Ischaemic heart disease Flashcards
What is ischaemic heart disease?
Disease of the coronary arteries
occurs when fatty/ fibrotic plaque blocks the coronary lumen
and blood flow is restricted= ischaemia
How does IHD occur and present?
Chest pains
When O2 demand of myocardium exceeds supply
less nutrients to tissue so cell death
presents when plaque ruptures and flow to artery is suddenly blocked
What happens when you get chest pains?
release of K, H and adenosine
disease progress insidiously until these symptoms
What is chest pain?
typically centered in the chest
radiates to neck and arm
levines sign
patients fist is clenched
Progression of coronary atherosclerosis
0-10= foam cells 10-20= fatty streak 20-30= intermediate lesion 30-40= atheroma 40-50= complicated lesion or rupture
Stats about IHD
leading cause of death
2013-7 million deaths
UK- 21,000 cases
>55 12% of men and 5% women
Risk factors
- non modifiable
- age sex gender
- family history - modifiable
- diet obesity and diabetes
- smoking
- high BP
- high cholesterol
What are the risks to patients with IHD?
- suspectible to acute coronary syndromes-ACS
- unstable angina
- Non-ST elevation MI (NSTEMI)
- ST elevation MI (STEMI)
ECG of IHD patients
The ECG can be normal in patients with IHD unless they have had a previous MI. To see the ECG changes – need to have current ischaemia or have had an MI
What are the differences in unstable angina, NSTEMI and STEMI?
unstable angina = pre MI condition
NSTEMI =a type of MI (more minor forms)
STEMI =caused by a complete blockage of one of the main coronary arteries. (can occur in emotional or physical stress and can progress as a full heart attack)
Lumen of stable angina and Non- stemi
stable angina, above plaque normal wall (thickened) ischemia (stable form
N ST- complete and permanent blockage
Epidemeology of ACS
Rare under 35
0.6%- 35-74
2.3%-75+
England= 233,600 new cases annually
amount of STEMI/NSTEMI in England
STEMI- 5/1000
Nstemi- increasing
How would a myocardial ischaemia be apparent and dealt with?
Chest pain- heavy or crushing
treatment would be based on the type of angina
Stable angina treatment
reduce cardiac work
treat the underlying condition- atherosclerosis (statin) or prohylaxis (anti-platelet)
unstable angina treatment
treat with MI strategy
- DAPT
- nitrates
Which types would have GTN relief?
Stable angina and unstable angina- not N/STEMI
Which would have a normal ECG?
Unstable and stable angina
Which types would have raised troponin?
NSTEMI
STEMI
What are the 4 steps for treating ischaemia?
restore blood flow asap
- reopen blocked arteries
- reduce the coagulability of blood
- control risk factors
- reduce myocardial O2 demand
Restoring blood flow method- PCI
PCI-percutaneous coronary intervention
- non surgical technique- aim to widen the artery using dilation from within
- place stent
- popular drugs attached to stent to inhibit cell regrowth
What is the crucial door balloon time?
120 min
for STEMI
immediate procedure
What would you use if there wasn’t uncontrolled angina?
Nitrates- they restore flow
What is combined treatment for IHD?
Use catheter and track into heart add dye see pictures -dilate vessels from veins and increase vessel size \+ - push away plaque
3 steps to stenting
- mounted on balloon
- inside stent and inflated
- stent positioned against wall and wire/ balloon is removed
Medical treatments after stenting
DAPT- dual antiplatelet therapy- incidience of thrombosis 1%
Aspirin-+ antiplatelet + abti-coagulant= continued years after stenting
Adverse effects and benefits of drugs after stenting
- excess bleeding
- pleiotropic positive effects of neutrophils and therefore pulmonary infection- reduce cell growth and clotting, keep your artery open
What is the main aim of pharmalogical treatments of IHD?
to keep the coronary plaque stable as possible to avoid an acute clot blockage (occlusion) which can be partial or full
and to reduce pain
two pharmacological treatment approaches?
