Flashcards in Stable Ischaemic Heart Disease and Angina Therapy Deck (56)
What are the risk factors for stable IHD and angina?
What is hyperlipidaemia a disease of?
Muscular arteries - cerebral or coronary, not veins
From what age do fatty streaks appear?
How does hyperlipidaemia affect the arteries?
Lesions start as fatty streaks
There is subendothelial accumulation of large foam cells derived from the macrophages and smooth muscles cells filled with lipids
How do fibrous plaques affect the arteries?
Develop from fatty streaks and project into the arterial lumen, reducing blood flow
Where do most of the changes to the artery in IHD occur?
In the intimal layer
What changes occur in the intimal layer in IHD?
Accumulation of monocytes, lymphocytes, foam cells and connective tissue
What are the usual features of foam cells?
Most are of smooth muscle origin
Necrotic core and fibrous cap
What does stable ischaemic heart disease result from?
Mismatch between myocardial blood and oxygen supply and demand
What are episodes of angina precipitated by?
Any activity which causes cardiovascular stress
How can drugs help to correct the imbalance in stable IHD?
Decrease myocardial oxygen demand by reducing cardiac workload
Increase supply of oxygen to ischaemic myocardium
What are the purposes of drug treatment of stable IHD?
Halt disease process
Regress disease process
What drugs can be used in the treatment of stable IHD?
CCBs - rate limiting and vasodilation
Potassium channel openers
Cholesterol lowering agents e.g. HMG CoA reductase inhibitors
Give an example of a beta blocker used in the treatment of stable IHD
How do beta blockers work to treat stable IHD?
Reversible antagonists of beta-1 and beta-2 receptors (newer drugs are cardioselective and act primarily on beta-1 receptors)
Block the physiological responses to adrenaline and noradrenaline and so decrease 3 major determinants of myocardial oxygen demand - HR, contractility and systolic wall tension
Also allow improved perfusion of subendocardium by increasing diastolic perfusion time
What effect do beta blockers have on HR, force of myocardial contraction, CO, velocity of contraction and BP?
Decrease all of these
What do beta blockers protect the caardiomyocytes from?
Oxygen free radicals formed during ischaemic episodes
By reducing HR, force of contraction and BP, beta blockers increase what?
Exercise threshold at which angina occurs and so move the balance point at which demand for oxygen outweighs the supply of oxygenated blood
What is rebound phenomena?
When sudden cessation of beta-blocker therapy may precipitate MI, those at risk include patients with angina and males over 50 years old who are receiving beta blockers for other reasons
What are the contraindications to beta blocker use?
Peripheral vascular disease (relative contraindication)
What are the potential adverse drug reactions from beta blocker use?
What are the possible drug-drug interactions with beta blockers?
Hypotension when used with other hypotensive agents
Bradycardia when used with other rate limiting drugs
Cardiac failure when used with negatively inotropic agents
NSAIDs antagonise antihypertensive actions
Exaggeration and masking of hypoglycaemic actions of insulin or oral hypoglycaemics
Give an example of a calcium channel blocker used in treatment of stable IHD
How do CCBs work?
Prevent calcium influx into the myocytes and smooth muscle lining the arteries and arterioles by blocking L type calcium channels
How do rate-limiting CCBs treat stable IHD?
Reduce HR and force of contraction which reduces myocardial oxygen requirements
How do vasodilation CCBs treat stable IHD?
Reduce vascular tone and so produce vasodilatation and reduce afterload, reducing myocardial workload
What are the contraindications for CCBs use?
Evidence that use of rapid acting vasodilatory CCB may precipitate acute MI or stroke
What are the possible adverse drug reactions from CCB use?
What percentage of patients on CCBs will experience ankle oedema?