Angina/ ACS Flashcards
(20 cards)
What is stable angina?
- pathogenesis
Transient myocardial ischaemia - imbalance between myocardial oxygen supply and demand
- Effort-related chest pain
Pathogenesis
• Most common = atherosclerosis (Coronary artery disease)
• Aortic valve disease
• Hypertrophic cardiomyopathy
• Vasculitits/aortitis of coronary arteries
• Coronary artery spasm
o Prinzmetal’s angina – if accompanied by transient ST elevation
Syndrome X o Typical angina on effort, objective evidence of myocardial ischaemia on stress testing, normal coronary arteries on angiography o Mostly women o Mechanism of symptoms unclear o Good prognosis
What makes angina worse?
- Physical exertion
- Cold exposure
- Heavy meals
- Intense emotion
- Rarer – vivid dreams (nocturnal angina), lying flat (decubitus angina)
What are the features of angina?
- what might you find in examination?
Central chest pain, breathlessness brought on by exertion/ other forms of stress & promptly relieved by rest
Note duration - recent-onset greater risk than long-standing/unchanged
Warm-up angina – discomfort starts when start walking; later may not return despite greater effort
Exam - Often unremarkable
LOOK for:
- Valve disease (esp. aortic)
- RFs – hypertension, diabetes, hyperlipidaemia
- Left ventricular dysfunction – cardiomegaly, gallop rhythm, dyskinetic apex beat
- Other manifestations of arterial disease – carotid bruits, peripheral arterial disease
- Unrelated conditions that may exacerbate– anaemia, thyrotoxicosis
What investigation should be done if also have murmur?
ECHO
Angina treatment
- what lifestyle advice should you give?
- when would you need to give anti platelet treatment?
- what is the treatment ladder?
- what drugs increase life expectancy?
Advice
- Weight
- Regular exercise (up to but not beyond point of discomfort → beneficial & may promote collateral vessels)
- Avoid severe unaccustomed exertion and vigorous exercise after a heavy meal or in very cold weather
- Take sublingual nitrate before exertion that may induce angina
All w/ angina secondary to CAD → receive antiplatelet therapy
- Low dose (75mg) aspirin – ALL & continued indefinitely since reduces risk of MI
- SE: dyspepsia
Clopidogrel = alternative
Start sublingual GTN and a B-blocker
- Add Ca channel antagonist or long-acting nitrate if needed
If drugs fail – revascularisation should be considered
- No evidence that these drugs will increase life expectancy
Drugs that make patient live longer – statins, anti-platelets drugs (aspirin - reduce risk of MI)
Angina nitrate treatment
- how do they work?
- when should GTN spray be used? SE of GTN spray?
Act directly on vascular smooth muscle → venous & arteriolar dilatation
- Coronary dilatation → Increase myocardial oxygen supply
- Lower preload & afterload → reduced myocardial oxygen demand
Sublingual GTN
- Aerosol – 400 ug per spray; Tablet – 300 or 500 ug
- Indication: acute attack
- Relieve in 2-3 minutes
- Use prophylactically before exercise likely to provoke symptoms
Short duration of action
- SE: headache, symptomatic hypotension, rare – syncope
Prolonged therapeutic effect → GTN transcutanously
- GTN transcutanously: Patch – 5-10mg daily
- Slow-release buccal tablet (1-5mg 4 times daily)
- Isosorbide dinitrate (10-20mg 3 times daily) or isosorbide mononitrate (20-60mg 1 or 2 daily) – given by mouth (unlike GTN which undergoes extensive metabolism by liver)
- Continuous nitrate therapy can cause tolerance
Avoid by having 6-8 hour nitrate-free period (usually at night - inactive)
Nocturnal angina – give long-acting nitrates at end of day
Beta blockers
- mechanism of action
- when should they be avoided
- can they be stopped abruptly?
- Side effects
- Lower myocardial oxygen demand by HR, BP and myocardial contractility
- Dampen effect of sympathetic nervous system
BUT may provoke bronchospasm in patients with asthma
Non-selective β-blockers may aggravate coronary vasospasm by blocking coronary artery β2- adrenoceptors → 1-daily cardioselective preparation used (e.g. slow-release metoprolol, bisoprolol)
Do not withdraw abruptly → rebound effects may precipitate dangerous arrhythmias, worsening angina or MI “β-blocker withdrawal syndrome”
SE: tired, dizziness, men – impotent, may drop BP
Ca channel antagonists
- mechanism of action
- when should they be avoided
- Side effects
- Inhibit slow inward current caused by entry of extracellular Ca through cell membrane of excitable cells, particularly cardiac & arteriolar smooth muscle
- reduced myocardial oxygen demand by reducing BP and reducing myocardial contractility.
