Ischemic Heart Disease(IHD) for medical students

Ischaemic Heart Disease

1. Ischemic Heart Disease(IHD).

2. Introduction.
•Synonym: coronary artery disease -CAD
•This is the generic name used for a group of
closely related syndromes resulting from
ischaemia, an imbalance between supply
(perfusion) and demand of the heart for
oxygenated blood
•Ischaemia is xterised by insufficiency of
oxygen, reduced availability of nutrient
substrates and inadequate removal of
metabolites .

3. •It is a disease characterized by ischaemia to
the heart muscles.
•usually due to coronary artery disease.
• Its risk increases with age, smoking,
hypercholesterolaemia, diabetes, and
hypertension
• more common in men and those who have
close relatives with ischaemic heart disease.

4. Ischaemic heart disease
•There are four clinical syndromes of IHD
namely.
1.Angina pectoris
2.Myocardial infarction
3.Chronic ischaemic heart disease.
4.Sudden cardiac death

5. Epidemiology
•Common cause of death in the US and
industrialized nations.
•Incidence increasing in developing world due
to changes in life style.
•Life style modification in the developed world
has resulted in the drop in incidence of IHD.
•Men develop IHD more than women

6. pathogenesis
•Four factors play roles in the pathogenesis of
IHD. These are
1.Coronary atherosclerosis
2.Acute plaque changes
3.Thrombosis
4.Vasospasm
Atherosclerosis is responsible for more than 90%
of the cases

8. Pathogenesis.
•Diminished coronary perfusion is as a result of the
superimposed thrombosis on a fixed coronary
atherosclerosis with at least 75% reduction in the
cross sectional areas.
•The thrombosis is a consequence of acute plaque
changes with stress, tachycardia and or vasospasm
resulting in fissuring, fractures and ulceration of
the plaque exposing the thrombogenic surfaces of
the vessels.

9. Pathogenesis (contd)
•Thrombosis results in the total occlusion of
the vessel and release of substances such as
thromboxane which further worsens
vasospasm.

10. Angina pectoris
•This is a symptom complex of IHD
characterized by paroxysmal attacks of
substernal or precordial chest discomfort caused
by transient (5secs-15minutes) myocardial
ischaemia that falls short of inducing an infarct.
•There are 3 types of angina pectoris
1.Stable or Typical angina
2.Prinzmetal or variant angina
3.Unstable or crescendo angina

11. Stable or typical angina
•Commonest form of angina
•Xterised by attacks of pain following physical
exertion, emotional excitement leading to increase in
demand of blood flow
•Relieved by rest, and vasodilators such as
nitroglycerin.
•Associated with ST segment depression in ECG
because ischemia is most intense in the
subendocardial zone of the lt ventricle.
•No elevation of cardiac enzymes in blood.

12. •The pathogenesis lies in chronic stenosing
coronary atherosclerosis that leads to
inadequate perfusion of the myocardium
when the workload on the heart increases

13. Prinzmetal (variant) angina.
• Episodic pain that occurs at rest.
•Associated with coronary spasms and unrelated to
physical activity, heart rate or blood pressure.
•Vasospasm may follow release of humoral factors in
the blood
•There is an elevation of the ST segment on ECG,
indicative of a transmural ischemia.
•Responds to vasodilators and calcium channel
blockers

14. Unstable or crescendo angina.
•This is angina pain occurring with progressively
increasing frequency and prolonged duration.
•Precipitated with progressively less effort, occurs at
rest.
•It is induced by fissuring, ulceration , or rupture of
an AS plaque with superimposed partial mural
thrombosis, vasospasm or both.
•Micro infarcts may occur and it forewarns an MI
•It is also known as pre-infarct angina or acute
coronary insufficiency.

15. Myocardial infarction(heart
attack)
•This is the leading cause of death in the
developed world.
•The risk factors for MI are those for AS.
•Major :diet, hyperlipidemia, hypertension,
cigarette smoking, DM, male gender, Fam
Hx, increasing age, genetic abnormalities
•Minor: obesity, phys. Inactivity,ress, oral
contraceptives, high CHO intake.

16. Pathogenesis.
•90% of transmural acute myocardial infarcts are
caused by an occlusive intra coronary thrombus
overlying an ulcerated or fissured AS plaque.The
ischemia is worsened by factors such as a fall in
blood pressure, tachycardia,
•The exposure of the sub endothelial collagen
results in platelet adhesion, aggregation, activation
release of aggregators
•The activated platelets release thromboxane A2,
platelet factors 3 and 4 which predispose to
coagulation and cause vasospasms
•Also there is activation of the extrinsic pathway of
coagulation due to the release of tissue
thromboplastin.

