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What are the adverse effects of bile acid binding resins?

GI effects limit the max dose and are a common reason for nonadherence - need to take with lots and lots of water to minimise upper GIT disturbance

Can interfere with drdug absorption esp anticoagulants, thyroxine, cyclosporin, and digoxin


What is third line after a statin plus ezetimibe for dyslipidemia of LDL-C variant?

Bile acid binding resin


What is fourth line therapy for dyslipidemia of the LDL-C kind?

Nicotinc acid - rarely used as is poorly tolerated mainly due to flushing (can give with food and prophylactic aspirin)
Can also cause gastric irration, gout and impaired glucose tolerance.
Need to monitor BSL, CK, and liver.

Use with caution with a statin (but can be done)


Can you use fibrates with a statin to reduce LDL-C?  What do you need to consider?

May lead to 5-10% reduction in LDL-C
Does not increase risk of myopathy beyond the level of statin monotherapy, EXCEPT...

Gemfibrozil - DO NOT DO IT, significantly increases the risk of myositis when given with a statin.

Use fenofibrate instead and monitor CK.


How do you treat hypertriglyceridaemia?

Dietary/behaviour/diabetic control are central.

If severe (>10), or >4 and have low HDL-C (<1) or is associated with increased absolute CVD risk:

Fibrate plus fish oil (Two Fs!) - and probably need to max both out.

Nicotinic acid is third line.  Statins are inappropriate


High CVD risk
Elevated LDL-C
Mild to moderate elevation of TGLs

What is the treatment?

Statins are first line


High absolute CVD risk
LDL-C elevated
TGLs >4

What is first line therapy?



How safely do you treat mixed hyperlipidaemia that is severe? (Mixed = high cholesterol and TGL)

Statin plus fish oil
Fibrate plus ezetimibe

Statin plus fenofibrate or statin plus nicotinic acid can be done but only with caution.


What are the side effects of Ezetimibe?

Myalgia and rhabdo have been repeated

NOT CYP450 so limited drug interactions
Avoid in mod-severe liver impairment (no data)


What are the risk factors for developing liver and muscle problems from lipid-modifying therapy?

Risk factors for these adverse effects include pre-existing muscle, liver or kidney disease, high-dose therapy, concomitant interacting drugs, intercurrent illness, frailty and advanced age.


How do you monitor lipid modifying therapy?

Basleine LFTS and when you assess response to lipids - 1-2 months post initiation/dose adjustment

No need to routinely monitor CK/LFT if asymptomatic - unless on combination therapy

If asymptomatic CK elevation - avoid exercise for a few days.  Continiue if CK is not >5 ULN


When should you stop lipid-modifying therapy?

Mild muscle sx - still benefit from max dose, try second daily or twice weekly

Stop lif:
previously normal ALT is persistently more than 3 times ULN
CK is more than 10 times ULN
CK is more than 5 times ULN and patient has muscle symptoms
patient has persistent unexplained muscle pain
patient has persistent unexplained muscle weakness.


What do you do if someones muscles or liver enzymes normalise after you stop lipid-modifying therapy?

If the symptoms were mild, drug can be restarted (at a lower dose), if it recurs - change statin or go to alternative lipid modifying drug


Which lipid-modifying agents impair glucose metabolism?

High-dose statins may slightly impair glucose metabolism, while nicotinic acid can cause impaired glucose tolerance as well as hyperuricaemia and gout. Check blood glucose before starting therapy, and repeat 1 to 2 months after starting therapy or adjusting the dose.


Which lipid modifying drugs affect the CK and ALT respectively?

CK: statin > fibrate > nicotinic acid or ezetimibe

ALT: nicotinic acid > ezetimibe > fibrate > statin


What lipid tests are required to calculate absolute CVD risk?

What are the drawbacks of this?

