Ischaemic Heart Disease Flashcards
What is Ischaemia?
Reduced tissue blood flow.
What’s hypoxia?
Oxygen deprivation which causes cell injury by reducing aerobic oxidative respiration.
What is an infarct / an infarction?
A localized area of ischaemic tissue necrosis (Death) - usually coagulative necrosis (tissue preserves its outline)
What is coagulative necrosis?
A form of necrosis in which tissue architecture is preserved for at least some time
What are the clinical presentations of IHD?
- Angina pectoris (chest pain)
- Myocardial infarction (MI)
- Chronic IHD with heart failure
- Sudden cardiac death
In which coronary arteries occur most often?
- Left anterior descending
- RCA
- Circumflex branch of LCA
What is the pathogenesis of IHD?
There simply isn’t enough blood supply to meet myocardial demand (in most cases this reduced blood supply is caused by atherosclerosis
What are the main risk factors for IHD - modifiable and non-modifiable
What is the pathogeness of the intimal thickening in ‘Response to injury’
- There is recruitment of smooth muscle cells or smooth muscle precursor cells to the intima.
- Smooth muscle proliferates
- There is elaboration of the ECM
What is the pathogenesis of atherosclerosis?
- Ednothelial injury and dysfunction causes increased vascular permeability, leakocyte and platelet adhesion.
- Lipoproteins accumulate in the vessel wall - mainly LDL in its oxidised form
- Cytokines released attract monocytes; which migrate into the intima, transform into activated macrophages that engulf lipids and become ‘foam cells’.
- Activated ECs, SMCs, platelets and macrophages lead to cytokine and growth factor release leading to SMC recruitment from the media or form circulating percursors
- smooth muscle cells proliferate, and there is extracellular matrix deposition. They also engulf lipids (foam cells)
- T cells are recruited (due to cytokine release)
- An atherosclerotic plaque forms with the intima; which encroaches on the vascular lumen
What are first signs of atherosclerosis grossly?
Formation of fatty streaks
What are the complications of atherosclerosis?
- You get mechanical obstruction of the vessel wall leading to ischaemia (critical stenosis of ~70%)
- It is increases the diffusion distance from the lumen to the media, leading to it weakening and to cause aneurym formation
- The new blood vessels can bleed cause haemorrhage into hte palque - leading to plaque expansion or rupture
- Plaque ulceration, erosion or rupture, leading to thrombosis and partial or complete occlusuon of the vessel
- since subendothelial collagen, vWF and tissue factor get exposed
- Clinical concequences: MI, stroke, peripheral vascular disease, and aortic aneurysm
Why does a vulnerable plaque have a higher risk of causing thrombosis?
Vulnerable plaques are more likely to rupture
What does a plaque rutpure cause?
Thrombosis leading to an occlusion
What is the pathogenesis of IHD?
- Chronic vascular occlusion by atherosclerosis
- 70-75% of stenosis is considered ‘critical’
- once or more of LAD, RCA, LCX affected
- Acute plaque change
- Intraplaque haemorrhage, erosion, rupture
- Superimposed thrombosis and possible complete vascular occlusion
- An element of coronary vasospasm
When a patient presents with angina pectoris, where is the pain felt, and why is the pain occuring?
- Paroxysmal recurrent attacks of substernal or precordial chest pain last for 15 sec to 15 mins.
- Pain is the consequence of ischemia-induced release of bradykinin and other mediatros that stimulate symapthetic and vagal nerve endings
silent ischema can occur in diabetic patients (due to neuropathy)
What types of angina are there?
Stable angina
Unstable angina
Prinzemetal angina
What happens in stable angina (most common)?
- Caused by significant coronary occlusion due to atherosclerosis - ‘critical stensosis’
- Triggered by increased O2 demand such as exerise, stress and emotional excitement
- usualy relived by rest of vasodilators
What is unstable angina?
- associated with ‘plaque change’ and superimposed non-occlusive thrombi &/or vasospasm
- pain is prolonged, more frequent, even at rest
What is prinzmetal angina?
Coronary artery spasm (not atherosclerosis)
What is MI caused by?
- MI is ischemia severe enough to cause myocyte death.
- It’s caused by acute plaque change, with superimposed thrombosis (causing vessel occlusion).
- Vasospasm also occurs under the effect of platelet-derived mediators
- Thrombus can expand to completely occlude the vascular lumen
What is the timeline of MI?
How is lab diagnosis of MI made?
By measuring blood levels of proteins that leak out of necrotic myocytes
- Cardiac specific troponins T and I (cTnT & cTnI)
- The MB fraction of creatine kinae (CK-MB)
what are the Morphology changes in the heart over from the attack to 8 weeks
