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Cardiology > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What does the pressure volume loop indicate?

A

Aortic stenosis

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2
Q

What could the following pressure-volume loop indicate

A 
Aortic regurgitation
consider MR (similar looking loop)
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3
Q

(Draw) Cardiac pressure-volume loop

A
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4
Q

ABSOLUTE contraindications to fibrinolysis (8)

A
  1. Previous ICH or stroke of unknown origin at anytime
  2. Ischaemic stroke in the preceding 6months
  3. CNS damage/neoplasms/AV malformations
  4. Recent major trauma/surgery/head injury within the preceding month
  5. Gastrointestinal bleeding within the past month
  6. Known bleeding disorder excluding menses
  7. Aortic dissection
  8. Non-compressible punctures in the past 24 hours (E.g. liver Bx, LP)
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5
Q

Acute HR control of AF

A
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6
Q

AF in HF

A
  • AF is the most common arrhythmia in HF - new onset AF in established HF predicts worse outcomes
  • ACEIs,ARBs, betablockers and MRAs,will reduce the incidence of AF, but ivabradine may increase it.
  • CRT has little effect on the incidence of AF
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7
Q

Anticoagulation rules post mechanical prosthetic valve vs bioprosthetic valve

A

Mechanical

  • PO anticoagulation with VKA - all patients lifelong
  • Bridge with clexane/UFH if VKA needs to be interrupted
  • Consider adding aspirin post TE events despite adequate INR or if concomitant atherosclerotic disease

Bioprosthetic

  • PO anticoagulation with VKA for the first 3 months post MV/TV bioprosthesis or repair
  • Either PO anticoagulation or low dose aspirin for the first 3 months post AV bioprosthesis
  • Aspirin or DAPT for the first 3 to 6 months post TAVI (depending on bleeding risk) then continue lifelong antiplatelet agent
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8
Q

Angiotensin–Neprilysin Inhibition vs ACEI PARADIGM-HF 2014 trial difference in outcomes

A

LCZ696 ARNI was superior to enalapril in reducing the risks of death and of hospitalization for heart failure.

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9
Q

Arrhythmogenic Right Ventricular Dysplasia (ARVD or ARVC)

A

Inherited cardiomyopathy - autosomal dominant in genes encoding desmosomal proteins
Risk factor for ventricular arrhythmias and sudden death
Advice - avoid competitive and/or endurance sports

ECG:

  • Epsilon wave mst specific finding, seen in 30% of patients)
  • T wave inversions in V1-V3 (85% of patients)
  • Prolonges S-wave upstroke of 55ms in V1-V3 (95% of patients)
  • Localised QRS widening of 110ms in V1-V3
  • Paroxysmal episodes of ventricular tachycardia with a LBBB morphology
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10
Q

ASD ostium primum - what kind of BBB
ASD ostium secundum - what kind of BBB

A

Primum - LBBB
Secundum - RBBB
Both present with wide, fixed splitting of S2 with an ESM in the L) 2nd ICS

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11
Q

Atherosclerosis principally affects which of the following components of the vessel wall

A

Intima and Media

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12
Q

Bare metal stent (BMS) vs. Drug eluting stent (DES) in PCI

A
  • newer generation DES (Everolimus, Zotarolimus) reduce risk of repeat target vessel revascularisation cf BMS in the first year
  • Very similar safety profile
  • To a lesser extent, there may be a mortality benefit DES cf BMS in the EXAMINATION trial
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13
Q

Beneficial effect of Mediterranean Diet in CVD

A
  • Lower incidence of major cardiovascular events when Mediterranean diet is supplemented with extra-virgin olive oil or nuts when compared to reduced-fat diet
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14
Q

Brugada Syndrome

A
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15
Q

Brugada Syndrome - indications for ICD

A
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16
Q

Cardiac Action Potential (draw)

