Ischemic heart disease (IHD) encompasses conditions resulting from myocardial ischemia, primarily atherosclerotic coronary artery disease. The disease can manifest as angina pectoris, myocardial infarction, or sudden cardiac death, with rising incidence in India despite a decline in Western countries due to better prevention and treatment. Risk factors align with those of atherosclerosis, and clinical management relies on timely diagnosis, recognizing symptoms, and assessing biochemical markers like troponin for myocardial infarction.

1. Ischemic Heart DiseaseIschemic Heart Disease
Dr.R.RupnarayanDr.R.Rupnarayan

2. IHDIHD
• Group of closely related syndromes allGroup of closely related syndromes all
due to Myocardial Ischemiadue to Myocardial Ischemia
• > 90% cases> 90% cases Atherosclerotic CoronaryAtherosclerotic Coronary
Artery Disease (CAD)Artery Disease (CAD)
• Most cases the disease is slowMost cases the disease is slow LongLong
latent periodlatent period SilentSilent LateLate
manifestationsmanifestations

3. IschemiaIschemia
due to obstruction to flow :due to obstruction to flow :
• Hypo perfusionHypo perfusion
• Increased oxygen demandIncreased oxygen demand
• Decreased oxygen supplyDecreased oxygen supply

4. IHD: CLINICAL SYNDROMESIHD: CLINICAL SYNDROMES
• Angina PectorisAngina Pectoris:: Less severe Ischemia.:: Less severe Ischemia.
Do not cause muscle death.Do not cause muscle death.
• Myocardial InfarctionMyocardial Infarction:: Most important:: Most important
form of IHD. Duration & severity ofform of IHD. Duration & severity of
ischemia causes muscle death.ischemia causes muscle death.
• Sudden Cardiac DeathSudden Cardiac Death..
• Chronic IHD with Heart Failure.Chronic IHD with Heart Failure.

5. EPIDEMIOLOGY OF IHDEPIDEMIOLOGY OF IHD
• Leading cause of death in males &Leading cause of death in males &
females in US & Europe.females in US & Europe.
• Its incidence is now declining in West. InIts incidence is now declining in West. In
India its increasing.India its increasing.
• Decline is due to prevention of modifiableDecline is due to prevention of modifiable
risk factors; Better diagnostic &risk factors; Better diagnostic &
therapeutic modalities.therapeutic modalities.
• Risk factors are same as forRisk factors are same as for
Atherosclerosis.Atherosclerosis.

6. PATHOGENESIS OF IHDPATHOGENESIS OF IHD
• Diminished coronary perfusion relative toDiminished coronary perfusion relative to
myocardial demandmyocardial demand
• Ischemia: Consequence ofIschemia: Consequence of
-Fixed atherosclerotic narrowing of-Fixed atherosclerotic narrowing of
epicardial CAepicardial CA
-Disrupted atherosclerotic plaques-Disrupted atherosclerotic plaques
-Intra-luminal thrombosis-Intra-luminal thrombosis
-Vasospasm-Vasospasm

7. 1. FIXED CORONARY ARTERY1. FIXED CORONARY ARTERY
OBSTRUCTIONOBSTRUCTION
• A fixed 75% obstructionA fixed 75% obstruction Ischemia atIschemia at
exercise.exercise.
• 90% stenosis90% stenosis Inadequate coronary flowInadequate coronary flow
even at rest.even at rest.
• Single, two or all three CA can beSingle, two or all three CA can be
affected.affected.
• LAD, LCA, RCA.LAD, LCA, RCA.

8. • Acute coronary syndromeAcute coronary syndrome
precipitated by plaque disruptionprecipitated by plaque disruption
• Erosion/ ulcerationErosion/ ulceration
• Rupture/ fissuringRupture/ fissuring
• Hemorrhage into atheromaHemorrhage into atheroma
2.2. Acute Plaque ChangeAcute Plaque Change

9. Acute Plaque Change: risk factorsAcute Plaque Change: risk factors
• Adrenergic stimulusAdrenergic stimulus
• Eccentric plaqueEccentric plaque
• Large soft coreLarge soft core
• Thin fibrous capThin fibrous cap