Dihydropyridine calcium antagonists
- Nifedipine, nicardipine
- May cause a reflex tachycardia – so use in combination with β-blocker.
Verapamil, diltiazem
- Can use as monotherapy - useful when β-blockers contra-indicated
- reduce SA node firing, inhibit conduction through AV node → tend to cause bradycardia.
SE: o May aggravate or precipitate heart failure – so use with care in patients with poor LV function o Peripheral oedema o Flushing o Headache o Dizziness
Potassium channel activators
- Nicorandil (10–30 mg twice daily orally)
- Arterial & venous vasodilator
- Do not exhibit tolerance seen with nitrates.
I(f) channel antagonist
• Ivabradine
• Induces bradycardia by modulating ion channels in sinus node
• In contrast to β-blockers and rate-limiting calcium antagonists, it does not have other cardiovascular effects (does not inhibit myocardial contractility)
• Safe to use in patients with heart failure.
Ranolazine
• Inhibits late inward Na current in coronary artery smooth muscle cells
• Secondary effect on Ca flux and vascular tone, reducing angina symptoms
Percutanous coronary intervention
- what is it?
- does it improve survival or just symptomatic treatment?
- complications
- Passing fine guidewire across coronary stenosis under radiographic control and using it to position a balloon, which is then inflated to dilate stenosis
- Coronary stent = coated metallic ‘scaffolding’ that can be deployed on a balloon and used to maximise & maintain dilatation of a stenosed vessel. - Reduce acute complications & incidence of re-stenosis
Symptomatic treatment but no evidence improves survival in chronic stable angina.
- Mainly used in single- or two-vessel disease.
- Stenoses in bypass grafts and native coronary arteries can be dilated
- Often used to provide palliative therapy for patients with recurrent angina after CABG.
- Three-vessel or left main stem disease - usually do coronary
Complications
- Occlusion of target vessel or side branch by thrombus or loose flap of intima (coronary artery dissection) → consequent myocardial damage.
- 2–5%
- Usually can be corrected w/ stent; emergency CABG sometimes
- Minor myocardial damage (troponins) 10%
Long term complication = re-stenosis
- 33%
- Due to elastic recoil & smooth muscle proliferation (neo-intimal hyperplasia)
- Tends to occur within 3 months.
- Stenting reduces risk of re-stenosis (as more complete dilatation is achieved)
- Drug-eluting stents reduced risk even further by allowing antiproliferative drug (sirolimus or paclitaxel) to elute slowly from coating and prevent neo-intimal hyperplasia and in-stent re-stenosis. - increased risk of late stent thrombosis with drug-eluting stents. Absolute risk is small (< 0.5%).
Recurrent angina (affecting up to 15–20% of patients receiving an intracoronary stent at 6 months) may require further PCI or bypass grafting.
Risk of complications & likely success of procedure - related to morphology of the stenoses, experience of operator and presence of comorbidity, e.g. diabetes, PAD.
- Poor prognosis – Complex target lesion, long, eccentric or calcified, lies on a bend or within a tortuous vessel, involves a branch or contains acute thrombus.
Adjunctive therapy –potent platelet inhibitors – clopidogrel or glycoprotein IIb/IIIa receptor antagonists – with aspirin, heparin, improves outcome, with lower short- and long-term rates of death and MI.
Coronary artery bypass grafting
- what arteries/veins may be used?
- what increases the risk?
- what is the operative mortality?
- what could be causing early post-operative angina?
- what could be causing late recurrence?
Use: internal mammary arteries, radial arteries or reversed segments of saphenous vein
Usually major surgery under cardio-pulmonary bypass BUT some cases, grafts can be applied to the beating heart: ‘off-pump’ surgery.
Operative mortality = 1.5%
- increased risk - elderly, poor LV function, comorbidity – renal failure
<60% asymptomatic after 5 or more years
Early postoperative angina
- Graft failure - technical problems during operation
- Poor ‘run-off’ due to disease in distal native coronary vessels.
Late recurrence - progressive disease in native coronary arteries or graft degeneration.
Aspirin (75–150 mg) and clopidogrel (75 mg) improve graft patency, indefinitely.
Lipid-lowering therapy reduce progression in native coronary arteries & bypass grafts & reduces cardiovascular events.
Increased cardio morbidity/mortality if continue to smoke.