TC (total cholesterol) and HDL-C

TC may overestimate risk of HDL-C is raised
TC may underestimate risk of TGLs are raised

Predictive value is improved by considering LDL-C and HDL-C independently


What impact does significantly elevated triglycerides have on the measurement of cholesterol and LDL-C?

LDL composition changes when TGL >2mmol
 - in this case, non-HDL-c becomes a better indicator than LDL-c
 - LDL-C requires a fasting sample and becomes unreliable if TGLs exceed 4mmol


How do statins reduce LDL?

Reduce liver cholesterol synthesis
Increased LDLr and SREBP gene expression
Receptors produced by normal gene (even in familial disease) will reduce LDL cholesterol levels.


What are the target lipid levels for patients on lipid-modifying therapy?

total cholesterol (TC) - less than 4.0 mmol/L

low-density lipoprotein cholesterol (LDL-C) - less than 2.0 mmol/L

high-density lipoprotein cholesterol (HDL-C) - more than 1.0 mmol/L

triglycerides -less than 2.0 mmol/L

non–high-density lipoprotein cholesterol (non–HDL-C) - less than 2.5 mmol/L


What are the target LDL-C levels in those with familial hypercholesterolaemia?

Target plasma levels for LDL-cholesterol for low, intermediate an d high risk FH are < 4, < 3 and < 2 mmol/L, respectively


Which subset of familial hypercholesterolaemia patients benefits the most from statins?

Statin treatment of FH males is one of the most cost-effective medical intervention
s available and several lines of evidence point towards major improvements in CVD event rates and total mortality of FH patients since its introduction.  Still evolving for younger patients.


What does this ECG show?

Broad QRS >120ms
RSR pattern in V1-V3
Wide slurred S wave in lateral leads (I, AVL, V5-V6)



What syndrome do you need to be mindful of when diagnosing a RBBB on ECG?

An RSR’ pattern in V1-3 may also be caused by Brugada syndrome – an ECG pattern associated with malignant ventricular arrhythmias.


When is treatment stress testing indicated?

Symptoms of known or probably ischaemic heart disease
Stable chest pain
Unstable chest pain stabilised by medical therapy
Post MI
Post revascularisation


What are the absolute contraindications to EST?

Acute MI
Unstable angina
Symptomatic uncontrolled cardiac arrhythmia
Severe AS
Acute PE or pulm infarct
Acute myocarditis or pericarditis
Acute aortic dissection


What are the most important pre-test predictive parameters of CAD?

Chest pain

Diagnostic power of EST is maximal when the pretest probability is intermediate (30-70%)


What are the indications for PCI?

Clinical indications for PCI include the following:

    Acute ST-elevation MI (STEMI)
    Non–ST-elevation acute coronary syndrome (NSTE-ACS)
    Stable angina
    Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
    Asymptomatic or mildly symptomatic patient with objective evidence of a moderate-sized to large area of viable myocardium or moderate to severe ischemia on noninvasive testing 

Angiographic indications include hemodynamically significant lesions in vessels serving viable myocardium (vessel diameter >1.5 mm). 


What is the evidence behind CTCA?

Meta-analyses of over 45 single-centre studies have consistently shown CTCA to have excellent sensitivity (98%) and very good specificity (88%) compared with invasive coronary angiography for significant disease (stenosis > 50%).5,8,9 The negative predictive values (96%–100%) were better than positive predictive values (93%), demonstrating CTCA to be an excellent tool for ruling out significant disease in patients with low-to-intermediate pretest probability of CAD. 


What are the indications for CTCA in the evaluation of non-acute chest pain?

Evaluation of chest pain with no previous known disease:

    able to exercise and no previous tests (intermediate risk)

    unable to exercise or ECG uninterpretable (low-to-intermediate risk)

    equivocal or uninterpretable stress test results

    normal ECG exercise test but ongoing symptoms.


What are the indications for CTCA with acute chest pain?

Evaluation of acute chest pain (emergency department):

    normal ECG and cardiac enzymes

    low-to-intermediate pretest probability of CAD.