11. 3. Coronary Thrombosis3. Coronary Thrombosis
• Platelets- Thromboxane A2Platelets- Thromboxane A2
• Increased fibrinogenIncreased fibrinogen
• Low plasminogen activator inhibitorLow plasminogen activator inhibitor
• High lipoprotein (a)High lipoprotein (a)
• Thrombus can emboliseThrombus can embolise
• Thrombus is an activator of growth signalsThrombus is an activator of growth signals
to SMto SM

12. 4. Vasoconstriction4. Vasoconstriction
• Adrenergic agonistAdrenergic agonist
• Locally released platelet contentsLocally released platelet contents
• Endothelial dysfunctionEndothelial dysfunction
• Mediators released from mast cellsMediators released from mast cells

13. IHD: CLINICAL SYNDROMESIHD: CLINICAL SYNDROMES
• Angina PectorisAngina Pectoris:: Less severe Ischemia.:: Less severe Ischemia.
Do not cause muscle death.Do not cause muscle death.
• Myocardial InfarctionMyocardial Infarction:: Most important:: Most important
form of IHD. Duration & severity ofform of IHD. Duration & severity of
ischemia causes muscle death.ischemia causes muscle death.
• Sudden Cardiac DeathSudden Cardiac Death..
• Chronic IHD with Heart Failure.Chronic IHD with Heart Failure.

15. ANGINA PECTORISANGINA PECTORIS
• Symptom complex of IHDSymptom complex of IHD
• Paroxysmal & recurrent sub sternal orParoxysmal & recurrent sub sternal or
precordial chest discomfortprecordial chest discomfort
• Constricting, choking, squeezing, knifelikeConstricting, choking, squeezing, knifelike
feelingfeeling
• TransientTransient 15 sec to 15 Min.15 sec to 15 Min.
• No cardiac muscle cell death.No cardiac muscle cell death.
• Falls short of infarctionFalls short of infarction

16. ANGINA PECTORISANGINA PECTORIS
• Three Overlapping Patterns of AnginaThree Overlapping Patterns of Angina
PectorisPectoris::::
- Stable or Typical Angina- Stable or Typical Angina
- Prinzmetal or Variant Angina- Prinzmetal or Variant Angina
- Unstable or Crescendo Angina- Unstable or Crescendo Angina
• There is increased myocardial demand;There is increased myocardial demand;
decreased myocardial perfusion;decreased myocardial perfusion;
stenosing plaques; disrupted plaques;stenosing plaques; disrupted plaques;
vasospasm.vasospasm.

17. STABLE ANGINASTABLE ANGINA
• Most Common FormMost Common Form
• Reduction of coronary perfusion due toReduction of coronary perfusion due to
chronic stenosing atherosclerosis.chronic stenosing atherosclerosis.
• Seen at times of increased demand.Seen at times of increased demand.
• Relieved by rest, nitroglycerin, or otherRelieved by rest, nitroglycerin, or other
vasodilators.vasodilators.

18. PRINZMETAL ANGINAPRINZMETAL ANGINA
• Uncommon typeUncommon type
• Occurs atOccurs at restrest. Due to. Due to VasospasmVasospasm ofof
coronaries.coronaries.
• Angina is unrelated to physical activity.Angina is unrelated to physical activity.
• Responds to vasodilators like nitroglycerinResponds to vasodilators like nitroglycerin
& calcium channel blockers.& calcium channel blockers.
• ECG shows ST segment elevation.ECG shows ST segment elevation.

19. UNSTABLE ANGINAUNSTABLE ANGINA
• Pattern of pain that is progressive withPattern of pain that is progressive with
increasing frequencyincreasing frequency
• Precipitated by less effortPrecipitated by less effort
• Often occurs at rest. Tends to be longOften occurs at rest. Tends to be long
duration.duration.
• Induced by disruption of atheroscleroticInduced by disruption of atherosclerotic
plaques, with superadded thrombosis,plaques, with superadded thrombosis,
embolisation & Vasospasm.embolisation & Vasospasm.
• Pre Infarction AnginaPre Infarction Angina

21. MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
• Death of the Cardiac Muscle by infarctionDeath of the Cardiac Muscle by infarction
• Most Important & Most severe form of IHDMost Important & Most severe form of IHD
• Leading cause of death in West & rising inLeading cause of death in West & rising in
INDIA.INDIA.
• Acute Coronary syndromesAcute Coronary syndromes::
- Myocardial Infarction- Myocardial Infarction
- Unstable Angina- Unstable Angina
- Sudden cardiac Death.- Sudden cardiac Death.

