Bems Kiran presentation1
Bems Kiran presentation1
INTRODUCTION
Ischemic heart disease also designated
  as coronary artery disease refers to a
  group of closely related syndromes
  caused by an imbalance between
  myocardial oxygen demand and blood
  supply.
ETIOLOGY
The most common cause of imbalance
 between need and supply of oxygen
 is atherosclerotic narrowing of the
 coronary arteries producing ischemia.
RISK FACTORS FOR
     ATHEROSCLEROSIS
Fixed Risk Factors
Age
Male Sex
Family History
MODIFIABLE RISK FACTORS

    STRONG ASSOCIATION
Hyperlipidemia
Hypertension
Cigarette Smoking
Diabetes Mellitus
OTHER ASSOCIATIONS

Obesity
Lack of exercise
Heavy alcoholism
Dietary factors
Oral contraceptives
Gout
High level of coagulation factor vii &
 fibrinogen
Anxiety & depression
PATHOGENESIS
    Defective Oxygen Delivery
    Increased Oxygen Demand
    IHD becomes symptomatic when there is 75% or
    more reduction of the lumen of one or more
    coronary arteries by atherosclerotic plaque.
 Superimposed Lesions
       Acute changes in plaque morphology
              Local platelet aggregation
              Coronary artery spasm
              Coronary artery thrombosis
Bems Kiran presentation1
CLASSIFICATION OF IHD

Stable angina
Unstable angina
Myocardial infarction
Sudden cardiac death
Bems Kiran presentation1
WHAT IS ANGINA?
Angina is a clinical syndrome
 characterized by intermittent chest
 pain caused by reversible myocardial
 ischemia.
The pain is usually substernal or
 precordial radiating to the shoulder
 and arm or to the jaw.
It lasts for several minutes.
TYPES OF ANGINA
  STABLE ANGINA
  VARIANT ANGINA
 UNSTABLE ANGINA
STABLE ANGINA
It occurs due to increased myocardial
 oxygen demand during exertion in a patient
 of narrow coronary arteries.
VARIANT ANGINA
It occurs at rest and produced by the
 reduction of the myocardial blood supply
 due to coronary artery spasm.
UNSTABLE ANGINA
In this type of angina, frequency, severity
 and duration of episodes are progressively
 increased. It occurs at rest due to thrombus
 formation and coronary artery spasm.
DIFFERENCE B/W STABLE &
            UNSTABLE ANGINA
STABLE ANGINA             UNSTABLE ANGINA


 Due to fixed stenosis      Due to dynamic
                                 stenosis
 Demand-led ischemia      Supply-led ischemia


 Related to effort         Symptoms at rest


 Symptoms over long       Symptoms over short
  term                            term
Bems Kiran presentation1
INVESTIGATIONS
ECG
ETT
Thallium scan
CT Angiography
Echocardiography
Coronary Angiography
ECG
During pain ECG shows
ST –segment depression with or without T
 wave inversion that reverses after ischemia
 disappears.
Elevation of ST segment in variant angina.
The resting ECG may be normal b/w
 attacks however it may show old MI, heart
 block or left ventricular hypertrophy.
ETT
When history is suggestive of angina
 but ECG normal ETT is performed for
 diagnosis.
Positive test is one in which ST
 segment is depressed by 1 mm.
Bems Kiran presentation1
MYOCARDIAL
INFARCTION
INTRODUCTION
•MI is death or necrosis of myocardial
cells.

 Myocardial infarction (MI or AMI for acute
myocardial infarction), commonly known as a
heart attack, occurs when the blood supply to
part of the heart is interrupted.
ETIOLOGY
Commonly caused due to occlusion of a coronary
artery following the rupture of a vulnerable
atherosclerotic plaque, in the wall of an artery. The
resulting ischaemia and hypoxia, if left untreated for
a sufficient period, can cause damage and or death
(infarction)     of     heart     muscle       tissue.
Bems Kiran presentation1
Bems Kiran presentation1
ETIOPATHOGENESIS
1. Mechanism of MI
  i) Diminished coronary blood flow
  ii) Increased myocardial demand
  iii) Cardiac hypertrophy without se of
   coronary blood flow

2. Role of Platelets
   - rupture of atherosclerotic plaque exposes
   subendothelial collagen to platelets
   - aggregation, activation, release of platelets
3. Complicated Plaques
  i) Superimposed coronary thrombosis
  ii) Intramural haemorrhage



4. Non-atherosclerotic causes
   - coronary vasospasm
   - arteritis
   - embolism
   - thrombotic diseases
   - trauma
5. Transmural versus subendocardial
    infarcts

