Ischemic heart disease( coronary artery disease)

1. Ischemic heart disease( coronary artery disease)Ischemic heart disease( coronary artery disease)
 IHD results from ischaemia due to an imbalance between the supplyIHD results from ischaemia due to an imbalance between the supply
& demand of the heart for oxygenated blood& demand of the heart for oxygenated blood
 IncludesIncludes
 Myocardial infarctionMyocardial infarction
 Angina pectorisAngina pectoris
 Chronic IHDChronic IHD
 Sudden cardiac deathSudden cardiac death

2. Risk factorsRisk factors
 Non modifiable risk factors:Non modifiable risk factors:
 AgeAge
 SexSex
 Genetics and familial predispositionGenetics and familial predisposition
 Modifiable risk factors:Modifiable risk factors:
 SmokingSmoking
 Heavy drinkingHeavy drinking
 Diabetes mellitusDiabetes mellitus
 Hypercholesterolemia and hyperlipidemiaHypercholesterolemia and hyperlipidemia
 HypertensionHypertension
 Obesity and sedentary lifestyleObesity and sedentary lifestyle
 StressStress

3. PathogenesisPathogenesis
Due to atherosclerosisDue to atherosclerosis
1.1. Atherosclerosis having fixed stenosis plaqueAtherosclerosis having fixed stenosis plaque
 90% of cases of IHD have Atherosclerosis90% of cases of IHD have Atherosclerosis
2.2. Acute change in the atherosclerotic plaqueAcute change in the atherosclerotic plaque
 Rupture, fissuring, ulceration or intraplaque hemorrhageRupture, fissuring, ulceration or intraplaque hemorrhage
3.3. Coronary thrombosisCoronary thrombosis
 Rupture of atherosclerotic plaque exposes sub endothelial collagen &Rupture of atherosclerotic plaque exposes sub endothelial collagen &
may lead to Platelet adherence, activation & autocatalytic chainmay lead to Platelet adherence, activation & autocatalytic chain
reaction leading to the formation of thrombusreaction leading to the formation of thrombus
4.4. Coronary Vasospasm or vasoconstrictionCoronary Vasospasm or vasoconstriction

4. OthersOthers
5. Nonatherosclerotic coronary disease5. Nonatherosclerotic coronary disease
Disorders when involving coronary arteries reduces perfusionDisorders when involving coronary arteries reduces perfusion
 Emboli to coronary arteriesEmboli to coronary arteries
 ArteritisArteritis
 Coccaine abuseCoccaine abuse
 Trauma to coronary arteriesTrauma to coronary arteries
6. Hemodynamic derangements6. Hemodynamic derangements
 Hypotension – shock, massive hemorrhage, spinal anesthesiaHypotension – shock, massive hemorrhage, spinal anesthesia
 Left sided heart failureLeft sided heart failure
 Increase myocardial demand – tachycardia, hypertrophyIncrease myocardial demand – tachycardia, hypertrophy
 Reduced oxygen carrying capacity of bloodReduced oxygen carrying capacity of blood


5. Coronary Artery DistributionCoronary Artery Distribution
 LAD (40-50%) - anterior wall LV, apex, anterior IV septumLAD (40-50%) - anterior wall LV, apex, anterior IV septum
 Right (30-40%) - posterior wall LV, posterior IV septumRight (30-40%) - posterior wall LV, posterior IV septum
 Left circumflex (15-20%) - lateral wall LVLeft circumflex (15-20%) - lateral wall LV

6. ANGINA PECTORISANGINA PECTORIS
 It is characterized by paroxysmal and usually recurrent attacks ofIt is characterized by paroxysmal and usually recurrent attacks of
substernal or precordial chest discomfort or pain caused bysubsternal or precordial chest discomfort or pain caused by
transient (15 seconds to 15 minutes) myocardial ischemia.transient (15 seconds to 15 minutes) myocardial ischemia.
 There is a sense of oppression or tightness in the chest like a bandThere is a sense of oppression or tightness in the chest like a band
round the chest or feeling of choking occursround the chest or feeling of choking occurs
 Sometimes in the left jaw,neck, shoulder, arm & handSometimes in the left jaw,neck, shoulder, arm & hand

7. There are three overlappingThere are three overlapping patterns of anginapatterns of angina pectoris:pectoris:
(1) Stable or typical angina,(1) Stable or typical angina,
(2) Prinzmetal or variant angina, and(2) Prinzmetal or variant angina, and
(3) Unstable or crescendo angina.(3) Unstable or crescendo angina.
Some ischemic heart disease are not perceived by patients, evenSome ischemic heart disease are not perceived by patients, even
though such events may have adverse prognostic implicationsthough such events may have adverse prognostic implications
( silent ischemia).( silent ischemia).

