Stable angina therapy Flashcards
hyperlipidaemia - how does it cause damage to arteries?
blood has too many lipids (or fats), such as cholesterol and triglycerides
Atherosclerosis is the start
disease of the muscular arteries (not veins) - coronary and cerebral vessels
progressive deposition of cholesterol esters
mortality due to ischaemic heart disease is usually due to what?
MI
mortality due to cerebrovascular disease is usually due to what?
stroke
what do lesions in atherosclerosis start as
fatty streaks
what do fatty streaks develop into
fibrous plaques - more advanced/established
-project into the arterial lumen and cause reduced blood flow
where do fatty streaks form
in high pressure areas so muscular arteries NOT veins
what happens when plaques rupture
releases thrombogenic material
triggers clotting cascade- platelets adhere to exposed collagen
The plaque may heal, burying the thrombus into the vessel wall and causing the plaque to grow, or the thrombus may embolise distally
how can drugs help to correct imbalance of supply/demand of O2
decreasing myocardial oxygen demand by reducing cardiac workload
so reduce heart rate, reduce myocardial contractility, reduce afterload
by reducing heart rate, the heart stays longer in diastole and you get improved perfusion through the myocardium and better O2 supply
purpose of drug treatment (5)
relieve symptoms halt the disease process regression of the disease process prevent MI prevent death
what rate limiting (reduce heart rate) drugs are used for stable angina?
beta blockers (beta adrenoceptor antagonists)
ivabradine
Ca2+ channel blockers
what vasodilators are used in therapy for stable angina
Ca2+ channel blockers
Nitrates like GTN - quick relief of symptoms - oral, sublingual
Ca2+ channel blockers can fall under which types of drug therapies?
rate limiting and vasodilators
Other than rate limiting and vasodilators what other types of drugs are used for stable angina
Potassium channel openers - induce relaxation of vascular smooth muscle
Anti-platelets Aspirin/Clopidogrel
Statins - cholesterol lowering agents
how does ivabradine work
it reduces heart rate by inhibiting the pacemaker current/slowing the depolarisation in the SA node
can cause issues in people with previous heart problems
reduces fatal and nonfatal myocaridial infarction if heart rate is higher than or = to 70
beta blockers:- types, how they work
bisoprolol, atenolol
Beta blockers are reversible antagonists of the beta 1 (in the heart) and beta 2 (in the lungs) receptors
Newer drugs are cardioselective acting primarily on the beta 1 receptors
Block the sympathetic system
what 3 major determinants of myocardial O2 demand do beta blockers decrease?
heart rate
contractility
systolic wall tension
why must you not suddenly stop taking beta blockers?
it could cause MI esp if patient has angina, or is male or >50
When should you not use a beta blocker
if a patient’s heart failure is unstable - it could kill them
if they have asthma, peripheral vascular disease
Raynauds syndrome
bradycardia - slow it down too much
Raynauds syndrome
disease causes some areas of your body — such as your fingers and toes — to feel numb and cold in response to cold temperatures or stress.
Smaller arteries that supply blood to your skin narrow, limiting blood circulation to affected areas
Adverse drug reactions with beta blockers (6)
Tiredness /fatigue Lethargy Impotence- helpless Bradycardia Bronchospasm
Rebound – suddenly stopping a beta blocker then you can become highly anxious – exaggerated response to A/NA. And may cause MI. Stop using them over the course of a week
drug-drug interactions
hypotension when used with other hypotensive agents
bradycardia when used with other rate limiting drugs
cardiac failure when used with negatively inotropic (modifying the force or speed of contraction of muscles) agents
NSAIDs antagonise antihypertensive actions
Ca2+ channel blockers:- types, how they work
DILTIAZEM, VERAPAMIL, AMLODIPINE
Prevent calcium influx into myocytes and smooth muscle lining arteries and atrerioles by blocking the L-Type calcium channel
reduce vascular tone and produce vasodilation and reduce afterload
rate limiting - like diltiazem and verapamil also reduce heart rate and force of contraction
vasodilatiing - amlodipine - may produce a reflex tachycardia
adverse drug reactions with Ca2+ channel blockers
ankle oedema
headache
flushing
palpitation
GTN therapy
when patients present with angina they are put on GTN - doesn’t do anything for morbidity or mortality but relieves symptoms
it dilates arteries and veins by releasing Nitric oxide which then stimulates release of cGMP - smooth muscle relaxation
reduces preload and afterload - reduces O2 consumption
