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