57 - Ischaemic Heart Disease Flashcards
Examples of acute ischaemic heart disease
Unstable angina, myocardial infarct, sudden cardiac death
Examples of chronic ischaemic heart disease
Stable angina, chronic myocardial ischaemia
Factors limiting coronary blood flow 1) 2) 3) 4)
1) Perfusion pressure 2) Coronary vascular resistance 3) External pressure 4) Intrinsic regulation
What could lead to decreased perfusion pressure in coronary arteries?
Systemic hypotension
What could lead to increased coronary vascular resistance?
Coronary artery atherosclerosis
What could lead to external compression of the coronary arteries?
Muscular wall of the ventricle contracts and compresses coronary arteries. Vessels of the subendocardium particularly get squeezed between contracting muscles and pressure inside the ventricle
Example of intrinsic regulation of coronary vessels 1) 2)
1) Endothelium releases prostacyclin, NO, endothelin 2) Adenosine, lactate, hydrogen are local metabolites
Typical blood flow in solid organs
Have a hilum. Blood flows from hilum to capsule or periphery
Typical blood flow in hollow organs
Fatty external layer contains vessels. Blood flows from outside to inside.
Where do infarcts often occur?
At end of blood supply (EG: Causing wedge-shaped necrosis in solid organs, causing infarcts near lumen in hollow organs)
Part of heart most vulnerable to infarction
Subendocardium
How do infarcts spread in the heart?
Begin in the inside, spread outwards (non-transmural -> transmural infarcts)
Coronary arteries 1) 2) 3) 4) 5)
1) Left main 2) Left anterior descending 3) Left circumflex 4) Right coronary 5) Posterior descending
How to tell where is up and down on a cardiac slice 1) 2) 3)
1) Posterior side is more flat 2) Posterior side is less fatty 3) Posterior descending coronary artery is at septum
*Blood supply of the heart
Blood vessel supplying anterior wall and 2/3 of the septum in the heart
Left anterior descending coronary artery
Blood vessel supplying lateral wall of heart
Left circumflex coronary artery
Blood vessel supplying posterior wall of the heart
Posterior descending coronary artery
Where does the posterior descending coronary artery arise from?
In right-dominant heart (majority of people), from right coronary artery. In left-dominant people, from left circumflex coronary artery.
What is a heart attack?
Myocardial infarction. Imbalance between O2 supply and demand of myocardium, resulting in ischaemia and cell death.
Most common cause of myocardial infarct
Acute plaque event. Rupture or haemorrhage of atherosclerotic plaque, with formation of occlusive thrombus of coronary artery
30 minutes after myocardial infarct 1) 2) 3) 4)
1) No macroscopic, microscopic changes 2) Intracellular changes (EG: mitochondrial swelling) visible on electron microscope 3) Functional loss of contractility 4) Might see ECG changes (ST depression, T wave inversion) 5) Angina - REVERSIBLE INJURY
How long after ischaemia sets in does irreversible injury occur?
~30 minutes
Indicators of irreversible cardiac damage 1) 2)
1) Leaking of cardiac proteins (creatine kinase, troponin) 2) Leaking of current (ST segment elevation, ST segment depression, myocardial irritability)
How long after an infarct are troponin blood levels detectable?
~3-4 hours post-infarction
Complications 30 minutes-12 hours post-infarction 1) 2)
1) Arrhythmia (damaged myocytes are unstable) 2) Cardiac failure (damaged myocytes can’t contract properly)
NSTEMI 1) 2) 3)
1) Non-ST elevated myocardial infarction. 2) Leads to a non-transmural infarct. 3) From a transient or partial obstruction of coronary arteries, leading to a regional subendothelial infarct.
STEMI 1) 2) 3)
1) ST elevated myocardial infarction 2) Leads to a transmural infarct. 3) From a permanent, full-thickness occlusion of coronary artery
Histology of heart 30 minutes-12 hours post-infarction 1) 2) 3)
1) Wavy myocytes
2) Cell death, with faded nuclei, interstitial red blood cells
3) Early necrosis is present (faintly eosinophilic)
Are there any gross morphological changes 30 minutes - 12 hours post-infarct?
No
What happens 12-24 hours post-infarct?
