Acute Coronary Syndromes & Stable Angina Flashcards
what is hs-TnI
high sensitivity Troponin I released from cardiac myocytes due to necrosis
what is troponin
a protein in myocardium and skeletal muscle
- TnI levels begin to rise 3-4 hours after myocardial damage and stay elevated for up to 2 weeks
also measure CK in STEMI patients
what the parameters for TnI levels in men and women suggesting myocardial necrosis
males: hs-TnI levels greater than 34 ng/L for men suggests a high likelihood of myocardial necrosis
females: hs-TnI levels greater than 16 ng/L for women suggests a high likelihood of myocardial necrosis.
what do rising and/or falling cardiac troponin levels help to differentiate from
acute from chronic cardiomyocyte damage
- the more pronoounced the change, the higher the likelihood of acute MI
- a rise in greater than 5ng/L may indicate ACS
when are hs-TnI levels taken
taken on admission and again at 1 hour
one 1 level is required if the onset of symtpoms was 3 or more hour previously
in which patients may there be a false positive elevation of hs-TnI (2)
- advanced renal failure
- large PE
in which patients may there be an elevated hs-TnI level
- severe congestive cardiac failure
- myocarditis
- prolonged tachyarrhythmias
- aortic dissection
- aortic stenosis
- hypertrophic cardiomyopathy
- severe sepsis
Hs-TnI levels may remain elevated for several days and care should be taken in their interpretation in the context of re-admissions within a couple of weeks of a myocardial infarction
what are the ECG changes seen in STEMI (2)
- ST segement elevation in 2 or more leads from the same zone (ie leads II, III or AVF as inferior leads)
- new LBBB
what ECG changes are seen in an NSTEMI
- ST depression
- T wave inversion or flattening
- T wave pseudo-normalisation
what does ST depression confined to leads V1-V4 suggest
true posterior MI
- should be treated in the same manner as STEMI
what leads should STEMI patients have routinely recorded and why
posterior (V7-V9) and RV leads on or soon after admission
- especially those with inferior STEMI as diagnostic changes may be transient
what is ST elevation in RV4 highly sensitive for
RV infarction
what conditions may mimic STEMI on the ECG (4)
- early repolarisation causes up-sloping ST elevation esp in leads V1/V2 (more commonly seen in younger, athletic patients)
- concave ST elevation in pericarditis; may be widespread
- Brugada syndrome - anterior STEMI
- Takotsubo cardiomyopathy
what do pathological Q waves suggest
deep infarction involving the full thickness of the heart i.e. transmural
- typically appear 6 or more hours after the onset of symptoms
what is the inital management of STEMI
- IV access
- Pain relief e.g. morphine/anti-emetic
- O2
- Aspirin 300mg loading + 75mg OD for life
what antiplatelet therapies can be used in management of STEMI (3)
- prasugrel: thienopyridine inhibits ADP receptors 60mg loading and 100mg daily for up to 12 months
- clopidogrel: inhibits ADP receptors, loading dose 600mg followed by 75mg OD for up to 12 months
- ticagrelor: non thienopyridine loading dose 180mg + 90mg BD for up to 12 months (in pt who cannot have prasugrel or 1st choice NSTEMI)
what is the criteria for prescribing prasugrel
restricted to patients undergoing PPCI for STEMI who are under the age of 75 and who weigh more than 60kg and who have not had a prior TIA or stroke
what investigations are mandatory in patients presenting with STEMI
full biochemical screen on admission
- lipid profile
- random glucose
- HbA1c
- FBC
what medications may be administered as part of management of STEMI
- bisoprolol: reduce HR, avoid in shock! starting dose 1.25mg OD
- ACEi: prevent muscle over-damage, starting dose 2.5mg OD after checking renal function OR ARB starting dose 25mg then uptitrate to max tolerated dose
- statins: 80mg OD target to reduce LDL-C < 1.8mmol/L (total cholesterol target <4.0 mmol/L + ezetemibe if all statins caused side effects
what are target HbAcs for diabetics with STEMI
- Type 1 diabetes is < 7%
