Angina Flashcards
What are the symptoms of angina?
- Tightness
- Squeezing
- Crushing sensation in the chest
- Referred pain to left arm/left jaw
What is unstable angina?
- Fibrous cap has been eroded
- Very thrombotic plaque
- doesnt follow a pattern
- more severe
- can occur with/without physical exertion at rest or medicine may not relieve the pain
What is atherosclerosis?
- The build up of cholesterol rich plaques
- The disease process leading to CHD
- causes stenosis of coronary arteries
Describe the 2 components of an atherosclerotic plaque.
- ) Fibrous cap: SMCs and CT
2. ) Atheroma: soft pool of extracellular lipid, cell debris,activated immune cells. Progressively calcifies over time
What may thrombosis lead to?
- unstable angina
- STEMI
- NSTEMI
What may cause angina?
- exertion/emotion
- results from increased oxygen demand with restricted blood flow due to fixed stenosis
What may cause angina of effort?
- exertion/emotion
- results from increased oxygen demand with restricted blood flow due to fixed stenosis
At which level of stenosis does angina develop?
-Stenosis of > or= 70%
How can decreased oxygen in cardiac tissue lead to coronary vasodilation?
- The decrease in oxygen in the cardiac tissue results in a release of protons & bradykinin
- This leads to activation of TRPV1 on sensory nerves which causes pain and the release of substance P
- This subsequently leads to coronary vasodilation
What are the different types of angina?
- ) Angina of effort
- ) Mixed(variable threshold angina)
- ) Vasospastic(Prinzmetal’s) angina:
- ) Microvascular (syndrome X)
- ) Unstable
Outline mixed angina.
- unpredictable, develops at different levels of exercise
- common
- probs due to stenosis&vasospasm
Outline vasospastic (Prinzmetal’s) angina.
- decreased oxygen supply
- due to spasm of coronary artery- tight enough constriction to cause ischemia
- can occur at rest
- often at night
- Transmural ischemia cos all layers of the heart wall are affected due to the tightness of the constriction
- Patients may/may not have atherosclerosis with it
Outline micro vascular(syndrome X) angina
-Chest pain
-Normal coronary angiogram
-Positive exercise test
-Endothelial dysfunction
-Constricted microvasculature
-Occurs more commonly in women.
with signs associated with decreased blood flow to heart tissue but with normal coronary arteries.
-Coronary arteries are normal
Outline unstable angina
- decreased oxygen supply
- due to transient formation of a non-occlusive thrombus
- an acute coronary syndrome
What can we use for immediate relief/short term prevention of angina?
-Short acting nitrate
What can we use for ongoing prophylaxis of angina?
- Beta blockers
- long acting nitrate
- ivabradine
- nicrorandil
- ranolazine
How can we treat angina
- GTN
- rest
Outline the use of organic nitrates in angina
- cellular mechanism= NO donor
- Haemodynamic mechanism: decreased CVP/preload, leads to and increased coronary blood flow
- GTN taken sublingually= v rapid &used for cutting short an angina attack of preventing an anticipated attack
- Other organic nitrates are longer acting and are taken on an ongoing basis( pills,ointments,patches)
How is the effectiveness of longer acting nitrates limited? How can this be avoided?
- development of TOLERANCE
- Can be avoided by a daily 8 hour drug free period (typically at night)
Outline the haemodynamic effects of nitrates.
Major actions:
-relax venules & veins, so decrease CVP and thus decreases cardiac wall tension so decreases cardiac demand
Minor actions:
-Dilate larger coronary arteries, increasing blood flow through coronary collaterals
-decrease TPR and afterload, therefore decreasing oxygen demand
Side effects:headache, facial flushing, decreased BP, reflex increase HR
What is the aim of drug treatments for angina?
- Limit the number, severity& sequellae of anginal attacks, thereby improving QOL
- main mechanism is to decrease cardiac oxygen demand
- secondary mechanism= increase the o2 supply to the ischaemic zone by decreasing the HR and increasing the blood flow in coronary arteries
- protect against the future
What is Ivabradine used for?
- Decreases heart rate because it inhibits the funny current
- Decreases force of contraction
- Increases perfusion
What is Ranolazine used for
- Anti-anginal medication
- Decreases wall tension
- By blocking late inward sodium currents, calcium overload and diastolic wall stress are reduced, leading to improved coronary blood flow.
- prevents arrythmias
Which drugs can be used to treat angina?
-Ivadbradine
-Beta blockers
-Ranolazine
-Nitrates
(Calcium channel blockers-e.g amylodipine and potassium-ATP channel activators-e.g nicorandil also)
How is GTN metabolised?
- GTN is converted to superoxide,NO and oxygen, using mitochondrial aldehyde dehydrogenase 2 enzyme
- NO and oxygen allow for vasodilation due to guanylate cyclase
What is the function of Nicorandil?
-K-ATP channel activator
-Has dual action…
1.)Opens ATP-sensitive K+ channels in vascular SMCs
2.)Stimulates guanylate cyclase, so increases vascular SMC
These effects lead to relaxation of vascular smooth muscle and therefore venous& arterial vasodilation
What would be the effect of an increased late sodium current?
- Action potential prolongation
- leads to afterdepolarisations
- could cause arrythmias
What are the different methods of revascularisation?
- Percutanous coronary intervention (PCI): A balloon is inflated to reopen a coronary artery that has undergone stenosis
- Coronary artery bypass grafting (CABG): uses pieces of saphenous vein or diverted internal mammary artery
What is the issue with PCI?
- Restenosis may occur and symptoms may return
- May be resolved with the use of stents
Compare and contrast PCI & CABG
- CABG is preferred in patients with more serious/advanced coronary artery disease
- CABG is much more invasive than PCI
- Much more invasive than PCI as the chest must be opened& the patient is usually on cardiopulmonary bypass
- Unlike PCI, CABG improves survival
Most of the drugs used to treat angina act by reducing one or more of the 4 factors which determine cardiac output and therefore work; what are these factors?
- ) Preload
- ) Afterload
- ) HR
- ) Cardiac contractility
What is syndrome X
- Cluster of abnormalities caused by a high intake of refined carbohydrates,
- leads to hypoglycemia, hyperinsulinemia, and glucose intolerance followed by diminished insulin sensitivity, further leading to hypertension, hypercholesterolemia, obesity, and T2DM.
What is the difference between unstable angina and MI
Unstable angina= heart tissue is alive but ischemic ( cos its usually caused by when an atherosclerotic plaque has ruptured, together with thrombosis. The occlusion may not block the whole vessel)
-MI= necrosis has begun in the heart tissue
Why should unstable angina be treated as an emergency
cos patients are at high risk of progressing to MI
What are coronary artery vasospasms?
- occurs in vasospastic/ Prinzmetal’s angina
- The smooth muscles around the arteries constrict extremely tightly- enough to cause ischemia
How does angina differ from MI
Explain the ECG differences between stable, unstable and Prinzmetal’s angina
- Both stable and unstable angina show an ST depression cos the ischemia is sub endocardial
- Prinzmetal’s shows a ST elevation because the ischemia reaches all layers i.e it is transmural
Outline the difference in presentation at rest in stable, unstable & Prinzmetal’s angina
- rest tends to relieve symptoms of stable angina
- All 3 can be treated by nitroglycerin or GTN ( the dilute form of nitroglycerin) which is a vasodilator
- Vasoplastic angina also responds to calcium channel blockers (NOT beta blockers)
What is responsible for ST depression
- myocardial ischaemia caused by coronary insufficiency
- Subendocardial ischaemia/infarction
