Angina Flashcards
What is angina?
Angina is a symptomatic reversible myocardial ischaemia.
It is chest pain or discomfort that is caused when heart muscle does not get enough blood
What is stable angina?
Stable Angina is a chronic coronary syndrome.
Additional information: It is characterized by predictable chest pain.
What are the features of stable angina?
- Constricting / heavy discomfort to the chest, jaw, neck, shoulders or arms. (Central crushing chest pain)
- Symptoms are brought on by exertion.
- Symptoms are relieved within 5 minutes by rest or GTN spray.
What is typical vs atypical angina vs non anginal pain?
Typical angina is when all 3 features are present.
Atypical angina is when only 2 features are present.
This is when 0-1 of the features are present.
What are other types of angina?
- Unstable angina
- Crescendo angina
- Prinzmetal’s angina
- (coronary spasm) - very rare
What are some precipitating factors of stable angina?
- Emotion
- Cold weather
- Heavy meals
Define angina
Angina refers to classic cardiac pain that is felt when there is a reduction in blood supply to the heart.
What is the aetiology of angina?
Atherosclerosis → Atheromas - due to the narrowed arteries
Exacerbating factors:
There is a mismatch of oxygen demand and supply.
- Exercise
- Emotional stress
So stable angina is induced by effort and is relieved by rest.
- Rarely anaemia
What are the predisposing factors of angina?
- Predisposing factors
- Age
- Cigarette smoking
- Family history
- Diabetes mellitus
- Hyperlipidemia
- Hypertension
- Kidney disease
- Obesity
- Physical inactivity
- Stress
- Male
What is the pathophysiology of angina?
- Fatty streak - foam cells (lipid laden macrophages)
- Intermediate lesion - vascular smooth muscle cells
- Fibro
- Your blood carries oxygen, which your heart muscle needs to survive.
- When your heart muscle isn’t getting enough oxygen, it causes a condition called ischemia.
- Ischaemia=reduction in blood flow
The most common cause of reduced blood flow to your heart muscle is coronary artery disease (CAD).
- Your coronary arteries can become narrowed by fatty deposits called plaques. This is called atherosclerosis.
How is ohms law affected?
Missed pathophysiology/aetiology detailed+ physics
What is the epidemiology of angina?
- Angina is a common presenting complaint, with over 500,000 new cases of angina occurring in the US every year.
- Common
- But more common in men.
- More common with increasing age
- Incidence:
- Importance of age and risk factors are absolutely key.
- Young women with no risk factors have very low chances.
What are the symptoms of angina?
Angina can be precipitated by exertion, heavy meals, cold weather and emotion. Symptoms are usually relieved within 5 minutes by rest or GTN.
- Cardiac-sounding chest pain
- Crushing (left sided) chest pain that radiates to left arms, shoulders, jaw and neck (Tightness and discomfort).
-
Dyspnoea
- Breathlessness
- No fluid retention
- Palpitations
- Syncope-faintness
- Nausea
- Sweating
What are the signs of angina?
- Chest pain comes on with exertion and rapidly resolved by rest and/or GTN
- Exacerbated by cold weather, anger and excitement
- Xanthomas or xanthelasma: suggests hypercholesterolaemia
-
Hypertension
- A risk factor for angina
- Retinopathy may be seen on fundoscopy
- Evidence of peripheral vascular disease: may coexist with ischaemic heart disease
- Levine - clenched fist over the chest
What can the investigations for angina be grouped into?
History
Primary
Non-anginal chest pain
Others to consider
Testing/diagnosis
Stress ECG (ischaemic inducing exercise stress test)
CXR - check heart size and pulmonary vessels
What history can be taken to diagnose angina?
- Personal details (demographics, identifiers)
- Presenting complain
- History of PC and risk factors
- Past medical history
- Drug History and allergies
- History - typical? Atypical?
- Examination
- Physical Examination (heart sounds, signs of heart failure, BMI)
What history can be taken to diagnose angina?
- Personal details (demographics, identifiers)
- Presenting complain
- History of PC and risk factors
- Past medical history
- Drug History and allergies
- History - typical? Atypical?
- Examination
- Physical Examination (heart sounds, signs of heart failure, BMI)
What are the primary investigations for angina?
