Histology of myocardial infarction Flashcards
revision
What is cell injury and when does it occurs?
- Cell injury occurs when cells are stressed beyond their ability to adapt
- Hypertrophy
- Hyperplasia
- Atrophy
- Metaplasia
- Reversible cell injury
- Irreversible cell injury and cell death
REVISION
Define and describe hypoxia and ischaemia
Hypoxia
- Extremely important cause of cell injury
- Deficiency of O2 → reduced aerobic respiration
- Causes:
- Reduced blood flow (ischemia)***
- Inadequate oxygenation of blood (cardiorespiratory failure)
- Decreased oxygen-carrying capacity of blood (severe blood loss, CO poisoning, anemia)
Ischemia
- Most common cause of cell injury in clinical medicine
- Reduced blood flow: mechanical arterial obstruction (most often); or reduced venous drainage
- Compromises:
- Supply of oxygen (aerobic metabolism ceases)
- Supply of metabolic substrate i.e. glucose
- Removal of metabolites
- Cell injury
Define infarction
- Area of ischemic necrosis, occurs in any tissue in which ischemia leads to cell death/ tissue necrosis
- Commonly myocardial, cerebral, pulmonary, bowel
- Arterial:
- Vast majority of infarctions
- Occlusion by thrombosis or embolism
- Venous:
- Tissues usually congested → bypass channel permits vascular outflow
- Infarct in organs with a single efferent vein (testis/ovary)
Revision
Define and describe necrosis
- Morphologic changes that follow cell death in viable tissue
- Can be visualized macroscopically and microscopically
- Morphologic appearances due to:
- Denaturation of cellular proteins
- Enzymatic leakage and degradation of the cell
- Inflammation
Types of Necrosis
- Coagulative necrosis:
- Denaturation of protein including enzymes → digestion of cells halted
- Preservation of the architecture of dead tissue for days/week
- Classic finding in ischemic necrosis caused by obstruction in a vessel (e.g. myocardial infarction and most forms of tissue infarction, except brain)
- Liquefactive necrosis:
- Digestion of dead cells → viscous liquid
- Classic finding in abscess (microbes stimulate enzyme release from leukocytes) → pus
- Classic finding in cerebral infarct (reasons unclear)
- Caseous necrosis:
- Distinctive form of necrosis → cheeselike (friable white appearance)
- Classic finding in TB
- Fat necrosis:
- Focal areas of fat destruction
- Classic finding in pancreatitis
Recall the arterial supply of the heart
- Heart is supplied by the right and left coronary arteries
- Both are branches of the ascending aorta
- Should know about:
- Right CA
- Right marginal
- Posterior interventricular
- Left CA
- Circumflex
- Left anterior descending
- Right CA
see also anatomy of heart
Describe IHD
Ischemic Heart Disease
- Generic designation for closely related entities resulting from myocardial ischemia
- Leading cause of death in both males and females → single largest cause of mortality worldwide, accounting for over 12% of global deaths
- However, overall death rate has fallen ~50%
- Prevention (modifiable risk factors: smoking, cholesterol, etc.)
- Diagnostic and therapeutic advances (statins, angioplasty/stent, CABG)
Briefly describe pathogenesis of IHD
- Risk of developing IHD depends on:
- Number
- Distribution (usually first few centimetres of LAD and LCX)
- Structure (LAD, LCX, RCA) of atheromatous plaques
- Degree of narrowing they cause
- > 70% → critical stenosis
- > 90% → inadequate flow, even at rest
- How quickly the plaques evolve
List acute coronary syndromes and briefly describe how they precipitate
- Unstable angina
- Myocardial infarction (STEMI/ NSTEMI)
- Sudden death
- Precipitated by conversion of a stable atherosclerotic plaque to an unstable atherosclerotic plaque via:
- Plaque erosion or ulceration with secondary occlusive luminal thrombus formation or
- Intraplaque hemorrhage causing sudden luminal narrowing
Describe causes of acute plaque change
- Events that trigger acute plaque change are poorly understood
- Intrinsic:
- Plaque structure and composition
- Extrinsic:
- Mechanical stress
- Platelet reactivity
- Rupture/fissuring
- Erosion/ulceration
- Haemorrhage
- Mechanical stress
Describe the incidence of MI and risk factors
Incidence
- “Heart attack” - death of cardiac muscle due to prolonged ischemia
- Frequency increases with increasing age, however may occur at any age (10% <45 years; 45% <65 years)
- Leading cause of death in industrialized nations
- In the USA affects 1.5 million people p.a., 1/3 die, 1/6 die before reaching the hospital
Risk factors
- Male
- Risk factors for atherosclerosis
