Angina/ ACS Flashcards
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