22. PATHOGENESIS OF MIPATHOGENESIS OF MI
• CORONARY ARTERY OCCLUSIONCORONARY ARTERY OCCLUSION
Disruption of PlaqueDisruption of Plaque Platelets exposed to Sub-Platelets exposed to Sub-
endothelial collagenendothelial collagen Platelet Adhesion,Platelet Adhesion,
Aggregation, Activation, Release of potentAggregation, Activation, Release of potent
Aggregators. Vasospasm is Stimulated.Aggregators. Vasospasm is Stimulated.
• VASOSPASMVASOSPASM
• EMBOLIEMBOLI
Atrial Fibrillation,Atrial Fibrillation,
Vegetative endocarditisVegetative endocarditis
Pardoxical emboliPardoxical emboli
• UNEXPLAINEDUNEXPLAINED

23. MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION
TYPESTYPES
• TRANSMURALTRANSMURAL
• SUBENDOCARDIALSUBENDOCARDIAL

25. GENERAL PATHOLOGY OFGENERAL PATHOLOGY OF
MYOCARDIAL ISCHAEMIAMYOCARDIAL ISCHAEMIA
FunctionalFunctional: Ischemic muscle ceases to: Ischemic muscle ceases to
contract within a few minutes. Necrosiscontract within a few minutes. Necrosis
is inhibited if flow is restored within 20-is inhibited if flow is restored within 20-
40 mins.40 mins.
BiochemicalBiochemical::
1. Oxygen tension falls,1. Oxygen tension falls,
Mitochondrial respiration DeclinesMitochondrial respiration Declines 
Ceases.Ceases.

26. Fatty fuels cannot be usedFatty fuels cannot be used
Anaerobic glycolysisAnaerobic glycolysis  IncreasedIncreased
concentration of lactic Acid.concentration of lactic Acid.
Limited Glycogen storesLimited Glycogen stores  ReduceReduce
Intracellular ATPIntracellular ATP Concentrations ReachConcentrations Reach
Zero in 40-60 mins.Zero in 40-60 mins.
Creatinine Phosphate Conc.Creatinine Phosphate Conc. ZeroZero
in 15 mins. Myosin ATPase Inhibitedin 15 mins. Myosin ATPase Inhibited
CESSATION OF CONTRACTIONCESSATION OF CONTRACTION

27. MIMI
• Myocardial Necrosis Begins approx 30Myocardial Necrosis Begins approx 30
Min after Coronary OcclusionMin after Coronary Occlusion
• Severe Reduction, Extended interval,Severe Reduction, Extended interval,
Prolonged IschemiaProlonged Ischemia Permanent Loss ofPermanent Loss of
Function.Function.
• Cell Death is By Coagulation Necrosis &Cell Death is By Coagulation Necrosis &
Apoptosis.Apoptosis.
• Reperfusion in Less than 20 Min canReperfusion in Less than 20 Min can
Restore Cell Viability.Restore Cell Viability.

28. FEATURESFEATURES TIMETIME
Onset of ATP DepletionOnset of ATP Depletion SecondsSeconds
Loss of ContractilityLoss of Contractility Less than 2 MinLess than 2 Min
50% Reduction in ATP50% Reduction in ATP 10 Min10 Min
90% Reduction in ATP90% Reduction in ATP 40 Min40 Min
Irreversible Cell InjuryIrreversible Cell Injury 20- 40 Min20- 40 Min
Micro-vascular InjuryMicro-vascular Injury More than 1 HourMore than 1 Hour
KEY EVENTS IN ISCHEMIC CARDIAC MYOCYTES

29. LOCATION OF INFARCTLOCATION OF INFARCT
• LADLAD  Anterior & Apical LVAnterior & Apical LV
& 2/3 IV Septum [40--50%]& 2/3 IV Septum [40--50%]
• RCARCA  Post & Basal LVPost & Basal LV
& Post 1/3 of IV Septum [30--40%]& Post 1/3 of IV Septum [30--40%]
• LCALCA  Lateral wall of LVLateral wall of LV
[15 - 20% ][15 - 20% ]