A

Cardiac actional potention approx 100x longer than skeletal muscle

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17
Q

Cardioversion: General principles

A

Can be done with drugs or electricity

  • in the short term electrical restores SR quicker and more effectively with shorter hospital stay
  • Pharmacological - does not require sedation or fasting
  • Flecainide and propafenone - effective but cannot use if patient has structural heart disease
  • Amiodarone > Flecainide > Sotalol at restoring SR
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18
Q

Catecholaminergic Polymorphic VT
-buzz words and 2 drugs used to treat

A
  • Bidirectional VT entricular (arrhythmia with an alternating 180°-QRS axis on a beat-to-beat basis)
  • during exercise or induced by catecholamines
  • Mx - betablockers and verapamil
  • This will inhibit VT
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19
Q

Catecholaminergic Polymorphic VT (CPVT)

  • Describe classic presentation
  • Describe key test
  • Describe genetics
  • Describe Mx
A
  • Polymorphic VT induced by physical or emotional stress
  • NO structural heart changes
  • 1 in 10,000 people, autosomal dominant
  • Resting ECG will be normal - key test is an exercise stress test
  • RyR2 (ryanodine receptor 2) gene mutation
  • Other - CASQ mutation
  • Management
    • Beta blockers, sympathectomy
    • ICD
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20
Q

Categories of Aortic Stenosis

A

1. High gradient AS
-valve area <1cm2, mean gradient >40mmHg
2. Low-flow, low-gradient AS with reduced EF
-valve area <1cm2, mean gradient <40mmHg, EF <50% SVi < 35mL/m2
=do dobutamine echo to decide if truly severe AS or pseudosevere AS
=pseudosevere if AVA >1.0cm2 with flow normalisation
3. Low-flow, low-gradient AS with preserved EF
-valve area <1cm2, mean gradient <40mmHg, EF >50% SVi < 35mL/m2
=do MSCT to gage valve calcification and therefore severity
4. Normal flow, low-gradient AS with preserved EF
-valve area <1cm2, mean gradient <40mmHg, EF >50% SVi >35mL/m2
-general = moderate AS

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21
Q

Catheter Ablation in AF

A
  • More effective than anti-arrhythmic drugs in maintaining SR
  • however currently recommended in symptomatic paroxysmal AF to improve symptoms in patients with symptomatic recurrences despite drug anti-arrhythmics
  • Pulmonary Vein Isolation (PVI) - best documented target for ablation
  • Most patients require more than procedure to achieve symptom control
  • Anticoagulate for at least 8 weeks post ablation
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22
Q

Causes of ACUTE heart Failure - CHAMP

A
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23
Q

Causes of aortic regurgitation

A
  • Degenerative tricuspid or bicuspid most common in developed countries
  • Also infective, rheumatic
  • acute AR in aortic dissection
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24
Q

Causes of Late Mortality post Cardiac Transplant

A

CAV = cardiac agraft vascupathy

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25
Q

Causes of Triscuspid Regurgitation

A

Secondary (more common)- due to RV dysfunction following pressure and/or volume overload in presence of structurally normal leaflets
Primary causes

  • Infective endocarditis (esp IV drug users)
  • Rheumatic heart disease
  • Carcinoid syndrome
  • Myxomatous disease
  • Endomyocardial fibrosis
  • Ebsteins anomaly
  • Congenitally dysplastic valves
  • Drug induced valve diseases
  • Thoracic trauma
  • iatrogenic valve damage
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26
Q

CHA2DS2VASc Score

A
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27
Q

Choice of anticoagulation in AF

A
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28
Q

Classification of Aortic Stenosis Severity

A
  • Mild: AVA >1.5cm2, mean gradient <20mmHg
  • Mod: AVA 1 - 1.5cm2, mean gradient 20 - 39mmHg
  • Severe: AVA <1cm2, mean gradient >40mmHg (and/or jet velocity >4.0m/sec or DVI <0.25)
  • Normal AVA is 3 - 4cm2 with gradient <10mmHg
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29
Q