- Investigation
-
First line:12-lead ECG (ST segment depression)
- 12 lead ECG
- Usually normal
- May show ST depression and T wave inversion
- 12 lead ECG
- CT angiography (gold standard)
- CT angiography
- Shows narrowing of a coronary artery
- Once narrowing is shown it is then possible to go in and open with a stent or balloon
- CT angiography
- Second line:functional imaging (stress echo, or cardiac MRI) is used if CT angiography is non-diagnostic
- Third line: transcatheter angiography
-
First line:12-lead ECG (ST segment depression)
What must you do to investigate non-anginal chest pain?
- If the patient has ischaemic changes on 12 lead ECG, then consider investigations as per typical and atypical angina
- If no changes are present on ECG, then no further cardiac investigations are required and non-cardiac causes should be considered
What other investigations can you consider?
- FBC:may reveal anaemia as an underlying cause of angina
- Fasting blood sugar and HbA1c: diabetes is associated with an increased risk of ischaemic heart disease
- Fasting lipid profile:hyperlipidaemia is associated with an increased risk of ischaemic heart disease
- Ambulatory blood pressure monitoring: if hypertension is suspected in clinic
- Thyroid function tests: check for hypo / hyper thyroid
- U&Es: prior to ACEi and other meds
- LFTs: prior to statins
What tests are required to diagnose angina?
- CT Coronary Angiogram - Good for spotted severe disease and ruling out disease. BUT DIFFICULT TO DISTINGUISH moderate LIKE 50 OT 70%
- Exercise testing - Good functional test - but relies on patients ability to walk on a treadmill
- Myoview scan
- Stress echo
- Perfusion MRI - gold standard non invasive
- ## Coronary angiogram - Gold standard
What can management of stable angina be grouped into?
Symptomatic relief
Anti anginal medication
Re-vascularisation Options
Prevention of cardiovascular events
Revascularisation
Treatment
- Address exacerbating factors
- Pharmacology: Lecture notes
What is symptomatic relief?
- GTN spray or tablet: vasodilator
- If pain persists for 5 minutes after the first dose, then repeat the dose.
- If after 5 minutes the pain still remains, then an ambulance should be called.
What are anti-anginal medication?
-
1st line: beta (β)-blocker OR non-dihydropyridine calcium channel blocker
- First-line treatment is with either of these agents. If the patient’s symptoms are not controlled on one, consider switching to the other or using both.
- Increase the dose of β-blocker and/or CCB to the maximum tolerated dose if there is apoor response(e.g. atenolol 100mg BD)
- 2-4 weeks after starting or changing medication, review for efficacy and side-effects
-
2nd line: dual therapy with dihydropyridine calcium channel blocker AND β-blocker
- Combining a non-dihydropyridine calcium channel blocker (such as verapamil)anda β-blocker poses a risk ofcomplete heart block. A dihydropyridine calcium channel blockershould, therefore, be used, e.g. nifedipine
- Remember to avoid a β-blocker in patients with severe asthma
-
3rd line: add additional anti-anginal medication e.g.
- Long-acting nitrates
- Ivabradine
- Nicorandil
- Ranolazine
- If the patientcan’t tolerate bothbeta-blockers and calcium channel blockers, consider monotherapy with one of the above drugs
- For people on beta blocker or calcium channel blocker monotherapy whose symptoms are not controlled andthe other option (calcium channel blocker or beta blocker) is not tolerated, consider one of the above drugs
- Consider adding a third anti-anginal drug only when the person’s symptoms arenot satisfactorily controlledwith two anti-anginal drugsandthe person is waiting for revascularisation or revascularisation is not considered appropriate
- Nitrates: note, the long-term use of nitrates is associated with tolerance and reduced efficacy. If tolerance occurs, the second dose of isosorbide mononitrate should be taken after 8 hours, instead of after 12 hours. Modified release isosorbide mononitrate isnotassociated with tolerance
What are re-vascularisation options?
-
Percutaneous coronary intervention (PCI):a**balloon is inflated in a stenosed vessel and a stent is placed to ensure the lumen remains open.
- Administer a combination of aspirin and clopidogrel for a minimum of 12 months to reduce the risk of thrombosis.
-
Coronary artery bypass graft (CABG): involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis.
- Associated with a better overall outcome, however,as it is an open procedure it is associated with greater perioperative risks.
What does prevention of cardiovascular event include in management?
