Ischaemic Heart Disease Flashcards
Notes on BP targets in managing cardiovascular risk
- SPRINT trial - among patients at increased CV risk, targeting BP ≤120 mmHg resulted in lower rates of major adverse CV events compared to 140mmhg. Similar outcomes in RCT with older patients.
- Rates of some adverse events higher in the intensive treatment group
Notes on insulin resistance syndrome and cardiovascular risk
Diabetic dyslipidaemia profile
- Reduced HDL
- Elevated triglycerides
- Preponderance of atherogenic small, dense LDL particles
- HDL consistent predictor of CV risk - increasing levels = decreased MI or coronary death
- Lowering triglycerides → not predictive of outcome
Hypofibrinolysis
- Elevated plasminogen activator inhibitor-1 (PAI-1) predicts CV disease
Metformin
- Reduces macrovascular complications in obese patients compared to intensive therapy with sulphonylurea or insulin
Notes on LDL and CHD
- Relationship between LDL-C and CHD - see slide
- Doubling a statin dose only yields a 6% incremental drop in LDL-C
Cholesterol synthesis
- Two sources of cholesterol → dietary and biliary → intestine → either excreted in faecal bile acids and neutral sterols or absorbed → liver where they are synthesised by HMG CoA Reducatase → mevalonate → cholesterol
Notes on lipid lowering therapies
-
Statins
- Simvastatin, atorvastatin, rosuvastatin
- Fibrates
- Bezalip
- Cholesterol binding resins
- Cholestyramine
- Nicotinic acid
-
Ezetimibe
- Added to simvastatin → greater reduction in LDL cholesterol compared to simvastatin alone
- PCSK 9 Inhibitors
- Inclisiran - siRNA PCSK-9 production
Notes on PCSK9 inhibitors
- Monoclonal antibodies to Proprotein convertase subtilisin/kexin type 9 inhibitors
- Monthly/bi monthly SC injection
- Idea arose fro observation that naturally occuring loss of function polymorphisms in PCSK 9 led to lower LDL-C
- E.g. Alirocumab, evolocumab
Trials
- When used with statins → significant decrease in LDL-C levels (<1) , with lower CV events and no excess in safety events
Notes on Inclisiran in lipid lowering therapy
-
MOA
- Small interfering double stranded RNA
- Distributed in liver due to conjugation
- Inhibits production of PCSK9 in hepatocyte
- SC injection
RCTs
- 2 separate RCTs → reduces LDL cholesterol by 50% at month 17, modest excess of injection site adverse events
Benefits of radial approach in angiogram
Reduced bleeding
Earlier ambulation
Increased comfort
Mortality benefit ONLY in the setting of STEMI
Mechanism of action GTN
Systemic vasodilatation -> decrease in LV end diastolic volume and wall stress -> decreased myocardial oxygen demand
Classification of MI - 1 -> 5
- Infarction due to atherosclerotic disease
- Infarction secondary to supply/demand mismatch
- Infarction causing sudden death without the opportunity for bio marker or ECG confirmation
4a = infarction related to a PCI
4b = infarction related to the thrombosis of a coronary stent - Infarction as a complication of CABG
Options for treatment for left main coronary artery disease
Usually CABG
EXCEL Trial 2016 -> PCI with second generation DES non inferior to CABG in the setting of low-intermidiate anatomic complexity, with respect to primary outcome of death, stroke or MI at 3 years
GRACE Score
Risk stratify ACS - predicts in-hospital, 6 month and 3 year mortality
Variables - age, renal function, troponin, CHF, ST segment deviation, SBP, HR, Cardiac arrest
1-108 = low risk, 109-140 = intermediate, > 140 = high rish
Early vs delayed intervention (PCI) - TIMACS Trial - if low risk GRACE score early intervention does not differ greatly from delayed intervention in preventing death, MI, stroke at six months
?Value in re-vascularisation of non-culprit vessels in the setting of a STEMI (vs revascularisation of culprit vessel alone)
Complete revascularisation A/W reduction in major adverse cardiovascular outcomes at 12 months compared to culprit lesion alone - recommended PCI for non-infarct related arteries in selected patients with STEMI and multivessel disease who are haemodynamically stable - either at the time of intial PCI or as a planned staged procedure
?Value in re-vascularisation of non-culprit vessels in the setting of a STEMI (vs revascularisation of culprit vessel alone)
Complete revascularisation A/W reduction in major adverse cardiovascular outcomes at 12 months compared to culprit lesion alone - recommended PCI for non-infarct related arteries in selected patients with STEMI and multivessel disease who are haemodynamically stable - either at the time of intial PCI or as a planned staged procedure
Differential for acute renal failure after cardiac catheterisation
- Contrast nepropathy - usually resolves within 7 days, greater risk in moderate to severe renal insufficiency or diabetes
- Cholesterol emboli - other signs of embolisation e.g. blue toes, livido reticularis, hollenhorst plaque in retina and abdominal pain, transient eosinophilia and hypocomplementaemia, renal function derangement persists beyond seven days
MOA Tirofiban
- Reversible non peptide receptor antagonist against Glycoprotein IIB/IIIA. \Tirofiban, in combination with heparin, is indicated for patients with unstable angina or non-Q -wave myocardial infarction to prevent cardiac ischaemic events.
Features of an RV infarction
Think about in inferior STEMI. RV infarction suggested by:
- ST elevation V1
- STE V1 and STD V2 (highly specific)
- Isoelectric ST segment in V1 with marked depression in V2
- STE III > II
- Confirmed by presence of STE in right sided leads (V3R - V6R)
RCA branches and significance
Risk of bradyarrhytmias/heart block
Caution with nitrates, beta blockers, ACEi
If RV infarction - usually imrpoves dramatically in first few days after revascularisation
Posterior myocardial infarction features
15-20% STEMIs - should look for in inferior and lateral infarction
Increased risk of LV dysfunction and death
Clues:
Horizontal ST depression, tall broad R waves, upright T waves, dominant R wave in V2
Diagnosis
Posterior wall MI
STEMI: Indications for thrombolysis vs PCI
- See diagram
- Note late thrombolysis out to 6-12 hours reasonable if ongoing pain, but the earlier the better
STEMI: Indications for thrombolysis vs PCI
- See diagram
- Note late thrombolysis out to 6-12 hours reasonable if ongoing pain, but the earlier the better
Notes on stable angina - medical therapy and revascularistion
- ISCHAEMIA - Revascularisation does not reduce risk of death, MI, other other major CV event when added to optimal medical therapy though some divergence at 4 years favouring invasive strategy
- Invasive strategy in short term does → improved angina symptoms
- Note results do not apply to ACS, class III/IV angina, HFrEF, left main disease
- Optimal medical therapy
- Aspirin (or other antiplatelet if contraindications)
- Beta blockers - first line
- Calcium channel blockers - if no LV impairment, as add on for symptoms
- ACEI for all with LV impairment or CKD
- Long acting nitrates
Role of revascularisation in angina individualised
