Week 2 - CVS Flashcards
MI/IHD, Atherosclerosis, Aneurysms
What is the best way to salvage ischaemic myocardium and how?
Rapid reperfusion:
- thrombolysis
- PTCA +/- stenting
- CABGs
*Keep in mind re-perfusion injury!
What is atherosclerotic plaque separation caused by?
Proteolytic enzymes
What are the 3 types of aortic dissection classifications?
- Debakey I –> whole aorta
- Debakey II –> ascending only
- Debakey III –> descending only
- Type A Stanford = Debakey I and II
- Type B Stanford = Debakey III
What is the most important cause of aneurysms?
Atherosclerosis
Where are berry aneurysms common?
Cerebral arteries
- haemorrhage (rupture)
- stroke (thromboembolism)
What are complications of aneurysms?
- mural thrombosis/embolism –> COMMONEST
- fatal hemorrhage (if rupture)
- surrounding organ compression
- ischaemic organ damage!
What is the pathogenesis of aneurysms?
Cystic medial degeneration
What are vasa vasorum?
small blood vessels that supply wall of blood vessels
What is an aneurysm and its types?
Abnormal dilatation of an artery
- True (all layers involved) –> saccular/berry; fusiform
- False (not truly enlarged - escaped blood causes bulge) –> hematoma; dissecting
Which cardiac marker is best for lab evaluation of an MI?
Troponins I + T
- increased within 2-4hrs
- peak @48hrs
- remain elevated for 7-10 days
What are the MI markers?
- myoglobin
- troponin I + T
- CK + CK-MB
- lactate dehydrogenase
What are chronic complications of MI?
- chronic IHD - CHF
- arrhythmias
- ventricular aneurysm
- mural thrombosis
- papillary muscle contraction –> Mitral regurgitation
What are acute complications of MI?
- heart failure
- arrhythmias
- CHF
- cardiogenic shock
- pericarditis
- mural thrombosis
- myocardial wall rupture –> tamponade (3-10days)
- papillary muscle rupture –> mitral regurgitation
Which coronary arteries are commonly affected by infarction?
- LAD (ant/septum) –> 50% (most commonly affected)
- RCA (posterior) –> 30%
- Left marginal (L circumflex) (lateral) –> 20%
What are the 3 types of myocardial infarcts?
- Sub-endocardial
- partial obstruction
- NSTEMI - Transmural
- complete obstruction
- STEMI - Multiple Small (Microscopic)
- small vessels affected
- normal ECG
- gives rise to chronic IHD
Where in the artery is an atheroma located within?
Tunica Intima
Compare the 3 types of aneurysms
- Berry
- from one side of artery producing a ‘fruit-like bulge’
- common in cerebral arteries - Fusiform
- whole circumference of artery dilates due to AS plaque with inflammation weakening the arterial wall - Dissecting
- plaque ruptures in middle, blood rushes inside splitting wall into 2 layers (blood between tunica intima and media)
- common in aorta; blood enters ruptured plaque
What are the complications of atherosclerosis?
- ischaemia/infarction of organ supplied
- progressive block
- thrombosis/thromboembolism
- aneurysm
- rupture –> haemorrhage
- MACROANGIOPATHY
What is the pathogenesis of atherosclerosis?
- Endothelial injury
- LDL entry and oxidation in intima
- Oxidised LDL causes adhesion and entry of monocytes/T-cells across endothelium via pro-inflammatory mediators
- Monocytes –> macrophages which consume large amounts of LDL –> Foam cells
- Foam cells release cytokines which cause inflammation and smooth muscle cell/fibroblast proliferation –> fibrous cap formation
Compare the 2 types of plaques
Unstable Plaque (10%):
- large lipid core
- severe inflammation (IFN-gamma) –> M1
- thin fibrous cap
- low SMC
- rapid change
- pain at rest (unstable angina)
Stable Angina (90%):
- small lipid core
- low inflammation (IL-4/IL-13) –> M2
- thick fibrous cap
- high SMC
- slow progressive
- pain on exertion (stable angina)
True or False?
Unstable plaque cannot regress back to stable plaque
False
- atheroma plaque = balance between inflammation and healing
- increased inflamm. = unstable
- increased healing = stable
- with modifications of risk factors, unstable plaque can –> stable (and vice versa)
What are the 2 pathways of macrophage activation?
- Classic Path
- Th1 –> IFN-gamma –> M1 - Alternate Path
- Th2 –> IL-4/IL-13 –> M2
Where does plaque accumulation start in BVs and why?
At the bifurcation of arteries
- due to increased trauma here from blood hitting this area with increased force
What are the risk factors for atherosclerosis?
- Non-modifiable
- age, male, family history, genetics - Modifiable
- hyperlipidemia, HTN, smoking, DM, lifestyle - Additional
- CRP, hyperhomocysteinemia, metabolic syndrome, pro-coagulants
What are the clinical manifestations associated with unstable plaque?
