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Ischemic Heart Disease

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 of nutrients and the removal of metabolites

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

IHD usually presents as one or more of the following clinical syndromes:


Myocardial infarction, the most important form of IHD, in which ischemia causes the death of heart muscle. Angina pectoris, in which the ischemia is of insufficient severity to cause infarction, but may be a harbinger of MI. Chronic IHD with heart failure. Sudden cardiac death.

Pathogenesis
The dominant cause of the IHD syndromes is insufficient coronary perfusion relative to myocardial demand, due to chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries Variable degrees of superimposed acute plaque change Thrombosis Vasospasm

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

Acute Plaque Change


The risk of an individual developing clinically important IHD depends in part on the number, distribution, structure, and degree 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 an unpredictable and abrupt conversion of a stable atherosclerotic plaque to an unstable and potentially lifethreatening atherothrombotic lesion through rupture, superficial erosion, ulceration, fissuring, or deep hemorrhage

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 of restenosis

luminal narrowing estimation


If accurate measurements of cross-sectional luminal narrowing are to be undertaken, perfusion fixation is necessary The coronaries are perfusion fixed with 10% buffered formaldehyde retrograde from the ascending aorta at 100 mm Hg pressure for at least half an hour The plug is attached to tubing that is connected to the perfusion chamber that is placed 135 cm above the specimen, approximately equivalent to 100 mm Hg

luminal narrowing estimation


For correlation with premortem angiography, and for medicolegal civil matters, accurate percent 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 fixation and processing

This artifact is greatest in eccentric plaques and those with mild to moderate stenosis 25% lesion could be seen as >90% if the vessel is collapsed In reality, because of differential shrinkage of intimal 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 a decrease in percent stenosis after processing to almost 70%

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 <50% to nearly 80%.

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 to contact the luminal blood

Plaque fissure
Plaque fissure is an early form of plaque rupture, in which there is a break in the fibrous cap without significant luminal thrombus, resulting in intraplaque fibrin deposits without luminal thrombus (Fig. 6.21). The distinction between plaque fissure and rupture may be difficult and sometimes arbitrary

Plaque ulceration
Plaque ulceration is a form of plaque rupture in which the contents of the lipid core have been extruded into the lumen and then embolized, resulting in a scooped out lesion covered by organizing thrombus Because of the hemodynamics of the coronary circulation, plaque ulcers are relatively uncommon in coronary arteries in comparison with the aorta and carotid arteries. Plaque ulcers may be identified angiographically and by intravascular ultrasound.

Plaque erosion
Typically, there is not a prominent necrotic core, in contrast to plaque rupture. Plaque erosion is characterized by lesser degrees of calcification and overall plaque burden Histologically, plaque erosion shows denudated endothelial 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 crystals and hemorrhage into plaque are absent

The role of the thrombus mechanism of action in ST-segment elevation ACS


Generally caused by a completely occlusive thrombus in a coronary artery Results from stabilization of a platelet aggregate at site of plaque rupture by fibrin mesh

platelet RBC

fibrin mesh
GP IIb-IIIa

The Role of the Platelet: Mechanism of NSTE ACS


Generally caused by a partially occlusive, platelet-rich thrombus in a coronary artery
Unobstructed lumen
GP IIb-IIIa platelet

Results from cross-linking of platelets by fibrinogen at platelet receptors GP IIb-IIIa at site of plaque rupture

thrombus
fibrinogen
Ruptured plaque

Artery wall

Not all acute plaque ruptures result in sudden death or even acute myocardial infarction; Healed plaque ruptures represent a mechanism of plaque enlargement

Factors Influences plaque integrity


The structure and composition of a plaque (foam cell , fibrous cap , smooth muscle cell) The balance of synthetic and degradative activity of collagen drugs such as statins Adrenergic stimulation can elevate systemic hypertension or local vasospasm Intense emotional stress