Undergraduates

1. Ischaemic Heart DiseaseIschaemic Heart Disease
Dr. Evith Pereira

2. Ischaemic Heart DiseaseIschaemic Heart Disease
Imbalance :Imbalance : Myocardial requirement Vs Supply ofMyocardial requirement Vs Supply of
oxygenated blood.oxygenated blood.
Synonymous with coronary artery disease as in 90 %Synonymous with coronary artery disease as in 90 %
cases the cause in atherosclerosis of of coronariescases the cause in atherosclerosis of of coronaries

3.  Is defined as acute or chronic form ofIs defined as acute or chronic form of
cardiac disability arising from imbalancecardiac disability arising from imbalance
between the myocardial supply &between the myocardial supply &
demand for oxygenated blood.demand for oxygenated blood.
 It is the leading cause of death in mostIt is the leading cause of death in most
industrialized countries.industrialized countries.

5. Ischaemic Heart Disease (contd..)Ischaemic Heart Disease (contd..)
AsymptomaticAsymptomatic Chronic Ischaemic heart diseaseChronic Ischaemic heart disease
IHDIHD
Angina pectorisAngina pectoris
Myocardial InfarctionMyocardial Infarction Sudden Cardiac DeathSudden Cardiac Death
Spectrum of Sudden deathSpectrum of Sudden death

6.  IHD is invariably caused by diseases of the coronary artery-IHD is invariably caused by diseases of the coronary artery-
1.1. Coronary atherosclerosisCoronary atherosclerosis
A.A. DistributionDistribution
 Anterior descending branch of LCAAnterior descending branch of LCA
 Right Coronary arteryRight Coronary artery
 Circumflex branch of LCACircumflex branch of LCA
 B. LocationB. Location
 Commonly involved sites areCommonly involved sites are
• Coronary artery area 3 to 4 cm from the coronary ostiaCoronary artery area 3 to 4 cm from the coronary ostia
• At or near biforcation of the arteries.At or near biforcation of the arteries.
 C. Fixed athersclerotic PlaquesC. Fixed athersclerotic Plaques
• Atherosclerotic plaques are often eccentrically locatedAtherosclerotic plaques are often eccentrically located
• The fixed coronary obstruction may result from gradualThe fixed coronary obstruction may result from gradual
luminal narrowing.luminal narrowing.

7. Superadded changes in A SSuperadded changes in A S
 Acute changes like ulceration,haemorrhage,fissuringAcute changes like ulceration,haemorrhage,fissuring
 Coronary artery thrombosis.Coronary artery thrombosis.
 Local platelet aggregation .Local platelet aggregation .
 Coronary artery spasm[thromboxane A2]Coronary artery spasm[thromboxane A2]

9. Non A S causesNon A S causes
 Vasospasm.Vasospasm.
 Stenosis of coronary ostia.Stenosis of coronary ostia.
 Arteritis.Arteritis.
 Embolism.Embolism.
 Thrombotic diseases.Thrombotic diseases.
 Trauma.Trauma.
 Aneurysm.Aneurysm.
 Compression.Compression.

10. Causes of increased myocardial demandCauses of increased myocardial demand
 Hypertrophy of Heart-Hypertrophy of Heart-
 Hypertension.Hypertension.
 Ventricular hypertrophy.Ventricular hypertrophy.
 Exercise. Etc.Exercise. Etc.

11. Types of Infarcts - Depending uponTypes of Infarcts - Depending upon
Age – Acute/ Recent / freshAge – Acute/ Recent / fresh
Old/Healed/ Organized .Old/Healed/ Organized .
Anatomic region of left ventricle involved -Anatomic region of left ventricle involved -
Lateral / Septal / CircumferentialLateral / Septal / Circumferential
Ant / Post / InferiorAnt / Post / Inferior
Combination of above e.g. Anteroseptal/Combination of above e.g. Anteroseptal/
Posterolateral/ AnterolateralPosterolateral/ Anterolateral

12. Thickness of ventricular wall.Thickness of ventricular wall.
 TransmuralTransmural
95% cases95% cases
 75% Lumen is75% Lumen is
compromisedcompromised
 Full thickness solidFull thickness solid
 Specific area ofSpecific area of
coronary supplycoronary supply
 Epicarditis +Epicarditis +
 Coronary thrombosis+Coronary thrombosis+
 SubendocardialSubendocardial
(laminar- 5%)(laminar- 5%)
 Hypoperfusion to theHypoperfusion to the
Myocardium.Myocardium.
 Inner 1/3 - ½Inner 1/3 - ½
Patchy .Patchy .
 Circumferential .Circumferential .

