Angina Flashcards
other names for Stable coronary artery disease
Angina pectoris
Silent ischemia
Risk factors for angina
Hypertension Smoking Hyperlipidemia Hyperglycaemia Male Post menopausal females
Stable coronary artery disease
A result of a mismatch between myocardial blood/oxygen supply and demand
Attacks of angina when stressed/increased demand, anything that increases HR, SV or BP
Determinants of demand
HR
Systolic BP
Myocardial wall stress
Myocardial contractility
Determinants of supply
Coronary artery diameter and tone
Collateral blood flow
Perfusion pressure
Heart rate (duration of diastole)
Types of atherosclerotic lesions
1- adaptive thickening of smooth muscle at lesion prone location
2- macrophage foam cells
3- small pools of extracellular lipid
4- core of extracellular lipid
5- fibrous thickening
6- complicated lesion eg thrombus, fissure and haemotoma
Purpose of drug treatment
Relieve symptoms Halt disease process Regression of disease process Prevent MI Prevent death
Beta blockers
Bisoprolol and atenolol
Reversible antagonists on B1 and (B2) receptors which block sympathetic system
Decrease HR, contractility, systolic wall tension, BP, velocity of contraction
Allow improved perfusion of subendocardium by increasing diastolic perfusion time which protects cardiomyocytes from O2 free radicals during ischaemic episodes
Increase exercise threshold that angina occurs at (demand outstrips supply)
Negative parts of beta blockers
Rebound phenomena- don’t stop suddenly
Contraindications- asthma, PVD, reynauds, HF if dependant on sympathetic drive, bradycardia
Adverse drug reactions- tiredness/fatigue, lethargy, bradycardia, bronchospasm
Drug-drug interactions- don’t use with other hypotensives too much or rate limiting drugs or negatively ionotropic agents, mask hypoglycemia
Calcium channel blockers
Diltiazem, verapimil, amlodipine
Prevent calcium influx into myocytes and smooth muscle around arteries by blocking l-type channels
Rate limiting CCBs
Diltiazem, verapimil
Reduce heart rate and force of contraction (reduce myocardial oxygen requirements)
Vasodilating CCBs
Amlodipine, can cause reflex tachycardia
Contraindications for CCBs
Never use nifedipine immediate release as can cause MI or stroke
Do not use post MI as can increase morbidity and mortality in patients with impaired LV function
Do not use for unstable angina as dihydropyridines (vasodilators) may increase infarction rate and death
Adverse drug reactions for CCBs
Ankle oedema that doesn’t respond to diuretics
Headache
Flushing
Palpitations
Nitrovasodilators
GTN(sublingual) to avoid fpm and also prophylaxis
Isosorbide mono and dinitrate (sustained release) prophylaxis
Relax almost all smooth muscle cells by releasing NO which stimulates release of cGMP
Reduces preload and afterload so reduce myocardial oxygen consumption, relieved coronary vasospasm and redistributes myocardial blood flow to ischemic areas
When are IV nitrates used
Unstable angina, with heparin
Negative parts of nitrates
Tolerance can develop unless asymmetric doses used or incorporating a nitrate free period
Adverse drug reactions- headache so increase dose slowly, hypotension (GTN syncope)
New approaches to myocardial ischemia
Metabolic modulation by trimetazidine
Sinus node inhibition by ivabradine
Late Na current inhibition by ranolazine
Preconditioning by nicorandil
Nicorandil
Activates ATP sensitive potassium channels which inhibits calcium reflux and helps ischemic preconditioning (cardioprotective)
Ivabradine
Selective sinus node If channel inhibitor, slows the diastolic depolarisation so decreases HR and myocardial O2 demand
Reduces fatal and non fatal MI in HR>70
Reduces primary end point in angina patients
Ranolazine
anti angina
Inhibits persistent or late inward sodium current in vg channels. This leads to reduction in intracellular calcium levels which reduces tension in heart wall
Decreases oxygen requirements
Aspirin
Antiplatelet
Low dose uses 75-150mg
Inhibits thromboxane production which stimulates platelet aggregation and vasoconstriction
Only works >70bpm
Used in adults who can’t use BB or in combo
Reduces acute MI and unstable angina risks and as secondary prevention
Most common cause of GI bleed admission
Clopidogrel
Inhibits ADP receptor activated platelet aggregation and prevents atherosclerotic events in PVD
Lower GI bleeding
Cholesterol lowering agents
SimvaSTATIN, pravaSTATIN, atorvaSTATIN
HMG CoA reductase inhibitors, reduces mortality
Treatment regimen
Beta blockers first
Then CCBs
Then something else eg aspirin, ivabradine, statin
All patients with stable angina due to atherosclerotic disease should have long term aspirin and statin
Secondary prevention drugs
Aspirin 75mg daily
Ace inhibitors if diabetes
Statin
Treat high BP
Possible causes of stable angina
By far most commonly due to a reduction in coronary blood flow to the myocardium, caused by:
Obstructive coronary atheroma (Very common)
Coronary artery spasm (Uncommon);
Coronary inflammation/arteritis (Very rare)
Uncommonly due to reduced O2 transport:
Anaemia of any cause
Uncommonly due to pathologically increased myocardial O2 demand:
Left ventricular hypertrophy (LVH); as seen in significant persistent hypertension, significant aortic stenosis and hypertrophic cardiomyopathy.