- Type 2 diabetes 6·5 - 7·5%
how is NSTEMI/unstable angina managed
- Pain relief (as above)
- Asprin 300 mg loading and 75 mg od
- Low molecular weight heparin (Enoxaparin for 48 hrs based on weight and creatinine)
- Repeat ECG
- Risk assessment of patient with elevated hs-TnI. Try grace score
- Ticagrelor if risk > 3% (medium) 180mg loading and 90mg BD
- Whilst waiting for inpatient angiography consider anti-anginals: nitrates, ranolazine, calcium channel blockers
what are intervention options for patients with STEMI presenting within 12 hours of onset
- PCI (if available within 2 hours of presenting)
- thrombolysis (if PCI not available within 2 hours)
what is PCI
- insert catheter into radial or femoral artery feeding up to coronary arteries under X-ray guidance
- inject contrast to identify area of blockage
- angioplasty to widen lumen ot insert device to remove/aspirate blockage
- stent inserted to keep artery open
what does thrombolysing a patient involve
- injecting a fibrinolytic agent by breaking down fibrin in blood clots
- significant risk of bleeding which makes thrombolysis dangerous
- e.g. streptokinase, alteplase, tenecteplase
what interventions are patients with NSTEMI considered for
immediate angiography
what is the GRACE score
gives 6 month probability of death after having NSTEMI
- 3% or less: low risk
- above 3% medium to high risk
patients with medium or high risk are considered for early angiography with PCI within 72 hours
after initial management of NSTEMI, what 3 things do patient require
- echocardiogram to assess functional damage to heart (LV function)
- cardiac rehab
- secondary prevention
what medication is involved in secondary prevention (6 As)
- Aspirin 75mg OD for life
- Antiplatelet (ticagrelor or clopidogrel for 12 months)
- Atorvastatin 80mg OD
- ACEi as high as tolerated
- Atenolol titrate as high as tolerated
- Aldosterone antagonist for those w clinical heart fialure e.g. eplerenone titrated to 50mg OD
Essential to monitor renal functon in patients taking ACEi + aldosterone antagonists as it carries a risk of fatal hyperK
what are the complications of MI
DREAD 💀
Death
Rupture of heart septum or papillary muscles
Edema (HF)
Arrhythmia and aneurysm
Dressler’s syndrome
what is Dressler’s syndrome and what is it caused by
post-MI syndrome presenting around 2 – 3 weeks after an acute myocardial infarction
- localised immune response that results in inflammation of the pericardium
how does Dressler’s syndrome present
- pleuritic chest pain
- low grade fever
- pericardial rub
- can cause pericardial effusion and rarely pericardial tamponade
how is Dressler’s syndrome diagnosed (3)
- ECG (global ST elevation and T wave inversion)
- echocardiogram (pericardial effusion)
- raised inflammatory markers (CRP and ESR)
how is Dressler’s syndrome managed (3)
- NSAIDs (e.g., aspirin or ibuprofen)
- more severe cases steroids (e.g., prednisolone)
- Pericardiocentesis may be required to remove fluid from around the heart, if there is a significant pericardial effusion
what are the 4 types of MI
- Type 1: Traditional MI due to an acute coronary event
- Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
- Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
- Type 4: MI associated with procedures such as PCI, coronary stenting and CABG
Type 1: A – ACS-type MI
Type 2: C – Can’t cope MI
Type 3: D – Dead by MI
Type 4: C – Caused by us MI
what is angina caused by
atherosclerosis affecting coronary arteries which narrows the lumen and reduces blood flow to myocardium
- in times of high demand, there is insufficient supply to meet demand which causes symptoms
what are the typical symptoms of angina
constricting chest pain ± radiation to jaw/arms
what baselines investigations should all patients with angina have
- Physical examination (e.g., heart sounds, signs of heart failure, blood pressure and BMI)
- resting 12-lead ECG provides information on rhythm, presence of heart block, previous myocardial infarction and myocardial hypertrophy and ischaemia