13. Location of InfarctsLocation of Infarcts
>Common in left ventricle – thick wall>Common in left ventricle – thick wall
Rt. Ventricles – Less susceptible - Thin wallRt. Ventricles – Less susceptible - Thin wall
- Less Metabolic requirement- Less Metabolic requirement
- Adequate nourishment by- Adequate nourishment by
thebesian Vs.thebesian Vs.
Coronary – LAD – Commoner (40-50%) – Ant. Part of LV, ApexCoronary – LAD – Commoner (40-50%) – Ant. Part of LV, Apex
(Lt. Ant. Descending) Ant 2/3 of IV Septum(Lt. Ant. Descending) Ant 2/3 of IV Septum
- Rt. Coronary – (30 – 40%)- Rt. Coronary – (30 – 40%) Post part of LVPost part of LV
Post 1/3 of I.V. SeptumPost 1/3 of I.V. Septum
- Left Circumflex coronary (15-20%) Lateral wall of LV .- Left Circumflex coronary (15-20%) Lateral wall of LV .

14. Gross& H/P changesGross& H/P changes.—1.—1stst
weekweek
0-6 hrs0-6 hrs No change.No change.
TTC/NBT -veTTC/NBT -ve
? Streching &? Streching &
waviness of fibres.waviness of fibres.
6-12 hrs6-12 hrs samesame CoagulativeCoagulative
necrosis,pmn,h’ge.necrosis,pmn,h’ge.
24 hrs24 hrs Cyanotic,red-Cyanotic,red-
purple,h’ge.purple,h’ge.
>coag.necrosis;>coag.necrosis;
> pmn’s.> pmn’s.
48-72 hrs48-72 hrs Pale,hyperaemic.Pale,hyperaemic. Coag.necrosisCoag.necrosis
complete.>>pmn’scomplete.>>pmn’s
3-7 day3-7 day Hyperaemic borderHyperaemic border
Centre-yellow,softCentre-yellow,soft
Macrophages inMacrophages in
ms,fibrovascular.ms,fibrovascular.

15. Gross & H/P changes.Gross & H/P changes.
22ndnd
weekweek
1010thth
dayday
Red-purple at theRed-purple at the
periphery.periphery.
Most of necrosedMost of necrosed
ms. Removedms. Removed
fibrovs.>>macro&fibrovs.>>macro&
Lymphocytes.Lymphocytes.
14 th day14 th day samesame << necrosed ms.<< necrosed ms.
Fibrosis++Fibrosis++
33rdrd
weekweek samesame <<Necrosed ms.<<Necrosed ms.
From large infarctFrom large infarct
44thth
-6-6thth
weekweek Thin grey-white,Thin grey-white,
hard,shrunken scarhard,shrunken scar
>>>fibrosis,collag>>>fibrosis,collag
enization.<<<infl.enization.<<<infl.

21. MICROSCOPYMICROSCOPY

24. COMPLICATIONSCOMPLICATIONS
80-90% cases develop complications that may be fatal.80-90% cases develop complications that may be fatal.
Immediate mortality – 25 %Immediate mortality – 25 %
1)1) Arrythmia - most common – Due to Ischaemic injury toArrythmia - most common – Due to Ischaemic injury to
conduction system.conduction system.
- Leakage of K + from ischaemic muscle.- Leakage of K + from ischaemic muscle.
- >> conc.of Lactate & FFA in tissue- >> conc.of Lactate & FFA in tissue
2)2) CCF :- 40% death in MI : CCFCCF :- 40% death in MI : CCF
3)3) Cardiogenic Shock :- 10%Cardiogenic Shock :- 10%
((Hypotension, Peripheral circulatory failure,Oliguria,Mental confusion )Hypotension, Peripheral circulatory failure,Oliguria,Mental confusion )