Classification of HF

A
  • HF with preserved ejection fraction (HFpEF) = LVEF > 50% (old diastolic)
  • HF with reduced ejection fraction (HFrEF) = LVEF <40% (old systolic)
  • HF with mid range ejection fraction (HFmrEF = LVEF 40 - 49%
  • It is only in patients with HFrEF that therapies have been shown to reduce BOTH morbidity and mortality
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30
Q

Classification of HTN

A
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31
Q

Comparitive risks of SAVR and TAVI

A
  • *Risk of cerebrovascular events - similar**
  • *Higher risk in SAVR**
  • severe bleeding
  • AKI
  • new onset AF

High risk in TAVI

  • vascular complications
  • pacemaker implantation
  • paravalvular regurgitation
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32
Q

Complications of Catheter ablation in AF

A
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33
Q

Complications of thorascopic atrial fibrillation surgery

A
  1. Pericardial tamponade ?highest risk
  2. Conversion to sternotomy
  3. Pacemaker insertion
  4. Drainage for pneumothorax
  5. TIA
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34
Q

Components of Tetralogy of Fallot

A
  1. VSD
  2. Overriding Aorta
  3. Pulmonary stenosis/RV outflow obstruction
  4. RV hypertrophy
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35
Q

Conditions in which Pregnancy is Contraindicated (7)

A
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36
Q

Congenital abnormality most commonly associated with WPW

A
  • Ebstein’s anomaly - septal and posterior leaflets of the tricuspid valve are displaced towards the apex of the right ventricle of the heart
  • 10 to 20% of Ebstein patients have accessory pathway
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37
Q

Constrictive Pericarditis vs Restrictive Cardiomyopathy

A
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38
Q

Contraindications to Heart Transplantation in Heart failure

A
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39
Q

Contraindications to Percutaneous Mitral Commissurotomy (7)

A
  1. MV area >1.5cm2
  2. LA thrombus
  3. More than mild mitral regurgitation
  4. Severe for bi-commissural calcification
  5. Absence of commissural fusion
  6. Severe concomitant aortic valve disease, or severe combined TS and TR requiring surgery
  7. Concomitant CAD requiring bypass surgery
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40
Q

Contraindications to the P2Y12 inhibitors Ticagrelor and Prasugrel

A

BOTH

  • Previous haemorrhagic stroke
  • Oral anti-coagulants
  • Moderate to severe liver disease

PRASUGREL specific

  • Previous stroke/TIA
  • Age >75 years
  • Weight <60kg

TICAGRELOR specific

  • treatment with strong inhibitors of CYP3A4
  • bleeding disorder
  • Caution in patients at risk of bradycardia (excluded from trials)

If both are contraindicated - alternative is clopidogrel

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41
Q

Defib vs pacemaker in HF

A
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42
Q

Definition: non-sustained VT

A
  • 3 or more consecutive beats of broad complex QRS >120ms with HR > 120 which self terminates within 30 seconds
  • ischaemic heart disease is the most common cause
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43
Q

Driving rules post IHD

  1. Private licence - post PCI no ACS, ACS, CABG and cardiac arrest
  2. Commercial licence post PCI no ACS, ACS, CABG and cardiac arrest
A
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44
Q

ECG findings in TCA overdose

A
    1. Broad QRS complexe
      * ->100ms predicts seizures
      * ->160ms predicts cardiotoxicity
    1. Positive R wave in AVR
    1. Prolonged PR interval
    1. Long QT interval
    1. Brugada-like pattern in V1
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45
Q