- Lifestyle changes: exercise, dietary alterations, lipid, diabetes and hypertension management, smoking cessation
- Aspirin 75mg daily and astatin(e.g. atorvastatin 80mg daily)
- Angiotensin-converting enzyme inhibitors(ACEi): if the patient has angina and diabetes
What does re-vascularisation include?
- After patient has been treated for a number of months / years
- Coronary angioplasty PCI: Percutaneous coronary Intervention
- CABG- highly invasive procedures, Mammary artery from chest and leg vessel, have to be moderately fit to undergo this procedure
What is the treatment for stable angina?
- Reassure
- Changes in lifestyle factors
- Diet
- Excercise
- Smoking
- Weight
- Advice for emergency
What does addressing exacerbating factors include?
- Anaemia
- Tachycardia
- Thyrotoxicosis
What is the pharmacology of stable angina?
- GTN Spray
- Beta blocker - slow heart and reduce the force of contraction. REDUCES HEART RATE AND CONTRACTILITY WHICH REDUCES CARDIAC OUTPUT AND REDUCES OXYGEN DEMAND.
- Risks/ side effects
- Bradycardia
- Cold hands and feet
- Erectile dysfunction
- Tiredness, nightmares
- Never give to someone with severe asthma - can cause bronchoconstriction
- Bradycardic pATIENTS - slow resting heart rate
- Heart Block patients
- Long acting Nitrates: Venodilators - reduce preload by venodilitation? and dilating healthy coronary arteries
- Vasodilator so thumping headache - goes away after several days.
- Ca channel blockers - amlodipine
- Swollen ankles
- Postural hypertension
- Antiplatelet agent
- Dyspenisa
- Caution - gastric ulcers
- Statins - Inhibit endogenous production of ldl cholesterol In the liver by 30-40%
- Ace inhibitors - reduce vasoconstriction and sodium and water retention by the kidney. Useful for remodelling of the left ventricle after heart attack
- Cough
- Can cause renal impairment
- Aspirin
Dihydropyridine
What are the complications of stable angina?
- Cardiovascular complications - eg, unstable angina and myocardial infarction.
- Myocardial Infarction:a plaque may continue growing until the coronary artery is completely obstructed
- Chronic heart failure:the**underlying causes of ischaemic heart disease are also associated with an increased risk of chronic congestive heart failure
- Stroke:atherosclerosis may also develop within the cerebrovascular system
- Anxiety and depression.
- Reduced general health and quality of life.
What are non modifiable risk factors for stable angina?
- Demographic risk factor
- Increasing age
- Sex (male)
- Ethnicity
- Genetics (family history of coronary heart disease )
What are the modifiable risk factors for stable angina?
- Lifestyle risk factors
- Smoking
- Diet
- Physical activity
- Sedentary lifestyle
- Stress
- Drug use (cocaine)
- Clinical risk factors
- Hypertension
- Lipids
- Diabetes
- Obesity
- Hypercholesterolaemia
- Environmental risk factors
- Air pollution
- Chemicals
What are the 4 psychosocial risk factors grouped into?
- Coronary prone behaviour pattern
- Depression and anxiety and CHD
- Psychocial work characteristics
- Social support
What is Coronary prone behaviour pattern?
- Type A pattern behaviour is not a personality trait (fixed trait or disposition). It is a modifiable behaviour pattern.
- Extreme competitiveness, striving for achievement, hostileness and a sense of urgency
- Identified by cardiologist Friedman and Rosenman (1959)
- Feelings of anger
- Annoyance and resentment
- Verbal or physical aggression
What is Coronary prone behaviour pattern?
- Type A pattern behaviour is not a personality trait (fixed trait or disposition). It is a modifiable behaviour pattern.
- Extreme competitiveness, striving for achievement, hostileness and a sense of urgency
- Identified by cardiologist Friedman and Rosenman (1959)
- Feelings of anger
- Annoyance and resentment
- Verbal or physical aggression
What are Psychocial work characteristics?
- High demand low control jobs - significant association to MI
- These types of jobs are also associate with lower employment grades. They are also low reward and less secure which are additional sources of psychological stress.
- Longer working hours
What is meant by social support as a psychosocial risk factor?
- Both quantity and quality of social relationships
- Loneliness
What is a differential diagnosis of stable angina?
