SIHD and Angina - Therapy Flashcards
Here are the learning outcomes
What are the acute coronary syndromes and the stable coronary artery diseases?
Acute:
Myocardial infarction (STEMI/NSTEMI)
Unstable angina pectoris
Stable:
Angina pectoris
Silent ischaemia
How does SCAD (stable coronary artery disease) arise?
•mismatch between myocardial blood/ oxygen supply and demand
What causes the onset of ischaemia in demand ischaemia vs Supply ischaemia?
What are the determinants of demand?
Heart rate
Systolic blood pressure
Myocardial wall stress
Myocardial contractility
What are the seterminants of supply?
Coronary artery diameter and tone
Collateral Blood flow
Perfusion pressure
Hear rate (duration of distole)
What does hyperlipidaemia result in the deposition of?
Cholesterol esters
Where is the accumulation of foam cells in atherosclerosis?
Subendothelial
What is the cause of disease in atherosclerosis?
Fibrous plaques that project into the arterial lumen reducing blood flow
How can drugs overcome the deman/suppply imbalance?
What is the purpose of drug treatment in stable coronary artery disease?
To releive symptoms
Halt the disease process
Regression of the disease process
Prevent myocardial infarction
Prevent death
Here is a summary of all the potental drug therapies for stable coronary artery disease
From summary of drugs for stable ischaemic heart disease, what is are the rate limiting drugs?
Beta blockers
Ivabradine
Calcium channel blockers
What are the vasodilators used in the treatment of stable ischaemic heart disease?
Calcium channel blockers
Nitrates
Give examples of beta blockers
Bisoprolol and atenolol
What receptors do beta blockers block?
Reversible antagonists of beta 1 and beta 2 receptors
Newer drugs are cardioselective acting on the beta 1 receptors
How do beta blockers serve to decrease demand?
Reduce heart rate, reduce contractility, reduce systolic wall tension, decreases blood pressure, protects cardiomyocytes from oxygen free radicalsf ormed during ischaemic episodes
•Also allow improved perfusion of the subendocardium by increasing diastolic perfusion time
What are the contraindications for beta blockers?
Asthma
Peripheral vascular disease
Raynauds syndrome
Heart failure (those patients who are dependatn on sympathetic drive)
Bradycardia / heart block
What are the adverse drug reactions of beta blockers?
- Tiredness /fatigue
- Lethargy
- Impotence
- Bradycardia
- Bronchospasm
- Rebound –
–Sudden cessation of beta blocker therapy may precipitate myocardial infarction
What are the drug drug interactions of beta blockers?
Hypotentsion when used with other hypotensive agents
Bradycardia when used with other rate limiting drugs such as verapamil or diltiazem
Cardiac failure when used with negatively inotropic agents such as verapamil, disopyramide or diltiazem
NSAIDS antagonise antihypertensive actions
Exaggerate and mask hypoglycaemic actions of insulin or oral hypoglycaemics
How do calcium channels work?
Prevent calcium influx into myocytes and smooth muscle lining arteries and arterioles by blocking the L-Type calcium channel.
Give examples of rate limiting CCB’s and what they do
Diltiazem and verapamil - reduce heart rate and force of contraction - reducing myocardial oxygen requirements
Give an example of a vasodilating CCB and what it does
Amlodipine - (may produce a reflex tachycardia)
Vasodilitation, reducing afterload
Reduces myocardial work load
Do CCB’s cause coronary vasodilatation?
Yesm but of little importance
What is the effect of a rapidly acting vasodilatory CCB? (nifedipine)
May precipitate acute MI or stroke
What are the common adverse drug reactions associated with calcium channel blockers?
Ankle oedema (–Affects 15-20% of patients and does not respond to diuretics)
Headache
Flushing
Palpitation
Give examples of nitrovasodilators
•GLYCERYL TRINITRATE (GTN)
–Sublingual, buccal, transdermal
•ISOSORBIDE MONONITRATE
–Sustained release formulation, tablets
•ISOSORBIDE DINITRATE
–Sustained release formulation, tablets
How do nitrovasodilators work?