8. Stable (typical) anginaStable (typical) angina
 Caused by the reduction of coronary perfusion by stenosingCaused by the reduction of coronary perfusion by stenosing
coronary atherosclerosis to increased demand e.g during physicalcoronary atherosclerosis to increased demand e.g during physical
activity, emotional excitement, or any other cause of increasedactivity, emotional excitement, or any other cause of increased
cardiac workload.cardiac workload.
 Caused by coronary artery atherosclerosis with luminal narrowingCaused by coronary artery atherosclerosis with luminal narrowing
greater than 75%greater than 75%
 Chest pain is brought on by increased cardiac demandChest pain is brought on by increased cardiac demand

9. Prinzmetal variant anginaPrinzmetal variant angina
 It is a type of angina caused by coronary arteryIt is a type of angina caused by coronary artery
vasospasm.vasospasm.
 There is episodic chest pain often occurring at rest.There is episodic chest pain often occurring at rest.

10. Unstable or crescendo anginaUnstable or crescendo angina
 Caused by formation of a non occlusive thrombus in an area ofCaused by formation of a non occlusive thrombus in an area of
coronary atherosclerosiscoronary atherosclerosis
 Increasing frequency, intensity, and duration of episodesIncreasing frequency, intensity, and duration of episodes
 Occurs at rest / less effortOccurs at rest / less effort
 High risk for myocardial infarction/ preinfarction anginaHigh risk for myocardial infarction/ preinfarction angina

11. Myocardial InfarctionMyocardial Infarction
Infarction of an area of a heart muscle, usually as a result of occlusionInfarction of an area of a heart muscle, usually as a result of occlusion
of coronary arteryof coronary artery
Clinically pain is like angina but of more severe intensityClinically pain is like angina but of more severe intensity
MI rises progressively with increasing ageMI rises progressively with increasing age
Types of MITypes of MI
 Transmural InfarctTransmural Infarct
 Subendocardial/ Non transmual infarctSubendocardial/ Non transmual infarct

12. 1. Reduction in coronary1. Reduction in coronary
blood flowblood flow
 AtherosclerosisAtherosclerosis
 Coronary Vasospasm orCoronary Vasospasm or
vasoconstrictionvasoconstriction
 Thrombosis due toThrombosis due to
complicated atheromacomplicated atheroma
 Emboli to coronary arteriesEmboli to coronary arteries
 ArteritisArteritis
 Trauma to coronary arteriesTrauma to coronary arteries
3. Availability of oxygen in3. Availability of oxygen in
bloodblood
Decreased inDecreased in
Severe anaemiaSevere anaemia
Advanced lung diseaseAdvanced lung disease
Carbon monoxide poisoiningCarbon monoxide poisoining
Cynotic congenital heart diseseCynotic congenital heart disese
2. Increase myocardial demand2. Increase myocardial demand
 Tachycardia as occurs in exercise,Tachycardia as occurs in exercise,
infection, pregnancy, hyperthyroidisminfection, pregnancy, hyperthyroidism
& hypermetabolism& hypermetabolism
 Hemodynamic derangements asHemodynamic derangements as
occurs in Hypotension due to shock,occurs in Hypotension due to shock,
massive haemorrage, spinalmassive haemorrage, spinal
anesthesia,anesthesia,
 Tricuspid regurgitation & Left sidedTricuspid regurgitation & Left sided
heart failure – hypertrophyheart failure – hypertrophy
MI results from imbalanceMI results from imbalance
between supply & demand of thebetween supply & demand of the
heart for oxygenated bloodheart for oxygenated blood
Myocardial InfarctionMyocardial Infarction

