Arrhythmias
 Congestive heart failure
 Cardiogenic shock
 Mural thrombosis & thromboembolism
 Rupture
 Cardiac aneurysm
 Pericarditis
 Post myocardial infarction syndrome

23. TREATMENTS
 Medications Homeopathic Ayurvedic Medical .
Remedies Medications Procedures
 *Anticlotting *Arnica *Hrudya vati *Coronary artery
 Medications *Aconite *Anarsha kshara bypass graftinCABG
 *Nitroglycerin *Laurocerasus *Sukha virechana percutaneous
*Thrombolytic Tarentula coronary
(clot- busting ) Interventions
 medications (PCI)
*Anti-arrhythmia *Coronary
medications angioplasty
 *Morphine

24. EPIDEMIOLOGY

25. FIRST AID FOR MI
 # EMERGENCY FIRST STEPS TO BE TAKEN IN A HEART ATTACK
 Call 911 or your local emergency medical assistance number if the pain persists for more than 3
minutes.
 Keep the person calm and still.
 Put the person in a sitting position with knees raised and back supported.
 Chew and swallow an aspirin (325mg) slowly. Unless you are allergic or otherwise prescribed by
your doctor.
 Take prescribed medicines if any.
 Loosen any tight clothing.
 Give CPR if the person is unconscious his breathing or pulse stops CPR is the combination of both
chest compressions, to support the heart, and artificial respiration , to support the lungs.
 Give artificial respiration if required : Oxygen support or AED (Automated External Defibrillation).
 Take nitroglycerin: Up to three pills, one at a time every 5 minutes.

26. IMPORTANCE OF FIRST AID
• For every single minute that a person is not breathing. The chance of survival decreases by 10%.
• In an emergency the first 10 minutes are most important.
• CPR doubles a persons chance of survival from sudden cardiac arrest.
• In 4 minutes the victim starts to develop brain damage.
• *If CPR is started within 4 minutes of collapse and defibrillation provided within
• 10 minutes a person has a 40 % chance of survival.

27. SEVEN STEPS TO A HEALTHIER HEART

28. THANKYOU…