Echo to characterise AS

A
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46
Q

Electrical Cardioversion

A

SYNCHRONISED direct current electrical cardioversion

  • quickly and effectively converts AF to SR
  • method of choice in severely haemodynamically unstable patients with new onset AF
  • requires sedation prior and continuous BP and Sats monitoring
  • Biphasic (standard) is more effective than monophasic
  • Anterior-posterior electrode position beter than anterolateral - stronger shock and more effective
  • If considering starting anti-arrhythmic drug post:
    • start 1-3 days prior to electrical cardioversion and continue post
  • SE - stroke in non-anticoagulated patients
  • Patients in AF > 48 hours should start OAC at least 3 weeks before cardioversion and continue it for at least 4 weeks after.
  • -IF needing to do early cardioversion: TOE can exclude majority of LA thrombi, allowing immediate cardioversion
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47
Q

Eruptive xanthomas

A

Type I and V hyperlipoproteinaemia

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48
Q

Familial Hypercholesterolaemia

  • Special fact about epi
  • 3 genetic mutations involved, which is the most common
  • Homozygote phenotype
  • Treatment
A
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49
Q

STITCHES TRIAL - 2016

A
  • Cohort: EF of < 35% and CAD amenable to CABG and NYHA III/IV
  • CABG + medical therapy is greater than medical therapy alone.
  • CABG + SVR (surgical ventricular reconstruction) not recommended as routine at this stage (in patients with NYHA III/IV and LVED <35%)
  • Although SVR was demonstrated to reduce LV end-systolic volume to a greater extent than CABG alone, this result did not translate into an improvement in cardiovascular morbidity or mortality in this study. Based on these results, routine SVR at the time of CABG should not be recommended at this time.
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50
Q

SYNTAXES trial 2019

A
  • At 10 years, CABG had 18% more mortality benefit compared to PCI for complex CAD - but not in patients with left main coronary artery disease.
  • Patients with a history of PCI or CABG, acute myocardial infarction, or an indication for concomitant cardiac surgery were excluded.
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51
Q

Cardiac Resynchronization Therapy indication in HF

A
  • for prolonged QRS >150ms with LBBB, LVEF <35 (in some cases up to 50%) and NYHA class II to ambulatory class IV
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52
Q

Features favouring SAVR in AS in patients with increased surgical risk

A

Clinical characteristics

  • STS/EuroSCORE II <4% or EuroSCORE I <10%
  • Age <75 years
  • Suspicion of infective endocarditis

Anatomical

  • Unfavourable access (any) for TAVI
  • Short distance between coronary ostia and aortic valve annulus
  • Size of aortic valve out of range for TAVI
  • Aortic root morphology unfavourable for TAVI
  • Valve morphology (bicuspid, high degree of calcification/abn calcification pattern) unfavourable for TAVI
  • Aortic or LV thrombus

Concomitant Cardiac Pathology

  • Severe CAD requiring CABG
  • Severe primary mitral valve disease, which is surgically manageable
  • Severe tricuspid valve disease
  • Aneurysm of ascending aorta
  • Septal hypertrophy requiring myectomy
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53
Q

Features favouring TAVI in AS in patients with increased surgical risk

A

Clinical Characteristics

  • STS/EuroSCORE II >4% or EuroSCORE I > 10%
  • Presence of other severe comorbid conditions not covered in SCORE
  • Age >75 years
  • Previous cardiac surgery
  • Frailty
  • Restricted mobility and conditions that may affect rehab post procedure

Anatomical

  • Favourable access for transfemoral TAVI
  • Sequelae of chest radiation
  • Porcelain aorta (cannot cross-clamp)
  • Presence of intact CABG grafts at risk when stenotomy is performed
  • Expected patient-prosthesis mismatch
  • Severe chest deformation or scoliosis
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54
Q

Features of constriction

A

Rapid y decent
Square root sign - rapid fall in diastolic pressure initally, rapid rise then plateau
Raised and equalised end-diastolic pressures

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55
Q

Form of dilated cardiomyomathy with best prognosis

A

Peripartum cardiomyopathy

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56
Q

General advice for patients with Eisenmenger Syndrome:

