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  1. Atheroma fibrofatty plaque
  2. Affects elastic arteries (aorta, carotid &iliac arteries) & large. & medium sized muscular arteries
  3. Begins in childhood, symptomatic later (MI, stroke, claudication, gangrene)
  1. Morphology: Raised focal 'plaque within intima having core of lipid (cholesterol & cholesterol esters) & covering fibrous cap. Q
  2. Distribution: Abdominal aorta - more commonly involved (prominent around ostia)
In descending order:                  
  1. Abdominal aorta                                  
  2. Coronary arteries                        
  3. Popliteal arteries
  4. Descending Thoracic aorta                
  5. Internal carotid artery                
  6. Circle of Willis
H/P ­
  1. Fibrous cap- Smooth muscle cells, macrophages, foam cells
  2. Shoulder: Cellular area beneath & to side of caps (macrophages, smooth muscle cells, T Lymphocytes
  3. Necrotic Core - Debris, cholesterol clefts
  4. Neovascularization at the periphery
  1. Complications:
    1. Calcification
    2. Focal rupture or gross ulceration cholesterol, emboli or atheroemboli
    3. Hemorrhage
    4. Superimposed thrombosis
    5. Aneurysmal dilation
  1. Fatty streaks:
  1. Not significantly raised, no disturbance, in blood flow
  2. Yellow flat spots, < 1 mm (fatty dots)
  3. Elongated streaks, 1 cm or longer (fatty streaks) seen in aorta of children < 1 years & in all > 10 years related to atherosclerosis complex Composed of lipid filled foam cells & T lymphocytes
American heart Associated classification of human atherosclerotic lesions:
American Heart Association Classification (1995) of Human Atherosclerosis    
Types Main histology Main pathogenesis
Type I: (Initial lesions)
Macrophages, occasional foam cell Accumulation of lipoprotein
Type II: (Fatty streaks)
Many layers of macrophages and foam cell Accumulation of lipoprotein
Type III: (Intermediate lesions)
Many lipid-laden cell and scattered extracellular lipid droplets Accumulation of lipoprotein
Type IV (Atheromatous lesion)
Intra as well as extra-cellular lipid pool Accumulation of lipid
Type V (Fibro fatty lesions)
Fibrotic cap and lipid core (Va), may have calcification Vb) and increased collagen Smooth muscle cell proliferation
Type VI: (Complicated lesions)
Ulceration, haemorrhage, hematoma, thrombosis Haemodynamic stress, thrombosis, haematoma
Risk Factors
1 HT
2 DM
3 Hyperlipidemia
4 Smoking
Non modifiable
­ Age
Male gender
, Family h/o
Cigarette smoking
(Lesser / Uncertain) causes:
  1. Obesity                                                                 
  2. Type A personality                                              
  3. Alcohol - Moderate intake - protective role  
  4. Physical Inactivity
  5. High S. Homocysteine        
  6. ­ Lipoprotein (a) - altered form of LDL that contain apolipoprotein B-100)
Response to injury hypothesis
  1. Chronic endothelial injury: Increased permeability, leukocyte adhesion and thrombotic potential
  2. Accumulation of lipoproteins, modification by oxidation Q
  3. Adhesion of blood monocytes Transformation into macro phages & foam cells in intima.
  4. Adhesion of platelets
  5. Release of factors from activated platelets, macrophages or vascular cells migration of smooth muscle cells from media to intima Q
  6. Proliferation of smooth muscle cells with elaboration of E/C matrix Q
  7. Enhanced accumulation of lipids
Clinically, IHD: 4 syndromes Q
  1. MI           
  2. Angina pectoris
  3. Chronic ischemic heart disease with heart failure
  4. Sudden cardiac death
  1. Role of fixed Coronary obstruction:
    1. 90% of pts with IHD have fixed obstruction
    2. At least 75% reduction of cross- sectional 'area of one of major epicardial arteries
  1. Role of Acute Plaque Changes:
    Most often initialing event is disruption of previously only partially stenosing plaque with
    1. Hemorrhage into atheroma      
    2. Rupture or fissuring
    3. Erosion or ulceration
  1. Unknown: Adrenergic stimulation (Peak incidence of MI: 6 Am to 12 noon) Q
    1. Eccentric configuration of plaque.
    2. Plaque with large soft core of necrotic debris & lipid
    3. Most Dangerous lesions: Moderately stenotic (50-75%), lipid rich atheromas, which are themselves insufficient to induce stable angina before disruption;
  2. Atheroma
    1. Of mod. size often has complex configuration with well developed soft core
    2. Plaque causing obstruction sufficient to limit flow severely have mechanical stresses in their wallQ
    3. High grade, slowly developing occlusion stimulate collateral formations' Q
    4. Repetitive non-lethal MI may be protective to infarction (Pre conditioning) (Mechanism - Unknown). Q
  3. Role of coronary thrombus:
    1. In acute Transmural (TM) MI, thrombus on partially stenotic plaque → total occlusion
    2. Contribution to growth of arthrosclerotic lesions. Q
Syndromes Stenosis PlaqueDisruption
Plaque ass.
Stable Angina
Unstable Angina Transmural MI Subendocardial MI
Sudden death
Non occlusive
Var; Partial/complete/ lysed. 
Often-small, platelet aggregates or thrombi &/or Thromboembolic
Angina Pectoris:
Caused by transient ischemia (15sec.-15min.) that fall short of inducing cell necrosis / infarction.