Necrosis and early acute inflammation
Histology of cardiac muscle 12-24 hours post-infarct 1) 2)
1) Neutrophils present
2) Contraction band necrosis
Gross appearance of heart 12-24 hours post-infarct
Mottled, haemorrhagic myocardium
Gross appearance of heart 1-3 days post-infarct
Soft yellowing of wall (necrosis is grossly-apparent)
Histological appearance of myocardium 1-3 days post-infarct
Heavy neutrophil infiltration Loss of structure.
Peak of troponin levels in the blood
Around 2 days post-infarct
How long post-infarct can troponin be detected?
Up to two weeks
What is happening 3-7 days post-infarct?
End of acute inflammation and beginning of granulation
Histological appearance of myocardium 3-7 days post-infarct 1) 2) 3)
1) Macrophages ingesting dead myocytes. 2) Fibroblasts, vessels of granulation tissue appear. 3) Collagen begins being laid down 5-6 days post-infarct
Gross appearance of heart 3-7 days post-infarct
Central yellowing (necrosis) surrounded by red rim (vascularised granulation tissue)
Complications 1-3 days post-infarct 1) 2) 3) 4) 5)
1) Arrhythmia (damaged myocytes are unstable) 2) Cardiac failure (damaged myocytes can’t contract) 3) Mural thrombus (damaged wall isn’t moving properly) 4) Rupture (necrotic wall is weak) 5) Pericarditis (preponderance of inflammatory mediators)
Three ways in which infarcted heart can rupture 1) 2) 3)
1) Rupture of free ventricular wall 2) Rupture of papillary muscle 3) Rupture of IV septum
Outcomes of a rupture of free ventricular wall 1) 2)
1) Blood can seep into pericardium - Haemopericardium 2) Haemopericardium can compress heart until it stops - Cardiac tamponade
Outcomes of a ruptured papillary muscle 1) 2) 3)
1) New onset murmur 2) Mitral regurgitation 3) Cardiac failure
Effect of a ruptured IV septum 1) 2) 3)
1) New onset murmur 2) Ventricular septal defect 3) Cardiac failure
What can lead to cardiogenic shock?
Rupture of papillary muscle of IV septum. Cardiogenic shock is when the heart can’t generate blood pressure to supply brain
Histological appearance of heart 1-8 weeks post-infarct 1) 2)
1) Early granulation tissue - High cellularity, vascularity, little collagen 2) Late granulation tissue - Gradual reduction in cells, vessels, increase in collagen
Possible complications of heart 1-8 weeks post-infarct 1) 2) 3) 4)
1) Lesser chance of arrhythmia or cardiac failure 2) Mural thrombus (damaged wall isn’t moving properly) 3) Aneurysm (the wall is stronger because of collagen, but is flexible to wall stress, and might bulge out) 4) Aneurysm exacerbates risk of mural thrombus.
Histological appearance of heart over 8 weeks post-infarct
Densely-collagenous scar
Complications over 8 weeks post-infarct 1) 2) 3)
1) Arrhythmia (damaged myocytes have been cleared, but there are isolated islands of autorhythmic myocytes) 2) Aneurysm, mural thrombus (aneurysm can form, but is unlikely to rupture with strong scar tissue) 3) Cardiac failure (biggest threat. Damaged myocytes can’t be replaced, LV remodelling might occur, decompensation can occur)
Non-atherosclerotic possible causes of MI 1) 2) 3)
1) Coronary artery dissection 2) Thrombosis due to vasculitis 3) thromboembolism from heart (EXTREMELY RARE. So much so that this isn’t really relevant)
Difference between stable and unstable angina
Stable angina is reproducible chest pain that is induced by exertion, disappears with cessation of exertion. Unstable angina presents as cardiac chest pain at rest or with minimal exertion
What is angina?
Transient ischaemia of cardiac muscle. Can lead to infarction (which is irreversible damage)
What is stable angina due to?
Atherosclerotic narrowing of coronary artery. Symptoms appear with over ~70% stenosis
What can bring about unstable angina?
Acute plaque event (EG: coronary artery thrombosis)
What brings about chronic myocardial ischaemia
Chronic narrowing of coronary arteries
Outcomes of chronic narrowing of coronary arteries? 1) 2) 3) 4)
1) Chronic myocardial ischaemia 2) Small areas of subendothelial ischaemia 3) Patchy myocyte necrosis, replacement by fibrosis 4) Similar risk of cardiac failure and arrhythmia as LV hypertrophy
Sudden cardiac death
Unexpected cause, death within an hour of symptoms. In a person with no previous diagnosis of a fatal condition. Frequently an arrhythmic event, but can also be a complication of a silent MI within the last few days
