Ischaemic heart disease clinical syndromes
- Myocardial infarction
- Angina pectoris (stable or unstable)
- Chronci ishcaemic heart disease with heart fialure
- Sudden cardiac death
What usually precipiated ischaemic heart disease?
An abrupt plaque change followed by thrombosis. The manifeststions of acute plaque change are termed acute coronary syndromes.
Over 90% of acute coronary syndromes (unstable angina, acute MI, and sudden death) result form coronary atherosclerotic plaque disruption and associated intraluminal thrombus formation.
Plaque changes resulting in acute coronary events
Rupture/fissuring: exposing the highly thrombogenic plaque constituents
Erosion/ulceration: exposing the thrombogenic subendocardial basement membrane to blood
Haemorrhage: into the atheroma, expanding its volume.
Outcomes of acute plaque changes
- Platelet adhesion, aggregation, activation, and release of potent aggregaors including thromboxane A2 and ADP.
- Vasospasm is stimulated by platelet aggregation and the release of mediators.
- Tissue factor activates coagulation pathway adding to the bulk of the thrombus.
- Frequently within minutes, the thrombus evolves to completely occlude the lumen of the coronary vessels.
The critical consequence is downstream myocardial ischaemia.
In angina the coronary artery occlusion is subtotal and causes ischaemia (but not myocardial necrosis) when the myocardial perfusion is decreased relative to demand.
There is a fixed obstruction within the cornary artery/ies with atherosclerotic plaque/s. 7% occlusion may lead to predictable exertional chest pain, relieved by rest and GTN.
Is the result of an acute change in an atheromatous plaque. This is still a subtotal occlusion but the pain is unpredictable, increasingly frequent, occurs upon rest or lower physical activity levels than usual - this is a warning that AMI may be imminent.
Prinzmetal variant angina
One uncommon variant of angina, that is an uncommon pattern of episodic angina that occurs at rest and is due to coronary artery spasm.
Acute myocardial infarction
An acute plaque change which induced total thrombotic occlusion.
Nerosis of cardiac muscle due to coronary arterial occlusion by athermoatous plaque complication with superimposed occlusive thrombosis.
What is the classiifcation of myocardial infarcts?
Transmural: known as ST elevelation infarcts (STEMI)
Subendocardial: known as non-ST elevation infarcts (non-STEMI)
These are transmural myocardial infarcts.
- Ischaemic necrosis involves the full or nearly full thicness of the ventricular wall in the distribution of a single coronary artery. This pattern is usually associated with coronary atherosclerosis, acute plaque change, and superimposed thrombosis.
Also termed a subendocardial infarct.
- Ischaemic necrosis limited to the inner half of the ventricular wall. The subendocardial zone is the least well perfused region of myocardium and is vulnerable to any reduction in coronary flow. This may occur when a coronary thrombosis is lysed before full thickness necrosis occurs or from prolonged reduction in systemic BP on top of atherosclerosis in the coronary arteries.
Causes of transmural MI other than changes in atheromatous plaque
Emboli: left arium in assoication with atrial fibrillation, a left-sided mural thrombus or vegetative endocarditis
Paradoxical emboli: from the right side of teh ehart which cross to the systemic circulation, through a patent foramen ovale, causing coronary occlusion
Unexplained: vasculitis, amyloid deposition in vascular walls, or other unusual disorders, such as vascular dissection.
Gross features and time scale in an AMI
0-4 hours: none
4-12 hours: occasionally dark mottling
12-24 hours: dark mottling
1-3 days: mottling with yellow-tan infarct centre
3-7 days: hyperaemic border; central yellow-tan softening
7-10 days: maximally yellow-tan and soft, with depressed red-tan margins.
10-14 days: red-gray depressed infarct borders
2-8 wks: gray-white scar, progressive from border toward core of infarct
>2 mths: scarring complete
LM features and timescale of an AMI
0.5-4hr: usually none; variably waviness of fibres at border
4-12hr: beginning coagulative necrosis; oedema; haemorrhage
12-24hrs: ongoing coagulative necrosis; pyknosis of nuclei; myocyte hypereosinophilia; marginal contraction band necrosis; begin netrophilic infiltrate.
1-3days: coagulative necrosis, with loss of nuclei and striation; interstitial infiltrate of neutrophils
3-7days: beginning disintegration of dead myofibres, with dying neutrophils, early phagocytosis of dead cells by macrophages at infarct border.
7-10 days: well developed phagocytosis of dead cells; early formation of fibrovascular granulation tissue at margins.
10-14 days: well-established granulation tissue with new blood vessels and collagen deposition.
2-8 wk: increased collagen deposition, with decreased cellularity.
>2 mo: dense collagen scar
- Contractile dysfunction
- Myocardial rupture
- Dressler's syndrome
- Infarct extension
- Ventricular aneurysm
- Formation of mural thrombus
- Papillary muscle dysfunction
- Healing by fibrosis (scar)
- Progressive late heart failure (chronic ischaemic heart disease)
Can be a complication of AMI.
This is severe 'pump failure' (cardiogenic shock), whic occurs in 10-15% of patients following AMI, generally with a large infarct (often greater than 40% of the left ventricle). Cardiogenic shock has a nearly 70% mortality rate and accounts for two third of in-hospital deaths.
- Sinus bradycardia
- Heart block (asystole)
- Ventricular premature contractions or ventricular tachycardia
- Ventricular fibrillation
Complication of AMI.
- Ventricular free wall (3-7 days)
- Ventricular septum
- Papillary muscle rupture
Complication of AMI.
A fibrinous or fibrohaemorrhagic pericarditis usually develops about the second or third day following a transmural infarct and usually resolves over time.
Post-MI complication, also seen in post cardiac surgery or PE.
This is a later complication, occuring weeks to months after MI. Clinical features include:
- Pleuritic chest pain
- Pericardial friction rub
Myocardial injury releases cardiac antigens and stimulates Ab formation. Subsequent immune deposits elicit inflammatory response.
Complication of MI.
New necrosis may occur adjacent to an existing infarct.
A late complication, aneurysms of teh ventricular wall result from a large transmural infarct that heals into a large region of thin scar tissue.
Complication of MI.
Endocardial damage + stasis.
Papilarry muscle dysfunction
Complication of MI.
Can lead to mitral regurgitation.