- symptomatic- reduce symptoms, reduce strain on heart and increase vasodilation
- prognostic- improve outcomes and eleviate neg outcome in future
Symptomatic drugs
- nitrates
- aspirin
- Ca channel
- K channel
- Analgesia
Prognostic
- Aspirin
- Statins
- beta blockers or ACE inhibitors
- anti-inflammation approaches are being developed
Nitrates- when they started, why we use them
- brunten 1867
- first line agents, GTN as a short acting spray sublingually
What is the primary and secondary effect of nitrates???
primary- to relax smooth muscle and veins, main effect on larger muscular arteries
secondary- reduce Cardiac work, redirection of flow towards ischaemic areas of heart muscle, improves coronary spasm
Mechanism of action of nitrates
GTN metabolism
activates GC and increases cGMP
this activates PKG and causes relaxation of the smooth muscle
What are the main adverse effects of nitrates
- hypotension- administer slow
- headaches
- tolerance= depletion of SH group and is more common with longer acting agents
NITRATES-What is GTN activated by?
Hepatic metabolism
What is the delivery time and the length of effect of nitrates?
- 1-2 mins- conversion from di to mono in a min
- 30 mins it lasts
What is isosorbide mononitrate?
orally administered
longer acting
2 a day with a nitrate free period at night to avoid tolerance
Mechanism of Ca channel blockers
block receptors, preventing ca channel opening therefore prevent influx of ca through membrane
blocks smooth muscle contractions
What do Ca channel blockers act on ?
L type Ca channels
Ca channel drugs
-phenylalkylamine= verapamil
- dihydropyridines= amlodipine
benzothiazepines= diltiazem
What are the selective actions of the Ca channel drugs?
verapamil- more active on the heart
nifedipine- smooth muscles
drugs also dilate the coronary vessel
Side effects of Ca channel blockers
flushing and headaches due to vasodilator action
verapamil= constipation (effects GI nerves and smooth muscle)
What is aspirin, why is it given?
NSAID/ acetylsalicylic acid
- given immediately on presentation or daily thereafter
Mechanism of aspirin?
cardiovascular area because it inhibits the COX-1 receptor on platelets and reduces platelet aggregation
irreversibly acetylates COX enzymes and platelet cannot replenish
Lifetime of a platelet
10 days
after that new ones form
Usage of aspirin? and risks?
First line CVD
GI bleeding, deafness, tinnitus, self poisoning and resistance
How was aspirin made?
One of the oldest drugs
synthesesied
derived from willow bark
Whats special about aspirin in comparison to other NSAIDS
non steroidal inflammatory drugs 75mg/day suppresses platelet aggregation
What does inhibiting COX1 effect?
it prevents the conversion of arachidonic acid to thromboxane A2 which causes platelet aggregation
Why can platelet replace enzyme?
Don’t have a nucleus
so cannot do de novo synthesis
remain inactivated
Pharmacokinetics of taking aspirin
given orally
hydrolysed in 30 mins by esterase from liver
1/2 life depends on dose
When happens to aspirin when taken orally
Week acid so protonated in stomach and able to pas through mucosa = major absorption site
hydrolysed by salicylate in tissues
Anti-coagulant and platelet approach how does it work
prevents clotting by inhibiting clotting factors
heparins= enoxaparin- activate antithrombin which activates thrombin and factor xa - prevent stable clot formation
Side effects of anti- coagulant and platelet
bleeding
Analgesia
Given with acute coronary syndrome
heart attack= painful so give morphine
Different types of opiates
- Morphine
- codeine
What id morphine?
extracted from poppy juice used for 1000s years
induce euphoria, analgesia and stop diarrhoea
partial agonist
How does morphine work?
Binds to opiod receptor (GI/Go coupled to ion channel)
phenanthrene derivative
What is codeine?
opiate
binds to Mu receptor as a partial agonist
effective respiratory depressor
Side effects of opiates?
Respiratory depression nausea and vomiting reduced tone and motily in gut histamine released tolerance effects *morphine given slowly it doesn't have effects
Unstable angina treatments
DAPT
heparin
analgesia
secondary prevention- ACE, statins, BB
Nstemi treatments
Antiplatelet
analgesics
PCI within 72 hours
possibly additional platelet depending on changes in ECG
Treatments for STEMI
PCI- If centre is too far away then clot buster
antiplatelet medications- aspirin
lifelong medications= aspirin 75mg/day for 1 year, statins, ace, BB
Personalisation of treatments
Platelet based- maybe inflammation
individual maps of the patients coronary arteries- help decide which lesions within which arteries need attention
PASTOR study
used bedside device at the time of PCI after STEMI to measure individual platelet activity and assign anti-platelet medication on this basis