25. COMPLICATIONS(Contd..)COMPLICATIONS(Contd..)
4)4) Mural Thrombosis & Thromboembolism – 15 – 45 % casesMural Thrombosis & Thromboembolism – 15 – 45 % cases
Develop Intracardiac Thrombi / Thrombi in leg veins.Develop Intracardiac Thrombi / Thrombi in leg veins.
Cause of death – 12 % casesCause of death – 12 % cases
5) Rupture of Heart – 5% cases.5) Rupture of Heart – 5% cases.
To Pericardium – Haemopericardium – Cardiac tamponadeTo Pericardium – Haemopericardium – Cardiac tamponade
I.V. SeptumI.V. Septum
Papillary muscle Mitral Incompetance/ RegurgitationPapillary muscle Mitral Incompetance/ Regurgitation
6) Cardiac aneurysm – 5% site for thrombi.6) Cardiac aneurysm – 5% site for thrombi.
7) Fibrinous pericarditis & effusion – resolves spontaneously7) Fibrinous pericarditis & effusion – resolves spontaneously
8) Post myocardial Infarction syndrome – Dresller’s syndrome8) Post myocardial Infarction syndrome – Dresller’s syndrome
3-4% patients. Occurs 1-6 weeks after attack. Charactrized by Pneumonitis3-4% patients. Occurs 1-6 weeks after attack. Charactrized by Pneumonitis
??Antiheart Abs + in patients serum.??Antiheart Abs + in patients serum.

26. Clinical Features – Sudden onset.Clinical Features – Sudden onset.
1)1) Pain – Sudden, Severe crushing, ProlongedPain – Sudden, Severe crushing, Prolonged
- Substernal / Precordial with sweating- Substernal / Precordial with sweating
- Radiating to one/both arms, neck, back- Radiating to one/both arms, neck, back
2) Indigestion - Nausea, vomiting with Heart burn2) Indigestion - Nausea, vomiting with Heart burn
3) Apprehension .3) Apprehension .
4) Shock – BP < 80 mm Hg.4) Shock – BP < 80 mm Hg.
Cold Clammy limbs,Cold Clammy limbs,
Peripheral CyanosisPeripheral Cyanosis
Pulse – Weak – tachy / Bradycardia.Pulse – Weak – tachy / Bradycardia.
5) Oliguria - < 20 ml/hr.5) Oliguria - < 20 ml/hr.
6) Law grade Fever with in 24 hrs. upto 1 week (necrosis of ms with pmn’s.6) Law grade Fever with in 24 hrs. upto 1 week (necrosis of ms with pmn’s.
7) Acute Pulmonary oedema – LVF- Suffocation/ Dyspnoea/Bubbling respiration.7) Acute Pulmonary oedema – LVF- Suffocation/ Dyspnoea/Bubbling respiration.

27. Serum cardiac markers.Serum cardiac markers.
Proteins & Enzymes released into blood from necrotic heartProteins & Enzymes released into blood from necrotic heart
muscle.muscle.
1.1. SGOT.SGOT.
2.2. Creatinine phosphokinase (CK) &CK-MB .Creatinine phosphokinase (CK) &CK-MB .
CK MM—Skeletal muscle.CK MM—Skeletal muscle.
CK MB—Cardiac muscle—CK MB2.CK MB—Cardiac muscle—CK MB2.
CK BB—Brain, Lungs.CK BB—Brain, Lungs.
Ratio of CK MB2: CK MB1 > 1.5Ratio of CK MB2: CK MB1 > 1.5
Diagnostic of MI 4-6 hrs after onset.Diagnostic of MI 4-6 hrs after onset.
Disappears in 48 hrs.Disappears in 48 hrs.

28. Serum cardiac markersSerum cardiac markers
4. Lactic dehydrogenase (LDH) Nonspecific.4. Lactic dehydrogenase (LDH) Nonspecific.
LDH1 specific for myocardium.LDH1 specific for myocardium.
Ratio LDH1:LDH2 >1 –helpful.Ratio LDH1:LDH2 >1 –helpful.
Appears to increase after 24 hrs.Appears to increase after 24 hrs.
Peak 3-6 days. Normal in 14 days.Peak 3-6 days. Normal in 14 days.
5.Cardiac specific Troponins (cTn)—Most specific.5.Cardiac specific Troponins (cTn)—Most specific.
Immunoassay T & I.Immunoassay T & I.
Not normally present.Not normally present.
Rise parallel to CK-MBRise parallel to CK-MB