- Pericarditis/Myocarditis
- Myocardial ischaemia
- Pulmonary Embolism
- Chest infection
- GORD
- Dissection of the aorta
- Anxiety
- Anaemia
What is the prognosis of stable angina?
- If lifestyle changes are made and the patient remains compliant with medication, 58% of patients are expected to be free of symptoms.
- However, poor lifestyle and poor anti-anginal compliance can predispose a stable atheromatous plaque to become unstable, increasing the risk of myocardial infarction
What are the different types of angina like?
- Stable angina: brought on by exertion, relieved by rest
- Unstable angina: occurs on minimal exertion or at rest, with increasing frequency and severity (acute coronary syndrome)Usually caused by rupture of atherosclerotic plaque with thrombosis (blood clot forms on top of plaque).There is even less room left for blood to flow by, and the heart tissue is starved for oxygen even during rest.Unstable angina involves subendocardial ischaemia and should be treated as an emergency as patients are at a high risk of progressing to myocardial infarction.ECG = ST segment depression
- Decubitus angina: induced by lying flat
- Prinzmetal angina: coronary artery spasm; typically brief chest pain at rest (non-exertional) and seen in younger patients. There is transient ST-elevation which self-resolves and normal serial troponins.Ischaemia and resulting chest pain is due to coronary artery vasospasms (smooth muscles around the arteries constrict tightly and reduce blood flow).The underlying mechanism causing vasospasms isn’t well understood, but likely involves vasoconstrictors e.g. platelet thromboxane A2.In this case the coronary artery’s constrict so severely that all layers of the heart wall being supplied are affected - transmural ischaemia.Episodes of vasospastic angina don’t correlate with exertion and can happen anytime, including at rest.ECG = transient ST segment elevation
- Nocturnal angina: occurs at night and may wake patient up
What is acute coronary syndrome?
Acute coronary syndrome (ACS) encompasses unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI).
An acute coronary syndrome typically manifests as sudden, new-onset angina, or an increase in the severity of an existing stable angina.
What is the epidemiology of acute coronary syndrome?
- STEMI = 5/1000 per annum in UK
- M>F
What are the non-modifiable risk factors of acute coronary syndrome?
- Non-modifiable risk factors:
- Age (>65 years of age)
- Male
- Family history of premature coronary heart disease
- Premature menopause
What is the pathophysiology of acute coronary syndrome?
In general, the process underlying all three conditions is atherosclerotic plaque formation.
- Thefirst stageof atherosclerotic plaque formation involves the accumulation of low-density lipoprotein cholesterol in the inner layer of the blood vessel
- Leukocytes adhere to the endotheliumand gain entry into theintima, where they combine with the lipids to becomefoam cells
- Artery remodellingandcalcification, alongside the presence offoam cells, causes atherosclerotic plaques to form
- Rupture of a plaquecauses platelet activation, thrombus formation and coronary artery occlusion. (The thrombus is mainly made up of platelets)
- This results in ischaemia and infarction
In unstable angina and NSTEMI, the occlusion is partial. In STEMI, the occlusion is complete.
In the case of a STEMI, ischaemia is initially just subendocardial, but eventually becomes transmural.
What are the signs of Acute coronary syndrome?
- Hypotension or hypertension
- Reduced 4th heart sound
- Signs of heart failure: e.g. increased JVP, oedema; **red flag symptom
- Systolic murmur: if mitral regurgitation or a ventricular septal defect develops
-
Chest pain
- Central, ‘heavy’, crushing pain
- Radiation to the left arm or neck
- Symptoms should continue at rest for more than 20 minutes
- Certain patients e.g. diabetics or elderly, have atypical presentation and may not have chest pain (‘silent MI’)
- May sometimes feel like indigestion
- Shortness of breath
- Sweating and clamminess
- Nausea and vomiting
- Palpitations
- Anxiety: often described as a ‘sense of impending doom’
-
Chest pain
What are the symptoms of acute coronary syndrome?
-
Chest pain
- Central, ‘heavy’, crushing pain
- Radiation to the left arm or neck
- Symptoms should continue at rest for more than 20 minutes
- Certain patients e.g. diabetics or elderly, have atypical presentation and may not have chest pain (‘silent MI’)
- May sometimes feel like indigestion
- Shortness of breath
- Sweating and clamminess
- Nausea and vomiting
- Palpitations
- Anxiety: often described as a ‘sense of impending doom’
What are the primary investigations for acute coronary syndrome?