13. Coronary artery with thrombus

14. Transmural InfarctTransmural Infarct
 Endocardium to epicardium/ full thickness in the distribution ofEndocardium to epicardium/ full thickness in the distribution of
involved arteryinvolved artery
 Usually associated withUsually associated with
 coronary atherosclerosiscoronary atherosclerosis
 Acute palque changeAcute palque change
 Superimposed thrombosisSuperimposed thrombosis
 Necrosis most likely begins in the subendocardiumNecrosis most likely begins in the subendocardium

15. Subendocardial InfarctSubendocardial Infarct
 This is limited to the inner 1/3This is limited to the inner 1/3rdrd
to 1/2 of the ventricular wallto 1/2 of the ventricular wall
 Associated with diffuse stenosing coronary atherosclerosisAssociated with diffuse stenosing coronary atherosclerosis
 Not associated with atherosclerotic palque rupture or superimposedNot associated with atherosclerotic palque rupture or superimposed
thrombosisthrombosis
 For this reason this is less dangerousFor this reason this is less dangerous

16. ChangesChanges
 Ischaemic myocardium undergoes progressive biochemical, functional &Ischaemic myocardium undergoes progressive biochemical, functional &
morphological changesmorphological changes
MorphologyMorphology
 SiteSite
 Undergoes progressive sequences of coagulative necrosisUndergoes progressive sequences of coagulative necrosis
 Necrosis elicits acute inflammation with neutrophils infiltration in 4- 12 hrNecrosis elicits acute inflammation with neutrophils infiltration in 4- 12 hr
 Later macrophages remove the dead materials most marked in 3-7 daysLater macrophages remove the dead materials most marked in 3-7 days
 Neovascularisation & proliferation of fibroblast at the margin leads toNeovascularisation & proliferation of fibroblast at the margin leads to
fibrous organisationfibrous organisation
 Finally producing an scarFinally producing an scar

17. Light microscopeLight microscope
1.1. Waviness of fibres at bordersWaviness of fibres at borders
2.2. Beginning of coagulation necrosis,Beginning of coagulation necrosis,
oedema, haemorrhage, beginoedema, haemorrhage, begin
neutrophilic infiltrationneutrophilic infiltration
3.3. Continuing coagulation necrosis,Continuing coagulation necrosis,
pallor(pyknosis of nuclei,pallor(pyknosis of nuclei,
shrunken eosinophilic cytoplasmshrunken eosinophilic cytoplasm
marginal contraction bandmarginal contraction band
necrosisnecrosis
Gross changeGross change
1.1. --
2.2. --
3.3. PallorPallor
4.4. PallorPallor
sometimessometimes
hyperemiahyperemia
Time
1.1-2 hours
2.4-12 hours
3.18-24 hours

18. Contraction bands in an early infarct. They are dark pink, and consist of greatly
contracted, ineffective actin and myosin fibrils.

19. Coagulative necrosis plus many neutrophils (2-3 day old infarct).

20. Light microscopeLight microscope
1.1. Total coagulation necrosis withTotal coagulation necrosis with
loss of nuclei & striations, heavyloss of nuclei & striations, heavy
interistial infiltrate of neutrophilsinteristial infiltrate of neutrophils
2.2. Beginning disintegration of deadBeginning disintegration of dead
myofibries & resorption ofmyofibries & resorption of
sarcoplasm by macrophages,sarcoplasm by macrophages,
onset of marginal fibrovascularonset of marginal fibrovascular
responseresponse
Gross changeGross change
1.1. PallorPallor
sometimessometimes
hyperemiahyperemia
2.2. HyperemicHyperemic
border,border,
central yellowcentral yellow
brownbrown
softeningsoftening
3.3.
Time
1.24 - 72hours
2.3-7 days

21. Infarct with numerous macrophages (slightly older, ~7 days).

22. Light microscopeLight microscope
1.1. Well developedWell developed
phagocytosis, prominentphagocytosis, prominent
granulation tissue withgranulation tissue with
fibrovascular reaction infibrovascular reaction in
marginmargin
2.2. --
Gross changeGross change
1.1. Maximally yellow 7Maximally yellow 7
soft, vascularisedsoft, vascularised
margins, red-brownmargins, red-brown
& depressed& depressed
2.2. Scarring completeScarring complete
Time
1.10 days
2.7th
week