30. CoronaryCoronary
ArteriesArteries
•Left Coronary A.
•L.A.Descending
•Left Circumflex
•Right Coronary A.
LCx
LAD

34. TIMETIME GROSSGROSS MICROSCOPYMICROSCOPY
0 to ½0 to ½
HourHour
NoNo
ChangesChanges
NoneNone
½ to 4 Hrs½ to 4 Hrs NoneNone Variable FibreVariable Fibre
WavinessWaviness
4 to 124 to 12
HrsHrs
Occ darkOcc dark
MottlingMottling
Odema, early CoagOdema, early Coag
Necrosis,Necrosis,
HemorrhageHemorrhage
12 to 2412 to 24
HrsHrs
DarkDark
MottlingMottling
Coag Necrosis,Coag Necrosis,
contraction bands,contraction bands,
Neutrophil infiltrnNeutrophil infiltrn

35. TIMETIME GROSSGROSS MICROSCOPYMICROSCOPY
1 to 3 days1 to 3 days Yellow tanYellow tan
InfarctInfarct
centrecentre
Loss ofLoss of
Striations,Striations,
InterstitialInterstitial
Neutrophils.Neutrophils.
3 to 7 days3 to 7 days HyperamicHyperamic
Border,Border,
central Softcentral Soft
Dead Cells,Dead Cells,
Phagocytosis,Phagocytosis,
macrophagesmacrophages
7 to 10 days7 to 10 days Red TanRed Tan
MarginsMargins
EarlyEarly
GranulationGranulation
TissueTissue
10 days to 210 days to 2
weeksweeks
DepressedDepressed
infarctinfarct
New BloodNew Blood
vessels,vessels,

36. TIMETIME GROSSGROSS MICROSCOPYMICROSCOPY
2-8 weeks2-8 weeks Gray whiteGray white
scarscar
formation.formation.
Border toBorder to
CoreCore
IncreasedIncreased
CollagenCollagen
DecreasedDecreased
CellularityCellularity
> 2 months> 2 months Firm scarFirm scar DenseDense
collagenouscollagenous
scarscar

37. The earliest change histologically seen with acute myocardial infarction
in the first day is contraction band necrosis.

38. This myocardial infarction is about 3 to 4 days old. There is an extensive acute inflammatory cell
infiltrate and the myocardial fibers are so necrotic that the outlines of them are only barely
visible

39. There is pale white collagen within the interstitium between myocardial
fibers. This represents an area of remote infarction

40. The myocardium beneath the endocardial surface at the top demonstrates
pale fibrosis with collagenization following healing of a subendocardial
myocardial infarction

42. Reperfusion :Infarct Modification
• Area at risksalvagepartial salvage
infarct
• Arrhythmias
• Hemorrhage +contraction bands
• Irreversible cell damage (injury)
• Myocardial stunning

43. Contraction band necrosis

45. DIAGNOSIS OF MIDIAGNOSIS OF MI
• Typical Symptoms + BiochemicalTypical Symptoms + Biochemical
Investigations + ECG PatternInvestigations + ECG Pattern
• Pain, Dyspnoea, Profuse Sweating, RapidPain, Dyspnoea, Profuse Sweating, Rapid
Weak Pulse, Pulmonary CongestionWeak Pulse, Pulmonary Congestion
• 10 to 15% have Silent MI10 to 15% have Silent MI
• Early Perfusion by Cardiac Intervention isEarly Perfusion by Cardiac Intervention is
Beneficial.Beneficial.

47. BIOCHEMICAL CARDIACBIOCHEMICAL CARDIAC
ENZYMESENZYMES
• The Enzymes are Released intoThe Enzymes are Released into
Circulation during Muscle NecrosisCirculation during Muscle Necrosis
• Myoglobin, Cardiac Troponin I & T,Myoglobin, Cardiac Troponin I & T,
Creatine Kinase-MB, LactateCreatine Kinase-MB, Lactate
dehydrogenase & Others.dehydrogenase & Others.
• Previous “Gold Standard” for MI diagnosisPrevious “Gold Standard” for MI diagnosis
was CK-MB. Now it is Troponin I & T.was CK-MB. Now it is Troponin I & T.
• CK- MB & Troponin I &T are Sensitive &CK- MB & Troponin I &T are Sensitive &
SpecificSpecific