ECG:perform within 10 minutes. Aim to perform serial ECGs every 10 minutes to detect dynamic changes.
- ## Troponin:for a STEMI and NSTEMI, troponin levels will begin to elevate 4-6 hours after injury and will remain elevated for roughly 10 days. In unstable angina, there isnoelevation in troponin.
What are the ECG findings for acute coronary syndromes?
-
ECG findings
- Unstable angina: non-specific changes
- NSTEMI: ST-segment depression; T-wave inversion; pathological Q waves; a normal ECG may be seen
- STEMI: ST-segment elevation; T-wave inversion; new left-bundle branch block
Which ECG changes correlate with which coronary artery?
What other investigations can be considered for acute coronary syndrome?
- Perform other tests that you would for stable angina e.g.
- Physical Examination (heart sounds, signs of heart failure, BMI)
- Lipid profile
- Thyroid function tests: check for hypo / hyper thyroid
- HbA1C and fasting glucose: check for diabetes
- Coronary angiogram:aim to carry out angiography within 90 minutes if required; diagnostic investigation of choice
- FBC:Hb and haematocrit may reveal a secondary cause in type 2 MI e.g. anaemia
- U&Es:electrolyte imbalances may predispose the patient to cardiac arrhythmias; also done prior to ACEi and other meds
- LFTs: done prior to statins
- Other biomarkers: less commonly used biomarkers of cardiomyocyte injury include creatine kinase-MB (increases at 3-6 hours), andmyoglobin (earliest to rise, usually within 2 hours)
- CXR:to exclude other potential causes, if needed
- Echocardiogram after the event to assess the functional damage
What other investigations can be considered for acute coronary syndrome?
- Perform other tests that you would for stable angina e.g.
- Physical Examination (heart sounds, signs of heart failure, BMI)
- Lipid profile
- Thyroid function tests: check for hypo / hyper thyroid
- HbA1C and fasting glucose: check for diabetes
- Coronary angiogram:aim to carry out angiography within 90 minutes if required; diagnostic investigation of choice
- FBC:Hb and haematocrit may reveal a secondary cause in type 2 MI e.g. anaemia
- U&Es:electrolyte imbalances may predispose the patient to cardiac arrhythmias; also done prior to ACEi and other meds
- LFTs: done prior to statins
- Other biomarkers: less commonly used biomarkers of cardiomyocyte injury include creatine kinase-MB (increases at 3-6 hours), andmyoglobin (earliest to rise, usually within 2 hours)
- CXR:to exclude other potential causes, if needed
- Echocardiogram after the event to assess the functional damage
What is the immediate management for unstable angina and NSTEMI?
- Oxygen:only if SpO2is <94%, and aim for 94-98%
- Analgesia:morphine and sublingual glyceryl trinitrate
-
Dual antiplatelets:
- Aspirin
- The choice of the second antiplatelet agent depends on if the person is having PCI or not, and will vary based on local guidance:
- Prasugrel or ticagrelor or clopidogrelif undergoing PCI
- Ticagrelor or clopidogrelif not undergoing PCI
-
Anticoagulation:
- Fondaparinux:offer to all patientsunlessundergoing immediate coronary angiography
- Unfractionated heparin:an alternative to fondaparinux if the patient has renal failure
- Beta blockers: e.g. atenolol or metoprolol, unless contraindicated
- Remember ‘MONA’: Morphine,Oxygen,Nitrates,Aspirin
What is the immediate management for unstable angina and NSTEMI?
- Oxygen:only if SpO2is <94%, and aim for 94-98%
- Analgesia:morphine and sublingual glyceryl trinitrate
-
Dual antiplatelets:
- Aspirin
- The choice of the second antiplatelet agent depends on if the person is having PCI or not, and will vary based on local guidance:
- Prasugrel or ticagrelor or clopidogrelif undergoing PCI
- Ticagrelor or clopidogrelif not undergoing PCI
-
Anticoagulation:
- Fondaparinux:offer to all patientsunlessundergoing immediate coronary angiography
- Unfractionated heparin:an alternative to fondaparinux if the patient has renal failure
- Beta blockers: e.g. atenolol or metoprolol, unless contraindicated
- Remember ‘MONA’: Morphine,Oxygen,Nitrates,Aspirin