17. •In 10% of cases there is no evidence of AS.
Infarct results from
–Vasospasm or
–Emboli - from left sided mural thrombosis,
vegetative endocarditis, or paradoxical emboli
from the right side of heart through a patent
foramen ovale.
•

18. Reperfusion injury.
•This follows the use of fibrinolytic agents
such as tissue type plasminogen activator or
streptokinase.
•Cell death results from free radical injury.
•Contraction bands occur in damaged muscle

19. Gross morphology.
•The gross morphologic appearance of a
myocardial infarction can vary. Patterns include:
•Transmural infarct - involving the entire thickness
of the left ventricular wall from endocardium to
epicardium, usually the LV anterior free wall and
posterior free wall and septum with extension into
the RV wall in 15-30%.
–Isolated infarcts of RV and right atrium are extremely
rare.
•Subendocardial infarct - multifocal areas of
necrosis confined to the inner 1/3-1/2 of the left
ventricular wall. These do not show the same
evolution of changes seen in a transmural MI.

20. Vessels and infarcted areas.
•Left anterior descending.40-50% of infarcts
–Affects
•Anterior wall of left ventricle near the apex
•Anterior two thirds of interventricular septum
•Right coronary artery 30-40%
–Affects
•Inferior/posterior wall of left ventricle.
•Posterior one third of interventricular septum
•Posterior right ventricular free wall
•Left circumflex coronary artery15-20%
–Affects
•Lateral wall of left ventricle

21. Time from OnsetGross Morphologic Finding
18 - 24 Hours




Pallor of myocardium
24 - 72 HoursPallor with some hyperaemia
3 - 7 Days Hyperaemic border with central yellowing
10 - 21 DaysMaximally yellow and soft with vascular
margins
7 weeks White fibrosis

22. Time from Onset Microscopic Morphologic Finding
1 - 3 Hours
 
Wavy myocardial fibers

 
2 - 3 Hours

 
Staining defect with tetrazolium or basic fuchsin dye

4 - 12 Hours Coagulation necrosis with loss of cross striations, contraction bands, edema,
hemorrhage, and early neutrophilic infiltrate
18 - 24 Hours
 

 
Continuing coagulation necrosis, pyknosis of nuclei, and marginal contraction
bands
 
24 - 72 Hours Total loss of nuclei and striations along with heavy neutrophilic infiltrate
3 - 7 Days
 
Macrophage and mononuclear infiltration begin, fibrovascular response begins

 
10 - 21 Days
 
Fibrovascular response with prominent granulation tissue
 
 
7 Weeks
Fibrosis

24. •MI fewer than 12 hours old are inapparent on
gross examination
•After 2-3 hours : immersion of tissue slides in a
solution of triphenyltetrazolium chloride imparts
to the intact non infarcted myocardium, where
dehydrogenase activity is preserved. Infarcted
area is revealed as an unstained pale zone due to
the leakage of dehydrogenase enzymes

39. Diagnosis
•Clinical features
•ECG changes
•Serum enzyme determination

40. Clinical features
•Pain- sudden, severe, prolonged, substernal or
precordial in location. Radiates to the arms,
neck and back. Not relieved by rest or
nitroglycerine
•Epigastric or retrosternal discomfort “heart
burn” with nausea and vomitting
•Apprehension
•shock

41. •Oliguria
•Low grade fever
•Acute pulmonary oedema due to left
ventricular failure: dyspnoea, orthopnoea,
suffocation

42. ECG changes
•ST segment elevation
•T wave inversion
•Deep Q waves

43. Serum cardiac markers
•Creatinine kinase
•Troponin
•Myoglobulin
•Lactate dehydrogenase

44. Creatinine kinase
•The total CK is a simple and inexpensive test that is
readily available using many laboratory instruments.
However, an elevation in total CK is not specific for
myocardial injury, because most CK is located in
skeletal muscle, and elevations are possible from a
variety of non-cardiac conditions.