  1. Stable/Typical Angina → M. comm. Type, chronic stenosing lesion.
  2. Prinzmetal / Variant angina →  occurs at rest, coronary artery spasm Q  
  3. Unstable/crescendo angina →↑freq; at rest, Partial thrombosis with embolism or vasospasm
  4. Pre infarction angina

Mycoardial Infarction

  1. Full thickness ischemia
  2. In distribution of single artery

B. Subendocardial

  1. Inner 1/3 rd of ventricular wall
  2. extends laterally beyond perfusion
  3. Wavy fibres: by forceful systolic tugs of viable fibres

C.  Myocytolysis:

  1. Vacuoles with in cells seen frequently in thin, variable subendocardial zone (sublethal Ischemic change)
  2. Hemorrhagic infarct     
  3. Necrosis with contraction band in already irreversibly injured myocytes (hyper contracted sarcomeres because of Ca2+ Q Salvages cells with non lethal injury
  4. Prolonged postischemic myocardial dysfunction, or stunned myocardium: Persistence of abn. in biochemistry & function of myocytes after alleviation of ischemia. Q
  5. Hibernating myocardium: Myocardium subjected to persistently low flow, has chronically depressed functions. Q



Reaches baseline


2-4 hrs. 24 hours 48-72 hours
LDH 24 hours 3-6 days 2 weeks
(I& T) 2-4 hours 48 hours 7-10 days

Others SGOT, Myoglobin

Troponin T is better than CK - MB (Myoglobin - more sensitive: Troponin I - more specific) Q


D. Complications

  1. Contractile dysfunction - can result in cardiogenic shock
  2. Arrhythmias
  3. Myocardial rupture: Q
    1. M. freq.: 3-7 days after MI
    2. Rupture of ventricular free wall - m. comm. - cardiac tamponadeQ
    3. Rupture of ventricular septum - left - right shunt
    4. Rupture of papillary muscles. - Mitral regurgitation
  4. Pericarditis - 2-3 days after MI
  5. RV infarct - May accompany infarction of posterior left ventricle or septum
  6. Infarct expansion - New necrosis may occur adjacent to an existing infarct Q
  7. Mural thrombus
  8. Ventricular aneurysm
  9. Papillary muscle dysfunction
  10. Progressive late heart failure (chronic IHD)
  11. Chronic ischemic heart disease: (Ischemic Cardiomyopathy)
  12. Cardiac findings in pts; often elderly, who develop progressive heart failure as a consequence of Ischemic myocardial   damage.Q 

E.  Myocardial Response:

  1. Cessation of Aerobic glycolysis - within seconds (onset of ATP depletion)
  2. Loss of contractility   < 2 min.
  3.   ATP To 50% of (n)  10 min
  4. ATP To 10% of (n)   40 min.
  5. Irreversible cell injury       20- 40 min.
  6. Microvascular injury > 1 hour.
  7. Irreversible injury in subendocardial zone 'wave front' of cell death moves through the myocardium
  8. Virtually all transmural infarcts involve at least a portion of LV
  9. Isolated RV infarct: 

F.  Frequency of Vessel Involvement:

  1. LAD - 40 to 50%
  2. RCA- 30 to 40%
  3. LCX - 15 to 20% 



 Light Microscopy

Reversible injury

0 – ½ in






1/2 – 4 in.



Waviness of Fibres at borders

4-12 hrs

Dark mottling

Beginning coag. necrosis, oedema hemorrhage


12 – 24

Dark Mottling

Ongoing coag. necrosis, marginal contraction, band necrosis, beginning neutrophil infiltrate

1-3 days

Mottling with yellow tan infarct center.

Coag. necrosis, interstitial neutrophilicinfiltrate Q


3 – 7 days

Hyperemic borders central yellow tan softening

Benign Disintegration Of dead myofibrils, with dying neutrophils, early phagocytosis by macrophagesQ Well dev. Phagocytosis,


7 – 10 days

Max - yellow tan & soft, depressed red-tan margin


Well dev. Phagocytosis,

Early formation of granulation tissue at margins Q

10 – 14 days

Red gray depressed infarct borders

well established granulation tissue


2-8 weeks

Gray -white scar, progressive from border towards. core


collagen deposition, , cellularity'


> 2 months

Scarring complete

dense collagenous scar



MI >12 hrs. old: not visible on gross examination so

Immerse tissue in Triphenyltetrazolium chloride:  Brick red colour to noninfarcted myocardium (therefore dehydrogenase is present) Q

At margins of infarcts:

Post infarction cardiac de-compensation due to exhaustion of the compensatory hypertrophy of viable noninfarcted myocardium. 

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