Angina Flashcards
What are the characteristics of these types of angina
- stable
- mixed
- vasospastic (Prinzmetals)
- microvascular (Syndrome X)
- unstable
Stable
- Stenosis >70%
- tight crushing pain on physical/emotional exertion (supply demand mismatch => adenosine, bradykinin release => pain)
Mixed
- stenosis + vasospasm
- unpredictable exertion
Vasospastic (Prinzmetals)
-no stenosis, coronary spasm
Microvascular (Syndrome X)
- can’t VD enough due to endothelial dysfunction
- no stenosis, linked to post/perimenopause
Unstable
-transient thrombus => partial occlusion
What are the main aims of drug treatment
-2 reasons
Decrease future attacks
- decrease coronary O2 demand
- increase coronary flow
Protect against future CV events
- decrease risk factors via
- Bblockers
- Statins
- ACEi
- Aspirin
Describe the mechanism behind B blockers
What are the SE and why
What are the CI
Decreased SNS => decreased contractility and renin release => increase flow, diastole
SE due to VD inhibition
- cold extremities
- hypoglyacaemia due to dampened SNS dominated adrenaline reaction
- exercise intolerance
- fatigue
CI due to VD inhibition
- asthma
- VS angina
Describe the mechanism behind Ca channel blockers
What are the 3 main drugs in this group
VD CORONARIES
Amilodipine
-increase VD arteries => decrease after load => decrease cardiac stress
Verapamil, Diltiazem
-decreased inotropy => increase diastole
Describe the mechanism behind organic nitrates
What are the SE and why
Why can you develop a tolerance to this
Decreased CVP (decreaseSM, depolarization => venous VD) => decrease wall stress => decrease O2 demand
Decrease TPR
VD of coronaries
SE due to VD
- low BP, reflex tachycardia
- headache, facial flush
Tolerance due to increased oxygen radicals
Describe the mechanism behind ranalazine
Ischemia => increased ROS => increased late Na I
Normally
- APs more likely
- afterdepolarization arrhythmias
-increased [Ca] I => myocardial stunning => decreased diastolic period => increased work, decreased coronary flow
Ranalazine inhibitions late Na I
Describe the mechanism behind ivabradine
What are the SE and why
What are the CI
Blocks If => decreased HR => increased diastole, decreased after load, O2 demand
SE due to reflex increases
- headache, dizzy
- bradycardia
- luminous phenomena
CI
-renal, hepatic impairment
Describe the mechanism behind nicorandil
What are the SE and why
What are the CI
KATP channel activator => opens channels in SM => hyper polarization and Ca removal/desensitization
=> VD => decreased pre/afterload => decreased work/O2 demand
SE due to VD
-headache, dizzy, flushed
CI
- hypotension
- PDE5 inhibitor (synergistic VD)
What are the 2 physical treatments for angina
How would you do this
PCI
- guide catheter via femoral/radial vein
- balloon inflates stent open
CABG
- saphenous/int mammary for serious cases
- more invasive, increase survival
- needs thoracotomy, CP bypass