A
  1. Physical activity within symptom tolerance
  2. Avoid dehydration
  3. Avoid exposure to excessive heat
  4. Avoid exposure to high altitude without supplemental O2
  5. Avoid pregnancy and use contraception
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57
Q

Goals in the treatment of AF

A
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58
Q

HASBLED score

A
  • Hypertension (1pt)
  • Abnormal renal or liver function (1pt for each)
  • Stroke (1pt)
  • Bleeding Hx or disposition (1pt)
  • Labile INR if taking warfarin (1pt)
  • Elderly >65 years
  • Drugs and excess alcohol (1pt for each)
    • Drugs includes - aspirin, clopidogrel, ticlopidine, NSAIDs
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59
Q

HLA group associated with anti-HMG CoA reductase autoantibodies

A

HLA DRB1*11:01

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60
Q

How to diagnose isolated, posterior MI (LCA territory)?

A
  • ST segment depression > 0.5mm in leads V1 - V3, to further confirm
  • Check posterior leads V7 - V9 which will have ST elevation >0.5mm
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61
Q

How to diagnose left main coronary artery obstruction

A
  • Presence of ST depression >1mm in 8 or more surface leads AND
  • ST elevation in aVR and/or V1 suggest = multivessel ischaemia or LMCA obstruction
  • these patients are usually haemodynamically unstable
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62
Q

How to manage STEMI if patient is ALREADY on oral anti-coagulation

A
  1. PCI is preferred
  2. Loading aspirin is STILL indicated +
  3. Loading clopidogrel before PCI - Note: Prasugrel and Ticagrelor are NOT recommended
  4. Triple therapy should be considered for 6 months –> followed by oral anticoagulation + Aspirin OR clopidogrel for an additional 6 months. Following this patient should continue on oral anticoagulation
  5. If very high bleeding risk –> consider 1 month of triple therapy followed by dual therapy (anticoagulant + aspirin OR clopigrel) up to 1 year. Then oral anticoagulantion ONLY thereafter
  6. In very high bleeding risk/pt with RFs - consider adding PPI
  7. DAPT can be reduced to 6 months in very high bleeding risk
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63
Q

How to pick a stress test

A

For unclear reasons LBBB pathology favours pharmacological stress testing over exercise

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64
Q

Indication for ICD in heart failure

A
  • *Symptomatic CCF**
    1. NYHA II or III AND
    2. LVEF <35% despite optimal medical therapy for >3 months AND
    3. It’s been > 6weeks after MI AND
    4. Patient is expected to survive at least 1 year with good functional status

Asymptomatic CCF
1. Systolic dysfunction: LVEF<30% of ischaemic origin, who are at least 40 days after acute MI
2. OR asymptomatic, non-ischaemic dilated cardiomyopathy LVEF <30% who recieve optimal medical therapy
To prevent sudden death and prolong life

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65
Q

Indications for cardiac transplant in heart failure

A
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66
Q

Indications for CRT

A
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67
Q

Indications for early invasive strategy (<24h) in NSTEACS

A
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68
Q

Indications for emergency CABG

A
  1. Unsuitable anatomy for PCI + large myocardial area in jeopardy OR cardiogenic shock
  2. Mechanical MI complications
  3. Failed PCI or occlusion not amenable to PCI
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69
Q

Indications for ICDs in heart failure

A
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70
Q

Indications for immediate invasive strategy (<2h) in NSTEACS

A
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71
Q

Indications for intervention in severe aortic stenosis

A
  1. All symptomatic patients
  2. All symptomatic patients with severe low-flow, low-gradient AS with reduced EF and evidence of flow reserve
  3. All symptomatic patients with severe low-flow, low-gradient AS with reduced EF and NO evidence of flow reserve but CT calcium score confirms severe aortic stenosis
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72
Q