   Transmural infarcts- involve full thickness of
   ventricular wall subendocardial (laminar)
   infarcts- affecting inner
   subendocardial one-third to one-half.
Bems Kiran presentation1
Classical symptoms
of acute myocardial
     infarction
   Sudden chest pain
   Shortness of breath
   Nausea
   Vomiting
   Palpitations
   Sweating
   Anxiety
Risk factors for
myocardial infarction

1. Older age
2. Sex (males)
3. Tobacco smoking
4. Hypercholesterolemia
5. Diabetes
6. Hypertension
7. Obesity
8. Stress
Pathological Changes

 Vary according to the age of the infarct

 Most infarcts occur singly (very less
  multifocal), 4-10 cm size

 Most often in left ventricle

 Subendocardial infarcts produce less well-
  defined infarcts gross changes than the
  transmural infarcts.
CLINICAL DIAGNOSIS

Clinical diagnosis is based on
 Symptoms
ECG changes
Elevation of specific serum enzymes
SYMPTOMS
Onset is sudden with severe
 constricting, crushing, burning
 substernal or precordial pain that
 radiates to the left shoulder and arm
 or jaw.
Pain is accompanied by
 sweating, nausea, vomiting or
 dyspnea.
Cardiogenic shock.
ECG Changes
 ST Segment elevation, follwed by
 abnormal new Q waves and inverted
 T wave.
 Serum Enzymes
Creatinine phosphokinase
Lactic dehydrogenase
Cardiac troponin I & Troponin T.
Bems Kiran presentation1
CHRONIC ISCHEMIC
  HEART DISEASE
Chronic IHD some times called
 ischemic cardiomyopathy is used to
 describe the development of
 progressive CHF.
It is characterized by multifocal areas
 of myocardial atrophy and fibrosis
 secondary to slowly developing
 coronary atherosclerosis leading to
 dilatation of cardiac chambers.
CLINICAL FEATURES
Usually it remains asymptomatic and
 progressively CHF develops.
Cardiac arrhythmias may occur when
 scarring involves conduction system.
Angina, MI
TYPES OF HEART FAILURE

   ACUTE HEART FAILURE
   CHRONIC HEART FAILURE
   RIGHT AND LEFT HEART FAILURE
   CONGESTIVE HEART FAILURE
   FARWARD HEART FAILURE
   BACKWARD HEART FAILURE
   CARDIAC ARREST
ACUTE HEART FAILURE
Sudden onset of heart failure without
  previous symptoms of ischemia or MI.
CHRONIC HEART FAILURE
Gradual onset of heart failure with
  symptoms of ischemia or MI.
CONGESTIVE CARDIAC FAILURE
Bi ventricular heart failure.
CARDIAC ARREST
Complete cessation of heart function.
Conductive system of heart completely
 block.
Bems Kiran presentation1
Bems Kiran presentation1