Relax almost all smooth muscle by releasing NO
Stimulates the production of cGMP which causes smooth muscle relaxation
Reduces preload and afterload so reduces myocardial oxygen consumption
What are the uses of GTN and oral nitrates?
GTN - rapid treatment of angina pain
Oral nitrates -
–Commonly given as a once a day sustained release formulation
–Used for prophylaxis
When are intravenous nitrates used?
Treatment of unstable angina used in combination with heparin
How do you overcome the development of tolerance to nitrate therapy?
–Giving asymmetric doses of nitrate 8am and 2pm
–Using a sustained release preparation which incorporates a “nitrate free period”
What are the adverse drug reactions for GTN?
Headache
Hypotension (GTN syncope)
Summary Table
Why is nicorandil said to have a negative ionotropic action?
It activates ATP sensitive potassium channels, •The entry of potassium into cardiac myocytes inhibits calcium influx and so has a negative inotropic action.
How does nicorandil cause a decrease in preload and afterload?
Activates Cyclic GMP, causing the dilation of capacitance vessels, decereases preload
Opens ATP sensitive potassium channels, these channels are involved in dilation of coronary resistance arterioles, these decrease afterload and are also thought to mimic ischaemic preconditioning - a potential cardioprotective effect
How does the activation of ATP sensitive potassium channels result in the relaxation of vascular smooth muscle and the dilitation of systemic and coronary arterioles?
ATP sensitive potassium channels cause potassium efflux, causing voltage gated calcium channels to close, intracellular levels of calcium decrease - relaxation of vascular smooth muscle
How does Ivabradine reduce heart rate?
Selective sinus node channel inhibitor, slows the diastolic depolarisation slope of the SA node
Which patients can ivabridine used for?
Those who have a heart rate of 70 and over.
Not effective at reducing the incidence of coronary artery disease outcomes in patients with heart rate less than 70 bpm
Symptomatic treatment of stable angina only effective if sinus rhythm and heart rate is greater than 70 beats per minute
What are the indications for ivabradine?
Patients who cannot use beta blockers
Patients who are inadequately controlled with optimal beta blocker dose
What is the action of thromboxane?
Stimulates platelet aggregation and vasoconstriction
How does aspirin inhibit platelet thromboxane production?
Aspirin acts by inhibiting the ability of the COX enzyme to synthesize the precursors of thromboxane within platelets
What is the effect of aspirin on acute MI and unstable angina?
Acute MI: Reduces mortality, in conjunction with streptokinase it can also reduce reinfarction
Unstable MI: Reduces MI and death
What is the most common cause of admission with GI bleed?
Aspirin
What is the effect of clopidogrel?
Inhibits ADP receptor activated platelet aggregation
What are the most effective cholesterol lowering agents?
HMG CoA reductase inhibitors - SIMVASTATIN, PRAVASTATIN, ATORVASTATIN
What is the point in cholesterol lowering agents post MI?
Can reduce cardiovascular mortality and total mortality
Treatment regimen
What is the NICE guidance for treatment for the relief of symptoms of stable angina?
Beta blockers first line therapy
Calcium channel blocker should be added if adequate control of symptoms is not achieved
•If the person’s symptoms are not satisfactorily controlled consider either switching to the other option or using a combination of the two
Which SIHD patients are offered •long term standard aspirin and statin therapy?
All patients with stable angina due to atherosclerotic disease
Who is offerec ACEi?
•All patients with stable angina should be considered for treatment with ACEi.
What drugs are given for the secondary prevention of cardiovascular disease?
- Aspirin 75 mg daily taking into account the risk of bleeding and comorbidities.
- ACE inhibitors for people with stable angina and diabetes.
- Statin treatment
- Treatment for high blood pressure
Overview
Overview for angina relief
Overview for event protection
