ischemic heart disease 19.9.90

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Ischemic Heart Disease


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Definition

IHD is the generic designation for a group of

pathophysiologically related syndromes

resulting from myocardial ischemiaan

imbalance between the supply (perfusion) and

demand of the heart for oxygenated blood.

Ischemia brings not only an insufficiency of

oxygen, but also reduces the availability ofnutrients and the removal of metabolites


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In more than 90% of cases, the cause of

myocardial ischemia is reduced blood flow due

to obstructive atherosclerotic lesions in the

coronary arteries. Thus, IHD is often termed

coronary artery disease (CAD) or coronary

heart disease


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IHD usually presents as one or more of the

following clinical syndromes:

Myocardial infarction, the most important form ofIHD, in which ischemia causes the death of heartmuscle.

Angina pectoris, in which the ischemia is ofinsufficient severity to cause infarction, but may be aharbinger of MI.

Chronic IHD with heart failure.

Sudden cardiac death.


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Pathogenesis

The dominant cause of the IHD syndromes isinsufficient coronary perfusion relative tomyocardial demand, due to chronic,

progressive atherosclerotic narrowing of theepicardial coronary arteries

Variable degrees of superimposed acuteplaque change

Thrombosis

Vasospasm


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Chronic Atherosclerosis

More than 90% of patients with IHD have

atherosclerosis of one or more of the epicardial

coronary arteries.

A fixed lesion obstructing 75% or greater of the

lumen is generally required to cause symptomatic

ischemia precipitated by exercise (most often

manifested as chest pain, known as angina Obstruction of 90% of the lumen can lead to

inadequate coronary blood flow even at rest


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Acute Plaque Change

The risk of an individual developing clinically important IHDdepends in part on the number, distribution, structure, anddegree of obstruction of atheromatous plaques

However, the varied clinical manifestations of IHD cannot

be explained by the anatomic disease burden alone The acute coronary syndromes are typically initiated by anunpredictable and abrupt conversion of a stableatherosclerotic plaque to an unstable and potentially life-threatening atherothrombotic lesion through rupture,

superficial erosion, ulceration, fissuring, or deephemorrhage


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There are two major methods of in vivo sampling of

coronary atherosclerosis as a surgical specimen:

Percutaneous via catheters

open procedures (surgery).

Coronary atherectomy was at one time a standard treatment

for coronary stenosis, with catheter-based removal of the

plaque

Thrombus Coronary endarterectomy (removal of intimal

disease at open surgery, usually with concomitant bypass

grafting) is not commonly performed because of relatively

high rates ofrestenosis


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luminal narrowing estimation

If accurate measurements of cross-sectionalluminal narrowing are to be undertaken,perfusion fixation is necessary

The coronaries are perfusion fixed with 10%buffered formaldehyde retrograde from theascending aorta at 100 mm Hg pressure for atleast half an hour

The plug is attached to tubing that is connectedto the perfusion chamber that is placed 135 cmabove the specimen, approximately equivalent to100 mm Hg


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luminal narrowing estimation

For correlation with premortem angiography,and for medicolegal civil matters, accuratepercent stenosis is often important to

determine There are two factors limiting accuracy in this

regard:

lack of perfusion fixation( more important)

Subsequent tissue shrinkage during fixationand processing


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This artifact is greatest in eccentric plaques andthose with mild to moderate stenosis

25% lesion could be seen as >90% if the vessel iscollapsed

In reality, because of differential shrinkage ofintimal tissues versus smooth muscle wall, the

effect on percent stenosis is minimal For segments with about 50% stenosis before

processing, there is an increase to about 65%after processing.

However, for 80% stenosis, there is actually adecrease in percent stenosis after processing toalmost 70%


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MORPHOLOGIC FEATURES OF CORONARY

ATHEROTHROMBOSIS

In patients dying after acute myocardial

infarct, thrombi are found in 98% of patients.

The frequency of acute thrombosis in unstable

angina is less than that seen in acute

myocardial infarction and ranges from


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Plaque ruptures

Plaque ruptures are characterized by a luminal

thrombus overlying a lipid-rich fibroatheroma,

often with areas of hemorrhage, usually with

a visibly interrupted cap

The thinned, inflamed fibrous cap

demonstrates an area of discontinuity,

allowing the underlying lipid-rich core tocontact the luminal blood


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Plaque fissure

Plaque fissure is an early form of plaquerupture, in

which there is a break in the fibrous cap

without significant luminal thrombus,resulting in intraplaque fibrin deposits withoutluminal thrombus (Fig. 6.21).

The distinction between plaque fissure andrupture may be difficult and sometimesarbitrary


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Plaque erosion

Typically, there is not a prominent necrotic core,in contrast to plaque rupture.

Plaque erosion is characterized by lesser degreesof calcification and overall plaque burden

Histologically, plaque erosion shows denudatedendothelial surface with luminal thrombus

The plaque underlying the thrombus is rich is

proteoglycans and smooth muscle cells There is often a small lipid core near the internal

elastic lamina, but prominent cholesterol crystalsand hemorrhage into plaque are absent


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The role of the thrombusmechanism ofaction in ST-segment elevation ACS

Results from stabilization of aplatelet aggregate at site of

plaque rupture by fibrin mesh

platelet

RBCfibrin mesh

GP IIb-IIIa

Generally caused by acompletely occlusive

thrombus in a coronary artery


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The Role of the Platelet: Mechanismof NSTE ACS

Results from cross-linking ofplatelets by fibrinogen at

platelet receptors GP IIb-IIIaat site of plaque rupture

platelet

fibrinogen

Rupturedplaque

GP IIb-IIIa

Generally caused by apartially occlusive, platelet-richthrombus in a coronary artery

Unobstructed

lumen

thrombus

Artery wall


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Not all acute plaque ruptures result in sudden

death or even acute myocardial infarction;

Healed plaque rupturesrepresent a

mechanism of plaque enlargement


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Factors Influences plaque integrity

The structure and composition of a plaque

(foam cell , fibrous cap , smooth muscle cell)

The balance of synthetic and degradativeactivity of collagen

drugs such as statins

Adrenergic stimulation can elevate systemichypertension or local vasospasm

Intense emotional stress

ischemic heart disease 19.9.90

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