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Bems Kiran presentation1

  • 3. INTRODUCTION Ischemic heart disease also designated as coronary artery disease refers to a group of closely related syndromes caused by an imbalance between myocardial oxygen demand and blood supply.
  • 4. ETIOLOGY The most common cause of imbalance between need and supply of oxygen is atherosclerotic narrowing of the coronary arteries producing ischemia.
  • 5. RISK FACTORS FOR ATHEROSCLEROSIS Fixed Risk Factors Age Male Sex Family History
  • 6. MODIFIABLE RISK FACTORS STRONG ASSOCIATION Hyperlipidemia Hypertension Cigarette Smoking Diabetes Mellitus
  • 7. OTHER ASSOCIATIONS Obesity Lack of exercise Heavy alcoholism Dietary factors Oral contraceptives Gout High level of coagulation factor vii & fibrinogen Anxiety & depression
  • 8. PATHOGENESIS Defective Oxygen Delivery Increased Oxygen Demand IHD becomes symptomatic when there is 75% or more reduction of the lumen of one or more coronary arteries by atherosclerotic plaque. Superimposed Lesions  Acute changes in plaque morphology  Local platelet aggregation  Coronary artery spasm  Coronary artery thrombosis
  • 10. CLASSIFICATION OF IHD Stable angina Unstable angina Myocardial infarction Sudden cardiac death
  • 12. WHAT IS ANGINA? Angina is a clinical syndrome characterized by intermittent chest pain caused by reversible myocardial ischemia. The pain is usually substernal or precordial radiating to the shoulder and arm or to the jaw. It lasts for several minutes.
  • 13. TYPES OF ANGINA STABLE ANGINA VARIANT ANGINA UNSTABLE ANGINA
  • 14. STABLE ANGINA It occurs due to increased myocardial oxygen demand during exertion in a patient of narrow coronary arteries. VARIANT ANGINA It occurs at rest and produced by the reduction of the myocardial blood supply due to coronary artery spasm. UNSTABLE ANGINA In this type of angina, frequency, severity and duration of episodes are progressively increased. It occurs at rest due to thrombus formation and coronary artery spasm.
  • 15. DIFFERENCE B/W STABLE & UNSTABLE ANGINA STABLE ANGINA UNSTABLE ANGINA  Due to fixed stenosis  Due to dynamic stenosis  Demand-led ischemia  Supply-led ischemia  Related to effort  Symptoms at rest  Symptoms over long  Symptoms over short term term
  • 18. ECG During pain ECG shows ST –segment depression with or without T wave inversion that reverses after ischemia disappears. Elevation of ST segment in variant angina. The resting ECG may be normal b/w attacks however it may show old MI, heart block or left ventricular hypertrophy.
  • 19. ETT When history is suggestive of angina but ECG normal ETT is performed for diagnosis. Positive test is one in which ST segment is depressed by 1 mm.
  • 22. INTRODUCTION •MI is death or necrosis of myocardial cells. Myocardial infarction (MI or AMI for acute myocardial infarction), commonly known as a heart attack, occurs when the blood supply to part of the heart is interrupted.
  • 23. ETIOLOGY Commonly caused due to occlusion of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, in the wall of an artery. The resulting ischaemia and hypoxia, if left untreated for a sufficient period, can cause damage and or death (infarction) of heart muscle tissue.
  • 26. ETIOPATHOGENESIS 1. Mechanism of MI i) Diminished coronary blood flow ii) Increased myocardial demand iii) Cardiac hypertrophy without se of coronary blood flow 2. Role of Platelets - rupture of atherosclerotic plaque exposes subendothelial collagen to platelets - aggregation, activation, release of platelets
  • 27. 3. Complicated Plaques i) Superimposed coronary thrombosis ii) Intramural haemorrhage 4. Non-atherosclerotic causes - coronary vasospasm - arteritis - embolism - thrombotic diseases - trauma
  • 28. 5. Transmural versus subendocardial infarcts Transmural infarcts- involve full thickness of ventricular wall subendocardial (laminar) infarcts- affecting inner subendocardial one-third to one-half.
  • 30. Classical symptoms of acute myocardial infarction  Sudden chest pain  Shortness of breath  Nausea  Vomiting  Palpitations  Sweating  Anxiety
  • 31. Risk factors for myocardial infarction 1. Older age 2. Sex (males) 3. Tobacco smoking 4. Hypercholesterolemia 5. Diabetes 6. Hypertension 7. Obesity 8. Stress
  • 32. Pathological Changes  Vary according to the age of the infarct  Most infarcts occur singly (very less multifocal), 4-10 cm size  Most often in left ventricle  Subendocardial infarcts produce less well- defined infarcts gross changes than the transmural infarcts.
  • 33. CLINICAL DIAGNOSIS Clinical diagnosis is based on  Symptoms ECG changes Elevation of specific serum enzymes
  • 34. SYMPTOMS Onset is sudden with severe constricting, crushing, burning substernal or precordial pain that radiates to the left shoulder and arm or jaw. Pain is accompanied by sweating, nausea, vomiting or dyspnea. Cardiogenic shock.
  • 35. ECG Changes ST Segment elevation, follwed by abnormal new Q waves and inverted T wave. Serum Enzymes Creatinine phosphokinase Lactic dehydrogenase Cardiac troponin I & Troponin T.
  • 37. CHRONIC ISCHEMIC HEART DISEASE Chronic IHD some times called ischemic cardiomyopathy is used to describe the development of progressive CHF. It is characterized by multifocal areas of myocardial atrophy and fibrosis secondary to slowly developing coronary atherosclerosis leading to dilatation of cardiac chambers.
  • 38. CLINICAL FEATURES Usually it remains asymptomatic and progressively CHF develops. Cardiac arrhythmias may occur when scarring involves conduction system. Angina, MI
  • 39. TYPES OF HEART FAILURE  ACUTE HEART FAILURE  CHRONIC HEART FAILURE  RIGHT AND LEFT HEART FAILURE  CONGESTIVE HEART FAILURE  FARWARD HEART FAILURE  BACKWARD HEART FAILURE  CARDIAC ARREST
  • 40. ACUTE HEART FAILURE Sudden onset of heart failure without previous symptoms of ischemia or MI. CHRONIC HEART FAILURE Gradual onset of heart failure with symptoms of ischemia or MI. CONGESTIVE CARDIAC FAILURE Bi ventricular heart failure.
  • 41. CARDIAC ARREST Complete cessation of heart function. Conductive system of heart completely block.