Treatment of Angina Flashcards
what shrinks the window between systole
• Shorteningdiastole
– e.g. increased heart rate
• Increased ventricular end diastolic pressure
– e.g. aortic valve stenosis
• Reduced diastolic arterial pressure
– e.g. mitral or aortic valve incompetence, heart failure
Coronary ischaemia
usually the result of atherosclerosis
– Causes angina
Sudden ischaemia
usually caused by thrombosis
- may result in cardiac infarction
Coronary spasms
sometimes causes angina
– “variant” angina
Cellular calcium over load results from ischaemia
– may cause cell death and dysrhythmias
Angina Pectoris
• Chest pain due to inadequate supply of oxygen to the heart – Typicallysevereandcrushing
– “Tight, constricting, dull or heavy”–SIGN Guidelines
Characteristic distribution of pain
– Often retrosternal, or left side of chest and can radiate to left arm,
neck, jaw and back
– Brought on by exertion, cold or excitement
– Thought chemical factors that cause pain in skeletal muscle (i.eK+,H+ and adenosine) are responsible
stable angina
– Predictable chest pain on exertion
– Caused by a fixed narrowing of the coronary arteries
• Unstable Angina
– Occurs at rest and with less exertion than stable angina
– Associated with a thrombus around a ruptured atheromatous plaque
but without complete occlusion of the vessel (similar to MI)
• Variant (Prinzmetal) Angina
– Uncommon
– Caused by coronary artery spasm
– Not completely understood, but sometimes associated with atherosclerosis
Treatments to reduce chest pain symptoms
– Beta-blockers – Nitrates –Calcium channel antagonists – Nirocandil – Ivabradine – Ranolazine
Treatments to prolong survival
– Beta-blockers – Aspirin – Statins - (Angiotensin Converting Enzyme Inhibitors) – (Angiotensin II Receptor Blockers)
Treatment of symptoms
Offer short-acting nitrate for preventing/treating episodes of angina.
Offer first-line treatment:
– Usually a β-blocker, but a calcium channel blocker (CCB)
can be considered if not optimal
If bode ineffective the other option is contraindicated, nicornadil or ivabradine
Antianginal drugs
• Mainly work by ↓ the metabolic demand of the muscle
• Organic nitrates, nicorandil and calcium antagonists are vasodilators
– ↓ preload or afterload
• b-blockers and ivabradine slow down the heart – ↓ the metabolic demand of the muscle
Glyceryl trinitrate and isosorbide mononitrate
– Powerful vasodilators
– Work by being metabolised to nitric oxide (NO) and relax smooth muscle (particular vascular smooth muscle)
– Act on veins to ↓ cardiac preload
• Higher concentrations can affect arteries,↓a Herload
– ↓ cardiac workload is helped by dilaIon of collateral coronary vessels
– ↓ cardiac workload is helped by dilaIon of collateral coronary vessels
- Improves distribution of coronary blood flow towards ischaemic areas
- Dilation of constricted coronary vessels is particularly beneficial in variant angina
Clinical Uses of Organic Nitrates in Angina - stable angina
– Prevention by sublingual glyceryl trinitrate shortly before
exertion or isosorbide mononitrate long before
Clinical Uses of Organic Nitrates in Angina - unstable angina
– intravenous glyceryl trinitrate (GTN)
Clinical Uses of Organic Nitrates in acute heart failure
– intravenous GTN
Clinical Uses of Organic Nitrates in Chronic Heart Failure(CHF)
– isosorbide mononitrate with hydralazine in patients of African American origin especially, (or patient cannot tolerate more commonly used CHF drugs)
b-blockers
• Important (first line treatment) in the prophylaxis and
treatment of stable and unstable angina
• ↓cardiac oxygen consumption by slowing the heart
• Also have an antidysrhythmic action
– reduce death after MI
• Bisoprolol,Atenolol
Calcium Channel Blockers (CCBs)
• Two main types:
– Dihydropyridine derivatives, e.g.amlodipine and lercanidipine
– Rate-limiting, e.g.verapamil and diltiazem
Action of Calcium Channel Blockers (CCBs)
• Preventing opening of voltage-gated L-type Ca2+ channels
– blockCa2+entry
– Mainly affect the heart and smooth muscle to inhibit calcium entry upon muscle cell depolarisation
• Vasodilator effect mainly on resistance vessels
– reducesafterload
– also dilate coronary vessels (important in variant angina)
• Verapamil and diltiazem
can reduce and impair AV conduction and myocardial contractility
– Amlodipine or lercanidipine
safe in patients with heart failure, used instead of a Beta-Blocker in Prinzmetal angina or alongside beta-blockers in most angina
– Diltiazem or verapamil
used but contraindicated in heart failure, bradycardia, AV block or in presence of Beta-Blocker
side effects of CCBs
– headache, constipation, ankle oedema
• Antidysrhythmics
– Mainly verapamil
• Slows ventricular rate in rapid atrial fibrillation
• Prevents recurrence of supraventricular tachycardia(SVT)
• No effect on ventricular arrhythmias
• Hypertension
– Mainly amlodipine or lercanidpine
Potassium Channel Activators
• Nicorandil
– combines activation of potassium K+ATP channels
with nitrovasodilator actions
• Causes hyperpolarisation of vascular smooth muscle
– both an arterial and venous dilator
– causes headaches, flushing and dizziness
– used for patients who remain symptomatic despite optimal management with other drugs
• Ivabradine
– Inhibits funny “f”-type channels in heart
– Reduces cardiac pacemaker activity • inhibits heart rate
• Ranolazine
– Unique anti-anginal used as a last resort