48. BIOCHEMICAL MARKERSBIOCHEMICAL MARKERS
• Creatine KinaseCreatine Kinase::::
- Has Brain, Muscle & Cardiac Isoforms.- Has Brain, Muscle & Cardiac Isoforms.
- Not Specific.- Not Specific.
- Rises in 2 Hrs, Peaks in 24 Hrs & Normal- Rises in 2 Hrs, Peaks in 24 Hrs & Normal
in 72 Hrs.in 72 Hrs.
• Creatine Kinase MBCreatine Kinase MB::::
-More Specific-More Specific
- Rises in 4 to 8 hrs, Peak 18 Hrs &- Rises in 4 to 8 hrs, Peak 18 Hrs &
Normal in 2-3 days.Normal in 2-3 days.

49. BIOCHEMICAL MARKERSBIOCHEMICAL MARKERS
• LDHLDH is Useful after 48 hrs.is Useful after 48 hrs.
• Cardiac Troponin I & TCardiac Troponin I & T is Sensitive,is Sensitive,
elevated for 7 to 10 Days. Marker forelevated for 7 to 10 Days. Marker for
Unstable Angina.Unstable Angina.
• Serum MyoglobinSerum Myoglobin::::
- Precedes CK- MB by 2 to 5 Hrs.- Precedes CK- MB by 2 to 5 Hrs.
Increases in 2 to 6 hrs & peaks in 8 to 12Increases in 2 to 6 hrs & peaks in 8 to 12
Hrs.Hrs.

51. EARLY COMPLICATIONSEARLY COMPLICATIONS
• Sudden cardiac arrestSudden cardiac arrest
• Arrhythmias and Conduction defects,Arrhythmias and Conduction defects,
• Left ventricular failureLeft ventricular failure
• Cardiogenic shockCardiogenic shock

52. LATE COMPLICATIONSLATE COMPLICATIONS
• Pericarditis ( Dressler’s)Pericarditis ( Dressler’s)
• Mural thrombosis, - EmbolizationMural thrombosis, - Embolization
• Myocardial rupture :Myocardial rupture :
Lateral wall- TamponadeLateral wall- Tamponade
IVS- intracardiac shuntIVS- intracardiac shunt
• Papillary muscle rupture,Papillary muscle rupture,
Ventricular aneurysmVentricular aneurysm

55. CHRONIC ISCHEMIC HEARTCHRONIC ISCHEMIC HEART
DISEASEDISEASE
• Seen inSeen in ELDERLYELDERLY
• Previous MI / Bypass SurgeryPrevious MI / Bypass Surgery
• Severe obstructive coronary arterySevere obstructive coronary artery
diseasedisease
• With or Without Acute MI or Healed MIWith or Without Acute MI or Healed MI

56. MORPHOLOGYMORPHOLOGY
MACROMACRO
Heart Enlarged & Heavy due toHeart Enlarged & Heavy due to LVH &LVH &
DILATIONDILATION
Moderate to Severely StenosedModerate to Severely Stenosed CoronaryCoronary
arteriesarteries
ScarsScars of healed previous infarctsof healed previous infarcts

57. CLINICAL FEATURESCLINICAL FEATURES
• Silent with HEART FAILURESilent with HEART FAILURE FirstFirst
Indication of chronic IHDIndication of chronic IHD
• Insidious onset of CCF in patientsInsidious onset of CCF in patients
withwith
past episodes of MI / Bypass.past episodes of MI / Bypass.
• Also called Ischemic CardiomyopathyAlso called Ischemic Cardiomyopathy

59. SUDDEN CARDIACSUDDEN CARDIAC
DEATHDEATH
Unexpected death from cardiacUnexpected death from cardiac
causescauses
withinwithin ONEONE HOURHOUR or without onsetor without onset
of symptomsof symptoms
80 to 90% : Complication of IHD80 to 90% : Complication of IHD
10 to 20% :10 to 20% : Non-AtheroscleroticNon-Atherosclerotic
causescauses
-Aortic valve stenosis-Aortic valve stenosis
- Mitral valve Prolapse- Mitral valve Prolapse
-Myocarditis-Myocarditis
-Cardiomyopathy-Cardiomyopathy