- Hypertension
- Cigarette smoking
- Diabetes mellitus
- Hypercholesterolemia
Describe the pathogenesis of MI
Pathogenesis
- STABLE PLAQUE
- ACUTE PLAQUE CHANGE
- Coronary arterial occlusion
- Increased myocardial demand
- Hemodynamic compromise
- Presence or absence of collateral vessels
Coronary Artery Occlusion
- Acute plaque change → disrupted plaque
- Platelets undergo adhesion, aggregation, activation
- Vasospasm (substance released from platelet)
- Activation of extrinsic pathway of coagulation → growing thrombus
- Within minutes, complete occlusion of the artery
NB
MI Not Associated With Atherosclerosis
- 10% of cases
- Vasospasm (e.g. cocaine)
- Emboli
- Vasculitis
- Hemoglobinopathies
- Amyloid
- Vascular dissection
Describe the myocardial response to MI
Myocardial Response
- Coronary arterial occlusion
- Loss of critical blood supply to the myocardium
- Profound functional, biochemical and morphological consequences
Myocardial Response
- Ischemia
- Cessation of aerobic glycolysis within seconds
- Loss of contractility <2 minutes
- Irreversible cell injury within 20-40 min will lead to necrosis of some myocytes
- Complete necrosis in 6 hours
- Dependent on location, severity, and rate of development of the occlusion
- Size of the vascular bed occluded
- Duration of occlusion
- Metabolic needs of the myocardium
- Extent of collateral vessels
- Alterations in BP, HR, and cardiac rhythm
Comapre and contrast transmural and subendocardial infarction
Transmural:
- Full thickness ischemic necrosis of the ventricular wall
- Permanent occlusion of an epicardial artery
Subendocardial:
- Non-transmural ischemic necrosis
- May involve the distribution of several coronary arteries (transient/partial obstruction)
Describe the progression of myocardial necrosis
- One Hour: No macroscopic changes
- Four Hours: +/- Wavy fibres
- One Day: Subtle macroscopic changes, dark mottling; Coagulation necrosis, haemorrhage, scant neutrophils microscopically
- Two Days: Mottled appearance with yellow/tan infarct center macroscopically; Coagulation necrosis + neutrophils microscopically
- One Week: Hyperemic border + central tan softening macroscopically; Disintegration of necrotic myofibers, dying neutrophils, macrophages microscopically
- Two Weeks: Maximally yellow/tan and soft, depressed infarct borders macroscopically; Phagocytosis, granulation tissue, early fibrosis microscopically
- Two Months: White scarring macroscopically; Dense collagenous scar microscopically
Describe the consequences and complications of MI
Outside to Inside:
- Contractile Dysfunction
- Conducting system
- Pericardium
- Pericardial space
- Myocardium
- Endocardium
- Papillary muscles/valves
Contractile Dysfunction:
- Immediate post-MI and ongoing (10% of patients with transmural MI)
- Abnormalities of left ventricular function
- Left ventricular failure (hypotension, pulmonary edema)
- Cardiogenic shock
Arrhythmias:
- Many arrhythmias occur post-MI, especially in STEMI
- Sudden cardiac death often a lethal arrhythmia
- MI can directly affect the bundle of His in the septum
- Cardiac muscle irritability secondary to ischemia is a common cause
Pericarditis:
- Epicardial manifestation of underlying myocardial inflammation
- Fibrinohaemorrhagic
- Transmural infarct
- Resolves slowly over days
- Rarely, intense pericarditis can develop weeks after MI (Dressler syndrome)
Haemopericardium and Cardiac Tamponade:
- Escape of blood from the ventricles into the pericardial cavity (haemopericardium)
- Constriction of the heart with decreased diastolic filling (cardiac tamponade)
- Usually fatal
Myocardial Rupture:
- Mechanical weakening due to myocardial necrosis
- Occurs 3-7 days post-MI
- Rupture can involve the ventricular free wall, ventricular septum, or papillary muscle
Infarct Extension / Expansion:
- Extension: New necrosis adjacent to the existing infarct
- Expansion: Weak necrotic muscle stretches, enlarging the infarct without further necrosis
Ventricular Aneurysm:
- Late complication
- Expansion of the infarct and healing by fibrosis
- Aneurysm bulges during systole
- Complications include mural thrombus, arrhythmia, and left ventricular failure
Mural Thrombus:
- Adherent thrombus in the left ventricular cavity
- Local inflammation of the endocardium and abnormal contractility contribute to thrombus formation
- Potential for thromboembolism
Papillary Muscle Dysfunction:
- Dysfunction of the papillary muscles leading to mitral regurgitation
- Dysfunction can be caused by rupture, fibrosis and shortening, or ventricular dilation