45. Creatinine kinase
•Creatinine kinase can be further subdivided into
three isoenzymes: MM, MB, and BB.
•The MM fraction is present in both cardiac and
skeletal muscle, but the MB fraction is much more
specific for cardiac muscle:
• about 15 to 40% of CK in cardiac muscle is MB,
while less than 2% in skeletal muscle is MB.
•The BB fraction (found in brain, bowel, and
bladder) is not routinely measured.

46. Creatine Kinase - MB Fraction:
•CK-MB is a very good marker for acute myocardial injury,
because of its excellent specificity, and it rises in serum within
2 to 8 hours of onset of acute myocardial infarction.
•Serial measurements every 2 to 4 hours for a period of 9 to 12
hours after the patient is first seen will provide a pattern to
determine whether the CK-MB is rising, indicative of
myocardial injury.
•The CK-MB is also useful for diagnosis of reinfarction or
extensive nature of an MI because it begins to fall after a day,
dissipating in 1 to 3 days, so subsequent elevations are
indicative of another event.
•A "cardiac index" can provide a useful indicator for early MI.
This is calculated as a ratio of total CK to CK-MB, and is a
sensitive indicator of myocardial injury when the CK-MB is
elevated

47. Troponin.
•Troponin I and T are structural components of cardiac muscle.
They are released into the bloodstream with myocardial injury.
They are highly specific for myocardial injury--more so than
CK-MB--and help to exclude elevations of CK with skeletal
muscle trauma.
•Troponins will begin to increase following MI within 3 to 12
hours, about the same time frame as CK-MB. However, the
rate of rise for early infarction may not be as dramatic as for
CK-MB.
•Troponins will remain elevated longer than CK--up to 5 to 9
days for troponin I and up to 2 weeks for troponin T.
•This makes troponins a superior marker for diagnosing
myocardial infarction in the recent past--better than lactate
dehydrogenase (LDH).

48. Troponin (contd)
•However, this continued elevation has the disadvantage of
making it more difficult to diagnose reinfarction or extension
of infarction in a patient who has already suffered an initial
MI.
•Troponin T lacks some specificity because elevations can
appear with skeletal myopathies and with renal failure.

49. Myoglobin
•Myoglobin is a protein found in skeletal and cardiac
muscle which binds oxygen. It is a very sensitive
indicator of muscle injury.
•The rise in myoglobin can help to determine the size
of an infarction.
• A negative myoglobin can help to rule out
myocardial infarction. It is elevated even before
CK-MB.
•it is not specific for cardiac muscle, and can be
elevated with any form of injury to skeletal muscle.

50. Lactate Dehydrogenase
•The LDH has been supplanted by other tests. It
begins to rise in 12 to 24 hours following MI, and
peaks in 2 to 3 days, gradually dissipating in 5 to 14
days.
• Measurement of LDH isoenzymes is necessary for
greater specificity for cardiac injury.
•There are 5 isoenzymes (1 through 5). Ordinarily,
isoenzyme 2 is greater than 1, but with myocardial
injury, this pattern is "flipped" and 1 is higher than
2.

51. LDH
• LDH-5 from liver may be increased with
centrilobular necrosis from passive
congestion with congestive heart failure
and following ischemic myocardial injury

52. Complications
•Arrhythmias and conduction defects, with possible
"sudden death"
•Extension of infarction, or re-infarction
•Congestive heart failure (pulmonary edema)
•Cardiogenic shock
•Pericarditis
•Mural thrombosis, with possible embolization
•Myocardial wall rupture, with possible tamponade
•Papillary muscle rupture, with possible valvular
insufficiency
•Ventricular aneurysm formation

53. Chronic Ischemic Heart Disease
•This refers to congestive heart failure
occurring usually in the elderly as a
complication of ischaemic cardiac disease.
•Previous history of angina or a remote MI.
•Sometimes the myocardial damage is silent
and the first indication of IHD is CIHD.

54. Morphology.
•Adhesions on pericardial surface
•Moderate to severe stenosing AS of the
coronary arteries
•Scars of previous infarcts
•Normal endocardium or with areas of patchy
fibrous thickenings
•Diffuse myocardial atrophy and sub
endocardial vacuolization.

56. Sudden Cardiac death
•Definition. This is an unexpected death from
cardiac causes within one hour after or without the
onset of symptoms.
•In most cases SCD is a complication of IHD
•SCD may be due to congenital structural
abnormalities,aortic valve stenosis, cardiac
conduction defects
•Mitral valve prolapse, idiopathic or hypertrophied
cardiomyopathy
•Death is usually from lethal arrhythmias