- 2x likely to die in 10 years post surgery
Increased survival in symptomatic patients with left main stem stenosis or 3-vessel coronary disease (i.e. involving LAD, CX and right coronary arteries) or 2-vessel disease involving proximal LAD coronary artery.
-Especially - left ventricular function or positive stress testing prior to surgery and in those who have undergone left internal mammary artery grafting.
Neurological complications common
- 1–5% risk of peri-operative stroke.
- 30% - 80% short-term cognitive impairment - resolves within 6 months.
- Long-term cognitive decline - >30% of patients at 5 years.
Acute coronary syndrome
- clinical features
- physical signs
Clinical features
Main one = Pain
- Same site as angina but usually more severe and lasts longer
- Tightness, heaviness or constriction in chest
- Radiation: throat, arms, epigastrium or back
Breathlessness
Vomiting
- Vomiting & sinus bradycardia often due to vagal stimulation – common in patients with inferior MI
- May be aggravated by opiates given for pain relief
Collapse
- Syncope – usually due to arrhythmia or profound hypotension
Anxiety and fear of impending death
Sudden death
- Due to ventricular fibrillation or aystole may occur immediately and often within first hour
Physical signs
- Signs of sympathetic activation: pallor, sweating, tachycardia
- Signs of vagal activation: vomiting, bradycardia
Signs of impaired myocardial function
- Hypotension, Oliguria, Cold peripheries
- Narrow pulse pressure
- Raised JVP
- Third heart sound
- Quiet first heart sound
- Diffuse apical impulse
- Lung crepitations
Signs of tissue damage: fever
Signs of complications: e.g. mitral regurgitation, pericarditis
What is the classification of NSTEMI/STEMI
Type 1: spontaneous MI
Type 2: increase in oxygen supply or decrease in supply (i.e. anaemia, hypotension/spasm)
Type 3: unexpected cardiac death before biomarkers obtained
Type 4a: PCI MI
Type 4b: Stent thrombosis MI
Type 5: CABG MI
What investigations should you do in a suspected MI?
ECG→ non-specific ST/T-wave changes
- ST elevations, pathological Q-waves over following days → STEMI
- ST depression, T-wav inversion→ NSTEMI
Trial of GTN→ ongoing pain
Cardiac troponin→ increased after 4-6hrs of onset, negative biomarkers should be remeasured within 6hrs of onset
FBC→ anaemia, thrombocytopaenia
Urea and creatinine→ adjust renally cleared drugs
Electrolytes
Liver function
Glucose
CXR→ may show pulmonary oedema Pneumonia, oesophageal rupture, aortic dissection (widened mediastinum) and pneumothorax can mimic cardiac ischaemia
What is the management of acute MI?
Morphine 10mg in 10ml with metoclopramide 10mg IV
Oxygen
Nitrates
Aspirin (300mg) with ticagrelor (for high risk 90mg)/ clopidogrel (300-600mg) then 75mg maintenance for at least 12 weeks
- Fondaparinux better in renal problems, LMWH if contraindicated
Beta-blocker: metoprolol, if ci: diltiazem, verapamil
ACEi indicated in LV dysfunction, hypertension, diabetes
Atorvastatin 80mg
GRACE scoring for possible PCI
- Low→ non invasive testing
- Moderate→ angiography within 24h
- High risk→ immediate angiography and PCI
Driving: can resume after 1 week after successful angioplasty or 4 weeks after ACS without angioplasty
STEMI management
Thrombolysis PCI Fondaparinux+ aspirin and clopidogrel/ticagrelor MONA Beta-blocker Statin
Three features of ischaemic heart disease (angina)
Constricting/ heavy discomfort to the chest, jaw, neck, shoulders or arms
Brought on by exertion
Relieved within 5 minutes rest or GTN
3= typical angina, 2= atypical angina, 1= not angina
Investigations in ichaemic heart disease
Resting ECG
FBC - anaemia
Fasting lipid (elevated)
Fasting BM (elevated)
Ischaemic heart disease management
75mg aspirin daily
Anti-anginal medication
- Bisoprolol 5-10mg
- Amlodipine 5mg OD
- Nitrates
- Ivabradine 5mg, reduces HR with minimal impact on BP
- s/e: ulceration of skin, mucosa, eye, GI tract
- Ranolazine 375mg BD, blocks late sodium current thus improving ventricular diastolic tension and oxygen consumption
- ci: HF, elderly, overweight, prolonged QT
Nicorandil 5-10mg, potassium channel activator
- Ci: pulmonary oedema, severe hypotension, hypovolaemia, LV failure