Thyrotoxicosis
history for stable angina
Essential to establish the characteristics of patients pain to differentiate from other causes of chest pain:
Site of pain (watch for patient gestures): retrosternal
Character of pain: often tight band/pressure/heaviness.
Radiation sites: neck and/or into jaw, down arms.
Aggravating e.g. with exertion, emotional stress
& relieving factors e.g. rapid improvement with GTN or physical rest.
Very occasionally myocardial ischaemia occurs with no chest pain but other symptoms on exertion:
Breathlessness on exertion
Excessive fatigue on exertion for activity undertaken
Near syncope on exertion.
More often in the elderly or those with diabetes mellitus: probably due to reduced pain sensation.
Features making angina less likely
Sharp/‘stabbing’ pain; pleuritic or pericardial.
Associated with body movements or respiration.
Very localised; pinpoint site.
Superficial with/or without tenderness.
No pattern to pain, particularly if often occuring at rest.
Begins some time after exercise.
Lasting for hours.
Differential diagnoses for chest pain, these will usually have characteristics different to angina:
Cardiovascular causes:
Aortic dissection (intra-scapular “tearing”), pericarditis
Respiratory:
Pneumonia, pleurisy, peripheral pulmonary emboli (pleuritic)
Musculoskeletal:
Cervical disease, costochondritis, muscle spasm or strain
GI causes:
Gastro-oesphageal reflux, oesophageal spasm, peptic ulceration, biliary colic, cholecystitis, pancreatitis
Canadian classification of angina severity (CCS)
I Ordinary physical activity does not cause angina, symptoms only on significant exertion.
II Slight limitation of ordinary activity, symptoms on walking 2 blocks or > 1 flight of stairs.
III Marked limitation, symptoms on walking only 1-2 blocks or 1 flight of stairs.
IV Symptoms on any activity, getting washed/dressed causes symptoms.
Risks factors for coronary artery disease
Non-modifiable
Age, gender, creed, family history & genetic factors.
Modifiable
Smoking
Lifestyle- exercise & diet
Diabetes mellitus (glycaemic control reduces CV risk)
Hypertension (BP control reduces CV risk)
Hyperlipidaemia (lowering reduces CV risk)
Making the diagnosis of stable angina: Examination
Tar stains on fingers
Obesity (centripedal)
Xanthalasma and corneal arcus (hypercholesterolaemia)
Hypertension,
Abdominal aortic aneurysm arterial bruits, absent or reduced peripheral pulses.
Diabetic retinopathy, hypertensive retinopathy on fundoscopy.
Signs of exacerbating or associated conditions:
Pallor of anaemia
Tachycardia, tremor, hyper-reflexia of hyperthyroidism
Ejection systolic murmur, plateau pulse of aortic stenosis
Pansystolic murmur of mitral regurgitation, and
Signs of heart failure such as basal crackles, elevated JVP, peripheral oedema.
Making the diagnosis of stable angina: Investigations
Bloods CXR ECG ETT Myocardial perfusion imaging Computed tomography (CT) coronary angiography CT coronary angiography Invasive angiography Cardiac catheterisation/coronary angiography
Bloods for stable angina
Full blood count, lipid profile and fasting glucose; Electrolytes, liver & thyroid tests would be routine.
CXR for stable angina
Often helps show other causes of chest pain and can help show pulmonary oedema.
Electrocardiogram for stable angina
normal in over 50% of cases
may be evidence of prior myocardial infarction i.e. pathological Q-waves.
may be evidence of left ventricular hypertrophy i.e. high voltages, lateral ST-segment depression or “strain pattern”.
ETT for stable angina (exercise tolerance test)
Often can confirm diagnosis of angina.
Relies on ability to walk for long enough to produced sufficient CV stress.
Typical symptoms and ST-segment depression for positive test.
