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In which cardiac patients is antibiotic prophylaxis recommended if undergoing dental surgery?

- prosthetic valve or material used for valve repair
- previous IE
- Congenital heart disease but only if
 - unrepaired cyanotic defects (inc pal shunts and conduits)
 - completely repaired with material or device either by surgery or cath and it's during the first 6 months afterward
- repaired defects with resiudal defects at or adjacent to the site of a patch or device (which inhibit endothelialisation

- cardiac transplant with subsequent development of valvulopathy

- RHD in in aboriginals only


For which dental procedures is antibiotic phrophylaxis always required in at-risk cardiac patients?

- extraction
- periodontal procedures inc surgery, subgingival scaling and root planing
- replanting avulsed teeth
- other surgical procedures ie implants

(Cleaning, braces, - only if repeated)

No need if just having anaesthetic, intracanal procedure, removal of sutures


What is the standard antibiotic prophylaxis for IE in at-risk patients undergoing dental procedures?

Amoxicillin 2g 1 hour before procedure

If hypersensitive/already on long-term/or in last month

Clindamycin 600mg 1 hour beforehand


Which respiratory tract procedures require endocarditis prophylaxis in those at-risk?

Anything involving incision or bx of resp mucosa
- tonsillectomy/adenoidectomy
- bronch PLUS incision or bx
Any surgery inc bronchial sinus, nasal or middle ear mucosa including tympanosomty tube insertion


For which GI and GUT procedures is antibiotic prophylaxis required in at-risk cardiac patients?

Any GU procedure in the prsence of a GU infection (unless already treating enterococci) - get an MSU beforehand!
Ditto GIT

Do NOT need for catheters, vaginal deliveries, TOE, endoscopy/colonoscopy +/- bx, perc gastrostomy


Name the points on the JVP

A- wave (S1) - atrial contraction

C-wave - tricuspid valve closure

X-descent - atrial relaxation

V-wave (S2) - atrial filling

Y-descent - rapid ventricular filling


What is the definition of a raised JVP?

More than 3cm from the zero point (or 8cm from the right atrium)

The zero point is the sternal angle when the patient is lying at 45 degrees


Define the anatomy of the JVP

Internal jugular vein is preferred (although does correlate well with external

This is lateral to the SCM


Why is the right sided internal jugular vein preferred for measuring the JVP?

The left sided veins cross from the left side of the chest before entering the right atrium so are less accurate


What does the pulmonary artery wedge pressure measure?

-¬†pressure within the pulmonary arterial system when catheter tip ‚Äėwedged‚Äô in the tapering branch of one of the pulmonary arteries

- in most patients this estimates LVEDP thus is an indicator of LVEDV (preload of the left ventricle)

- PCWP >18 mmHg in the context of normal oncotic pressure suggests left heart failure


In what situations is the PAWP not equivalent to LVEDP?

(Wedge pressure greater) than LVEDP 

Mitral stenosis or MR
Atrial myxoma
Pulmonary venous obstruction (i.e. fibrosis, vasculitis)
L-R shunt

Wedge pressure less than LVEDP
- severe LV failure
- high PEEP
- noncompliant LV (i.e. hocm)
- AR


What is the normal distribution of the ECG leads?

        Inferior =  II, III, aVF
        Lateral =  I, aVL, V5-6
        Anterior =  V2-6


What does LBBB and RBBB do to the t-wave?

Left bundle branch block produces T-wave inversion in the lateral leads I, aVL and V5-6.

Left bundle branch block produces T-wave inversion in the lateral leads I, aVL and V5-6.


How do you interpret a troponin?

A test should be interpreted as positive if level
99th centile for reference population OR
there is a change of
50% above an initial base-
line level. A positive finding identifies patients
at increased risk, but does not provide defini-
tive evidence of MI. A positive troponin result
should be followed up by a search for an
alternative plausible diagnosis and/or cardiac
consultation if ACS is suspected in the context
of the clinical presentation. 