- FBC (anaemia)
- U&Es (required before starting an ACE inhibitor and other medications)
- LFTs (required before starting statins)
- Lipid profile
- Thyroid function tests (hypothyroidism or hyperthyroidism)
- HbA1C and fasting glucose (diabetes)
what are extra investigations a patient with stable angina may undergo
-
cardiac stress testing: having the patient exercise (e.g., walking on a treadmill) or giving medication (e.g., dobutamine) to stress the heart
- ECG, echo, MRI, myocardial perfusion scan - CT coronary angiogram: injecting contrast and taking CT images timed with the heart contractions to give a detailed view of the coronary arteries, highlighting the specific locations of any narrowing
- invasive coronary angiography: gold standard for determining CAD
what is the medical management of stable angina for immediate symptomatic relief
sublingual glyceryl trinitrate (GTN) in the form of a spray or tablets - causes vasodilation, improving blood flow to the myocardium
* Take the GTN when the symptoms start
* Take a second dose after 5 minutes if the symptoms remain
* Take a third dose after a further 5 minutes if the symptoms remain
* Call an ambulance after a further 5 minutes if the symptoms remain
Key side effects of GTN are headaches and dizziness caused by vasodilation
what is the medical management of stable angina for long term symptomatic relief (2)
- Beta blocker (e.g., bisoprolol)
- Calcium-channel blocker (e.g., diltiazem or verapamil – both avoided in heart failure with reduced ejection fraction)
Specialist considerations:
* Long-acting nitrates (e.g., isosorbide mononitrate)
* Ivabradine
* Nicorandil
* Ranolazine
what is the medical management of stable angina for secondary prevention
A – Aspirin 75mg once daily (clopidogrel where allergic or intolerant)
A – Atorvastatin 80mg once daily
A – ACE inhibitor (if diabetes, hypertension, CKD or heart failure are also present)
A – Already on a beta blocker for symptomatic relief
when are surgical interventions appropriate for stable angina
generally offered to patients with more severe disease and where medical treatments do not control symptoms
what are 2 surgical interventions for stable angina
- Percutaneous coronary intervention (PCI)
- Coronary artery bypass graft (CABG)
what is a CABG
may be offered to patients with severe stenosis
- opening the chest along the sternum, with a midline sternotomy incision
- graft vessel is attached to the affected coronary artery, bypassing the stenotic area.
- three main options for graft vessels are: saphenous vein (harvested from the inner leg), internal thoracic artery, also known as the internal mammary artery, radial artery
what are the advantages of PCI compared to CABG
- Faster recovery
- Lower rate of strokes as a complication
- Higher rate of requiring repeat revascularisation (further procedures)
CAD scars to look out for in OSCE examination
what is ivabradine and what is its use
- sinus node blocking agent which can be used as an alternative rate controlling agent where B-blocker is contraindicated or not tolerated
- do not initate in angina if HR < 70bpm
- do not co-prescribe with diltiazem or verapamil
- 5-7.5mg BD
how is ranolazine used
give dosage and contraindication
as adjunctive therapy in patients who are inadequately controlled or intolerant of first-line anti-anginal drugs
- dose is initially 375mg BD increasing to max of 750mg BD
- use should be mainly in patients with chronic stable angina rather than in the acute setting
- contraindicated if the GFR is < 30
what are non-cardiac causes of chest pain
- Costochondritis
- Gastro-oesophageal
- PE
- Pneumonia
- Pneumothorax
- Psychogenic/psychosomatic
if angina is not controlled with a beta-blocker, what medication should be added
longer-acting dihydropyridine CCB e.g. amlodipine
what is the management of NSTEMI patients with a GRACE score >3%
coronary angiography with PCI if needed - within 72 hours of admission
infective endocarditis in IV drug users commonly affects which valve
tricuspid valve