-ve ETT doesn’t exclude significant coronary atheroma but if negative at high workload overall prognosis is good.
Myocardial perfusion imaging for stable angina
Superior to ETT in detection of CAD, localisation of ischaemia and assessing size of area affected.
Expensive, involves radioactivity; depending on availability used where ETT not possible/equivocal.
Either exercise or pharmacological stress: adenosine, dipyridamole or dobutamine .
Radionuclide tracer injected (iv) at peak stress on one occasion, images obtained; and at rest on another.
Comparison between stress and rest images.
Normal myocardium takes up tracer.
Tracer seen at rest but not after stress = ischaemia
Tracer seen neither rest, or after stress = infarction
when to do invasive angiography for stable angina
Early or strongly positive ETT (suggests multi-vessel ds).
Angina refractory to medical therapy.
Diagnosis not clear after non-invasive tests.
Young cardiac patients due to work/life effects.
Occupation or lifestyle with risk e.g. drivers etc.
Cardiac catheterisation/coronary angiography for stable angina
Definition of coronary anatomy with sites, distribution and nature of atheromatous disease enables decision over what treatment options are possible.
Whether medication alone or percutaneous coronary intervention (PCI)- most often angioplasty and stenting or coronary artery bypass graft (CABG) surgery.
Almost always done under local anaesthetic
Arterial cannula inserted into femoral or radial artery.
Coronary catheters passed to aortic root and introduced into the ostium of coronary arteries.
Radio-opaque contrast injected down coronary arteries and visualised on X-ray.
Invasive coronary angiography is 2-D “lumenogram” as iodinated contrast or “dye” is passed through the arteries
treatment strategies for stable angina
General measures
Address risk factors: BP, DM, Cholesterol, Lifestyle
Medical treatment
Drugs to reduce disease progression & symptoms
Revascularisation (if symptoms not controlled)
Percutaneous coronary intervention (PCI) & coronary artery bypass grafting (CABG)
medication for angina disease progression
Statins: consider if total cholesterol >3.5 mmol/l.
Reduce LDL-cholesterol deposition in atheroma and also stabilise atheroma reducing plaque rupture and ACS.
ACE inhibitors: if increased CV risk and atheroma
Stabilise endothelium and also reduce plaque rupture.
Aspirin; 75mg or clopidogrel if intolerant of aspirin.
May not directly affect plaque but does protect endothelium and reduces of platelet activation/aggregation
medication for angina symptoms
ß-blockers; achieve resting hr <60 bpm.
Reduced myocardial work and have anti-arrhythmic effects
Ca2+ channel blockers; achieve resting hr <60 bpm.
Central acting eg diltiazem/verapamil if ß-blockers C-I
Ik channel blockers; achieve resting hr <60 bpm.
Ivabridine is a new medication which reduces sinus node rate
Ca2+ channel blockers; produce vasodilatation
Peripherally acting dihydropyridines eg amlodipine, felodipine
Nitrates; produce vasodilatation
Used as short or prolonged acting tablets, patches or as rapidly acting sublingual GTN spray for immediate use.
K+ channel blockers; nicorandil
Nitrate molecule and K+ channel helpful in ‘pre-conditioning
Percutaneous coronary intervention (PCI)
Percutaneous transluminal coronary angioplasty (PTCA) and stenting (now in ~95% procedures)
Similar beginnings to coronary angiography but cross stenotic lesion with guidewire and squash atheromatous plaque into walls with balloon and stent.
If stent used aspirin and clopidogrel taken together whilst endothelium covers the stent struts and it is no longer seen as a foreign body with associated risk of thrombosis.
PCI effective for symptoms, but
No evidence it improves prognosis in stable disease.
Small risk of procedural complication: death=0.1%, MI=0.2%, emergency CABG=0.05%
Risk of restenosis: varying from 10-15% with bare metal stents and <10% with drug eluting stents.
Also still need to continue disease modifying medication.
Coronary artery bypass surgery (CABG)
In diffuse multi-vessel CABG often best option for stable angina
‘Up front’ risks are significantly > PCI
death=1.3%, Q-wave MI=3.9%; these increase in presence of co-morbidity
But good lasting benefit- 80% symptom free 5 years later.
CABG may confer prognostic benefit in certain subgroups:
>70% stenosis of left main stem artery
significant proximal three-vessel coronary artery disease
two vessel coronary artery disease that includes significant stenosis of proximal left anterior descending coronary artery and who have ejection fraction < 50%.
Patients must continue disease modifying medication and predictable deterioration in vein grafts after 10 years.