What is the epidemiology of familial hypercholesterolaemia?

Prevalence in offspring of 50%


What is the clinical presentation of familial hypercholesterolaemia?

1) Severe hypercholesterolaemia that is not explained by secondary causes,
2) A strong personal or family history of premature atherosclerotic cardiovascular disease (CVD),
3)Tendon Xanthomas


How do women differ from men with regard to familial hypercholesterolaemia?

Protected prior to menopause
Natural hx delayed by about one decade
But still accelerated b y 2 decades in both women and men


What are the specific signs of familial hypercholesterolaemia

Tendon xanthomas (achilles and extensors on dorsum of the hand) --> pathognomonic

Arcus (white ring around around iris - corneal margin) in a young person is suggestive.


What are the nonspecific clinical presentations of familial hypercholesterolaemia?

Arcus and xanthelasma
Premature CHD/CVD
Aortic stenosis


What are the metabolic features of hypercholesterolaemia?

Increased LDL
Increased remnants including precursor IDL


What are the top 3 specific features of familial hypercholesterolaemia?

8 points DNA Mutation, or LDL-C > 8.5
6 points Tendon xanthomas
5 points¬†LDL-C 6.5 ‚Äď 8.4
4 points Arcus senilis < 45 yrs
3 points¬†LDL 5.0 ‚Äď 6.4
2 points Xanthomas or premature arcus in 1 st degree relative, childhood LDL > 95th percentile, or premature CHD
1 point¬†1st deg relative with premature CVD or LDL > 95¬†th¬†percentile, personal history of LDL 4.0¬†‚Äď 4.9 or premature CVD


When should you suspect familial hypercholesterolaemia?

Patients presenting to cardiology and stroke units with premature CVD (aged < 60 yr), and in primary care amongst those with a family history of hypercholesterolaemia and
premature CVD. 

Risk factor counting, non-invasive testing for atherosclerosis (carotid ultrasonography, cardiac CT) and documented CVD should be used to stratify patients for routine, enhanced and high intensity treatment. 


What is the main value of molecular diagnosis of familial hypercholesterolaemia?

The major value in making a molecular diagnosis is its use in predictive testing
of other family members for FH. This is useful in early detection of cases that need intervention to prevent CVD and in re-assuring family members who may not have the condition. 


What genes are associated with familial hypercholesterolaemia?

LDL receptor (most common)

LDL receptor ligand (apolipoprotein B100) - second most common

Proprotein Convertase Subtilsin Kexin 9 (PCSK-9) - third most common


When would you be most likely to find a causative mutation for familial hypercholesterolaemia?

Definite clinical familial hypercholesterolaemia --> causative mutation found 80% of the time.


What is the management of predominantly elevated LDL-C?

Statins are first-line therapy for predominant elevation of LDL-C. The efficacy of statins in reducing the risk of cardiovascular events is proven, and there is a low rate of serious adverse effects with long-term use.


When is use of a bile acid binding resin inappropriate?

Addition of a bile acid binding resin can enhance LDL-C reduction, but is inappropriate when triglycerides are elevated because hypertriglyceridaemia can be exacerbated.


What does doubling the dose of a statin do to the LDL-C?

Each doubling of statin dose is likely to reduce LDL-C by an additional 5% to 10%.


What is the next step after maximal statin therapy fails to bring down the LDL-C enough?

The addition of ezetimibe to statin therapy is often synergistic, with the additional lowering of LDL-C ranging from 20% to 25%.

Ezetimibe is well tolerated in about 75% of patients who are unable to tolerate statin therapy, with LDL-C decreasing by 15% to 20%.


Under what circumstances are bile acid binding resins used in dyslipidemia?

If LDL-C is still not well controlled, or there are adverse effects from ezetimibe, consider adding a bile acid binding resin. Bile acid binding resins are mainly used in combination with statins, but they can be used alone or in combination with other drugs, including ezetimibe. Resins increase triglyceride levels and are inappropriate in moderate to severe hypertriglyceridaemia.