Page 271 - Concise Pathology for Exam Preparation ( PDFDrive )

256 SECTION II Diseases of Organ Systems

Clinical syndromes associated with IHD are
1. Myocardial infarction (MI)
2. Angina pectoris:
(a) Stable
(b) Prinzmetal or variant
(c) Unstable or crescendo
3. Chronic ischaemic heart disease with heart failure
4. Sudden cardiac death
These clinical syndromes are a result of a complex dynamic interaction between
• Fixed atherosclerotic narrowing
• Intraluminal thrombosis overlying a disrupted atherosclerotic plaque
• Platelet aggregation and vasospasm
Q. Write briefly on the role of fixed coronary obstruction in the
pathogenesis of IHD.
Ans. Ninety percent patients with IHD have underlying atherosclerosis with presence of
solitary or multiple lesions, causing at least 75% reduction of cross-sectional area of at
least one major artery.
• Common locations for clinically significant stenosis include the first several cm of LAD
(left anterior descending artery) and LCX (left circumflex artery), and the entire length
of RCA (right coronary artery).
• Usually 2 or all 3 arteries (LAD, LCX and RCA) are involved.
• Major secondary epicardial branches may also be involved but atherosclerosis of intra-
mural branches is rare.
Q. Write briefly on the role of acute plaque change in the pathogenesis
of IHD.
Ans. Role of acute plaque change in the pathogenesis of IHD (Flowchart 11.1):

Acute plaque change (includes haemorrhage into atheroma or
rupture or fissuring/erosion or ulceration of the plaque)

Exposure of thrombogenic substances to blood

Thrombus formation
FLOWCHART 11.1. Role of acute plaque change in the pathogenesis of IHD.

Factors that trigger/contribute to acute plaque alterations:
• Adrenergic stimulation
• Structure and composition of plaque (eccentric location, large soft core and thin fibrous
cap predispose to plaque alterations)
• Most dangerous lesions are the moderately stenotic (50–60% stenosis) lipid-rich athero-
mas (plaques causing >60% obstruction reduce blood flow; thus, decreasing mechanical
stress in the vessel wall, reducing chances of its disruption. Slowly developing occlu-
sions even if they are high grade, are less dangerous because they stimulate collateral
vessel formation)

Q. Write briefly on the role of coronary thrombosis in the
pathogenesis of IHD.

Ans. Acute transmural MI is usually caused by superimposition of a thrombus on a dis-
rupted, previously partially stenotic plaque, causing total occlusion.

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