23. Macrophages and granulation tissue (~ 10-day-old infarct)

24. Pale area in recent infarct

25. Old infarct. It is a firm scar

26. MI - ComplicationsMI - Complications
 ArrhythmiasArrhythmias
 Commonest cause of death is ventricular arrhythmia, usuallyCommonest cause of death is ventricular arrhythmia, usually
within the first hourwithin the first hour
 CHF and pulmonary edemaCHF and pulmonary edema
 Cardiogenic shockCardiogenic shock
 Pericarditis and pneumonitis( Dressler’s syndrome)Pericarditis and pneumonitis( Dressler’s syndrome)
 Mural thrombosisMural thrombosis
 Rupture of papillary muscle causing acute mitral insufficiency( day 3)Rupture of papillary muscle causing acute mitral insufficiency( day 3)

27. MI - ComplicationsMI - Complications
 Rupture of ventricular wall causing cardiac tamponade( day 4-7)Rupture of ventricular wall causing cardiac tamponade( day 4-7)
 Rupture of ventricular septum causing VSDRupture of ventricular septum causing VSD
 Ventricular aneurysmVentricular aneurysm

28. Recent infarct with perforation

29. Recent infarct with huge mural thrombus

30. Chronic Ischemic Heart DiseaseChronic Ischemic Heart Disease
 Is cardiac muscle insufficiency due to ischaemic myocardial damageIs cardiac muscle insufficiency due to ischaemic myocardial damage
leading to slow progressive heart failureleading to slow progressive heart failure
 Replacement of myocardial fibers by fibrous tissue which tends toReplacement of myocardial fibers by fibrous tissue which tends to
be progressivebe progressive
 Compensatory hypertrophy of non- infarcted musclesCompensatory hypertrophy of non- infarcted muscles
 40% of mortality in IHD40% of mortality in IHD
 Ischemic cardiomyopathyIschemic cardiomyopathy

31. Diffuse fibrosis in chronic ischemic heart disease. There is also myocyte
hypertrophy and a decrease in small vessels.

33. Sudden cardiac death
o Definition: death within 1 hour of cardiac events
Etiology
o In the vast majority of cases in adults, sudden cardiac death is a
complication and often the first clinical manifestation of IHD.
oMechanism: fatal cardiac arrhythmia; usually ventricular fibrillation
Common causes are:
o Coronary artery disease (80%)
o Hypertrophic cardiomyopathy
o Mitral valve prolapse
o Aortic valve stenosis
o Congenital heart abnormalities
o Myocarditis

34. Diffuse fibrosis in chronic ischemic heart disease. There is also myocyte
hypertrophy and a decrease in small vessels.

35. Lab diagnosis of MILab diagnosis of MI
 HistoryHistory
 ECGECG
 Routine blood examinationsRoutine blood examinations
 Neutrophil leucocytosisNeutrophil leucocytosis
 ESR raisedESR raised
 Estimation of serum enzymeEstimation of serum enzyme

36. ECG change seen in MIECG change seen in MI
- ST segment elevation- ST segment elevation
- Abnormal Q waves representing myocardial necrosis develop in 24- Abnormal Q waves representing myocardial necrosis develop in 24
to 48 hrsto 48 hrs
- Inverted T wave- Inverted T wave

37. Cardiac enzymes with their time of riseCardiac enzymes with their time of rise

38.  What are the risk factors for atherosclerosis / IHDWhat are the risk factors for atherosclerosis / IHD
 What are the complications of atherosclerosisWhat are the complications of atherosclerosis
 Give the morphology of atherosclerosisGive the morphology of atherosclerosis
 Give the pathogenesis of atherosclerosisGive the pathogenesis of atherosclerosis
 Define IHD. Classify IHDDefine IHD. Classify IHD
 What are the complications/fates of IHDWhat are the complications/fates of IHD
 Describe the pathogenesis of MIDescribe the pathogenesis of MI
 Give the lab diagnosis of MIGive the lab diagnosis of MI
 What are the sequences of changes / morphology of MIWhat are the sequences of changes / morphology of MI