What is ischaemia?
Loss of blood supply from impeded arterial flow or reduced venous drainage. This compromises the supply of oxygen and metabolic substrates (e.g. glucose)
What is Infarction?
Infarction occurs in any tissue in which there is sufficient ischaemia to cause death or tissue necrosis.
Describe an arterial infarction
A complete blockage of an artery by thrombosis or embolism
What is a venous infarction?
Venous infarctions occur when there is compression of the vascular supply. E.g. in hernias when the bowel may fold on itself and cut off blood supply
What is necrosis?
The morphologic changes that follow cell death in a living tissue
What are the morphlogic appearances of necrosis due to?
Denaturation of intracellular proteins and enzymatic degradation of the cell
What are the four types of necrosis?
Describe coagulative necrosis
Most common type of necrosis in ischaemia
Denaturtion of proteins with preservation of the cell outlines.
Classic finding in myocardial infarction and most forms of tissue infarction
Describe Liquefactive necrosis
Classic finding in abcesses and cerebral infarct
Enzyme degradation dominant
Describe caseous necrosis
Distinctive form of necrosis.
Classic finding in TB
Describe Fat Necrosis
Focal areas of fat destruction.
Classic finding in pancreatitis --> release of pancreatic enzymes that then travel to distant sites
What are the four main classifications for ischaemic heart disease?
Angina (Stable, Unstable, Prinzmetal)
Chronic ischaemic heart disease with heart failure
Describe the pathogenesis of Ischaemic Heart Disease (IHD)
90% due to coronary artery atherosclerosis. This decreases coronary perfusion relative to myocardial demand
What factors of the atherosclerotic plaques determine the risk for developing IDH?
The number of plaques
The distrobution of plaques (are they on proximal vessels?)
The structure of the plaques
The degree of narrowing they cause
How quickly the plaques evolve
What are some risk factors for Myocardial Infarction?
Risk factors for atherosclerosis (hypertension, cigarette smoking, diabetes mellitus, hypercholesterolaemia)
Describe acute plaque change
When the nature and structure of an atherosclerotic plaque changes due to certain intrinsic (plaque structure and composition) and extrinsic (mechanical stress, platelet reactivity).
Plaque change can result in rupture (leading to thrombi or emboli), erosion/ulceration and haemorrhage.
Describe the events in coronary artery occlusion
Acute plaque change leads to a disrupted plaque
This results in adhesion, aggregation and activation of platelets.
The extrinsic pathway of coagulation is stimulated and the thrombus increases in size
Within minutes the coronary artery can become completely occluded
Describe the response of the myocardium to ischaemia
Cessation of aerobic glycolysis within seconds --> lactic acidosis
Loss of contractility within 60 seconds
Severe ischaemi for 20-40mins will lead to some necrosis
Complete necrosis in 6 hours
This depends on the location, severity and rate of development of the occlusion
Compare and Contrast Transmural and Subendocardial Infarction
Transmural: full thicknes ischaemic necrosis of ventricular wall. Distribution of a single coronary artery.
Subendocardial: ischaemic necrosis limited to inner third of ventricular wall. May involve the distribution of several coronary artery
Describe the macroscopic and microscopic morphologic changes in myocardial infarction after four hours
Micro: thin wavy myocytes
Describe the macroscopic and microscopic morphologic changes in myocardial infarction after one day
Macro: subtle changes, dark mottling
Micro: coagulation necrosis, haemorrhage, scant neutrophils, contraction bands
Describe the macroscopic and microscopic morphologic changes in myocardial infarction after two days
Macro: mottled appearance with yellow/tan infarct centre and is soft to touch
Micro: coagulation necrosis, neutrophils
Describe the macroscopic and microscopic morphologic changes in myocardial infarction after one week
Macro: hyperaemic border with central tan softening
Micro: disintegration of necrotic myofibres, dying neutreophils, macrophages
Describe the macroscopic and microscopic morphologic changes in myocardial infarction after two weeks
Macro: maximally yellow/tan and soft, depressed infarct borders
Micro: phagocytosis, granulation tissue, early fibrosis
Describe the macroscopic and microscopic morphologic changes in myocardial infarction after two months
Macro: white scarring
Micro: dense collagenous scar
What is the outside-->inside system to understanding the complications of MI
Outside to inside:
Contractile dysfunction, conducting system, pericardium, pericardial space, myocardium, endocardium, papillary muscles/valves
What are the complications of MI?
Haemopericardium & cardiac tamponade
Papillary muscles dysfunction
Describe the consequences of contractile dysfunction in MI
Immediate and ongoing
Left ventricular failure --> hypotension and pulmonary oedema
Describe the consequences of haemoepicardium and cardiac tamponade in MI
Haemoepicardium: Escape of blood from the ventricles in to the pericardial cavity. Occurs through a rupture of the myocardium
Cardiac tamponade: Constriction of the heart with decreased diastolic filling. usually fatal
Compare infarct extension and infarct expansion
Extension: new necrosis adjcent to the existing infarct
Expansion: weak necrotic muscle stretches, the infarct enlarges in size without further necrosis
Describe mural thrombus
Local inflammation of the endocardium. Abnormal contractility results in blood stasis.
Both contribute to thrombus formation and the potential for a thromboembolism
Describe the timeline of complications in MI
Arrhythmia: Immediate leading to sudden death. Can also be ongoing i.e. bundle branch block
Contractile Dysfunction: Immediate, within 60 seconds. Cardiogenic shock, chronic left ventricular failure
Pericarditis: 2-3 days usual
Myocardial rupture: 3-7 days when necrotic myocardium at it’s weakest
Mural thrombosis with risk of embolism: Highest rist at 10 days, lasting for 3 months
Aneurysm: Late complication