- unstable angina
- acute MI
- sudden cardiac death
What is the earliest microscopic feature in atheroma formation?
Foam cells
Outline gross and microscopic changes to heart post-MI
Gross: <4hrs - none 4-12hrs - occasional dark mottling 12-24hrs - dark mottling 1-3days - mottling + yellow tan centre 3-7days - pale/yellow centre with hemorrhagic border 7-10days - max. yellow tan + red margins 1-3wks - red-grey depressed borders, thin (loss of tissue mass) >3wks - small silvery white scar
Micro:
<4hrs - none (loss of LDH/glycogen - special stain*)
4-12hrs - oedema, hemorrhage, beginning of necrosis
12-24hrs - coagulative necrosis, contraction bands, oedema, hemorrhage, neutrophils, pyknosis of nuclei
1-3days - necrosis, loss of nuclei, interstitial neutrophils
3-7days - dead myocytes, dying neutrophils, phagocytosis by macrophages
7-10days - macrophages, granulation tissue
1-3wks - no muscle, new BVs, granulation, fibroblasts (collagen), macrophages
>3wks - dense fibrosis (collagen scar), NO inflammation
What is granulation tissue?
Collective term for structure composed of new BVs and collagen fibres formed in the healing process approximately 7-10 days post-MI
When is the most dangerous time during healing post-MI for rupture of ventricular walls to occur and why?
Between 3-7days
-macrophages are present and begin phagocytosing dead debris (neutrophils and dying myocytes) –> thus potentially thinning the wall to the point of rupture –> CARDIAC TAMPONADE
What is Metabolic Syndrome X?
Collection of disorders that occur together and increase the risk of developing T2DM and CVD. Dx. is made when a person has >/= 3 of:
- central obesity
- HTN
- increased triglycerides
- increased LDLs/decreased HDLs
- increased BSLs
Where do coronary arteries arise from and when do they receive blood supply?
- from behind the the cusps of aortic valve
- receive blood during DIASTOLE, from L+R coronary sinuses
What are gross and microscopic features of chronic IHD?
Gross:
- LV dilatation and hypertrophy
- myocardium will show multiple grey-white scars (old MIs)
- evidence of atherosclerosis
- patchy white scars in endothelium –> mural thrombi
Micro:
- myocyte hypertrophy and vacuolisation
- fibrosis
What is the commonest cause of clinical angina?
Decreased coronary blood flow (90%)
-90% of this is atherosclerosis
What are contraction bands and when do they occur?
- bright, eosinophilic bands of condensed contractile proteins that run at right angles to the long axis of the cardiac myocyte
- occur after acute MI (12-24hrs)
What are the stages of AS plaques?
Foam cells –> fatty streak –> intermediate lesion –> atheroma –> fibrous plaque –> complicated lesion/rupture
What is cystic medial degeneration?
- elastic fibre degeneration
- small cyst-like spaces of necrosis in media
- commonest pathogenesis of aortic aneurysms
- caused by atherosclerosis
- separation of media tissue by elastic fragmentation forming cleft-like spaces in media
What is IHD?
Primarily a consequence of inadequate coronary perfusion relative to myocardial demand –> angina pectoris
What % of the coronary artery is required to be occluded to cause symptoms?
- <70% = asymptomatic
- > 70% = critical stenosis (symptomatic on exertion - stable angina)
- > 90% = symptomatic at rest - unstable angina
What is collateral perfusion?
Remodelling of coronary vessels over time to provide compensatory blood flow for at-risk areas
After how long does loss of function and necrosis occur with lack of O2?
loss of function –> 1-2mins
necrosis –> 20-40mins
What is the pathogenesis of ischaemic pain in cell injury/inflammation?
-decreased oxidative phosphorylation = decreased ATP = increased anaerobic glycolysis = increased lactic acid = decreased pH –> PAIN
What are the CXR findings of cardiac failure?
A - alveolar bat wings B - kerley B lines C - cardiothoracic ratio > 50% D - dilated upper lobe vessels E - pleural effusion
What is Nutmeg liver?
Passive venous congestion of liver, characteristic of RHF
Give examples of ischaemic vs. non-ischaemic causes of cardiac pain.
Ischaemic:
- stable angina
- unstable angina
- MI
Non-ischaemic:
- myocarditis
- pericarditis
- aortic dissection
Outline management process for ACS pts.
M - morphine/fentanyl (analgesia)
O - oxygen if hypoxic
N - nitrates if pain not controlled by opioids
A - aspirin ASAP
L - leads (ECG)
I - IV access + blood tests taken (cardiac markers)
S - streptokinase (+ other thrombolytics)
A - anti-platelet therapy as required
*Re-perfusion Tx. if pts. present within 12hrs of symptom onset