Indications for invasive strategy (<72h) in NSTEACS

A
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73
Q

Indications for oral anticoagulation in AF for men and women

A
  • Men - CHA2DS2VASc >2, consider if score = 1
  • Women - CHA2DS2VASc > 3 (2 in addition to being female), consider if score = 2
  • VKA (Warfarin) are recommended in moderate-severe mitral stenosis OR mechanical heart valves (Valvular AF)
  • NOACs are preferrable to VKAs if they can be used
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74
Q

Indications for rescue PCI post fibrinolysis

A

<50% ST resolution at 60 - 90min OR at any time if

  • haemodynamically or electrically unstable OR
  • worsening ischaemia

(Aim to do standard, non rescue angio and PCI, 2 - 24 hours post successful fibrinolysis if indicated)

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75
Q

Indications for Revascularisation in Stable CAD

A
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76
Q

Indications for surgery in severe chronic primary mitral regurgitation with symptoms

A
  1. LVEF >30% = surgery, if not then
  2. Refractory to medical therapy and durable valve repair is likely and low comorbidity = surgery
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77
Q

Indications for surgery in severe chronic primary mitral regurgitation without symptoms

A
  1. LVEF <60% or LVESD >40mm, if not then:
  2. New onset AF or SPAP >50mmHg, if not then:
  3. High likelihood of durable repair, low surgical risk and presence of risk factors
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78
Q

Indications for tricuspid valve surgery

A
  1. Symptomatic patients with severe TS or TR
  2. Severe TS or TR (primary or secondary) undergoing left sided valve intervention
  3. Consider surgery in patients with moderate primary or secondary TR undergoing left sided valve intervention
  4. Consider surgery in asymptomatic/mildly symptomatic patients with severe isolated primary tricuspid regurgitation and progressive RV dilatation or deterioration of RV function
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79
Q

Inherited cardiomyopathies, channelopathis, and pathways associated with AF

  • WPW gene mutation
  • Oram Holt gene mutation
A
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80
Q

Interventions with a mortality benefit in asymptomatic CCF - delays onset of HF and prolongs life

A
  1. BP control
  2. Statins - in pts with or high risk for CAD, regardless of systolic dysfunction
  3. Smoking cessation and alcohol reduction (in abusers)
  4. Weight loss in the obese
  5. Empagliflozin in T2DM pts
  6. ACEIs - if asymptomatic LV systolic dysfuction. Mortality benefit only on those post MI
  7. Beta blockers - asymptomatic LV systolic dysfunction in PHx of MI
  8. ICD (details on other flash card)
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81
Q

JVP waveform - just learn and copy

A
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82
Q

Key ECG features in WPW
AND
Most common accessory pathway locations

A

ECG
1. Shortened PR interval
2. Widened QRS complex due to delta wave - slurred upstroke in the QRS complex
Location
Left lateral > posteroseptal > right anteroseptal > right lateral

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83
Q

Key lifestyle interventions in coronary artery disease (5)

A
  1. Smoking cessation - most cost effective secondary prevention measure, 36% reduced mortality
  2. Optimal blood pressure control
  3. Diet advice - Mediterranean diet
  4. Weight control
  5. Encourage physical activity
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84
Q

Key Time Intervals in STEMI management

A
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85
Q

Lipids and their related apoproteins

A
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86
Q

Long-term medical management of NSTEACS

A
  1. High intensity statin
  2. Aspirin +P2Y12 inhibitor (DAPT for 1y, aspirin life long)
  3. ACEI/ARB - if LV systolic dysfunction, HF, HTN, DM
  4. Beta blockers - if LVEF <40% (unless contraindicated)
  5. MRA - if LVEF <40% and HF, or DM post NSTEACS
  • eplerenone in particular shown to reduce morbidity and mortality
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87
Q

Long-term RATE control of AF

A
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88
Q

Main Causative Genes in Hypertrophic Cardiomyopathy

A

Boxed - responsible for 70% of positive gene tests

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89
Q

Main long term issue post TOF repair

A

Pulmonary Regurgitation

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90
Q

Main Targets and Goals in CVD

A
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91
Q

Management of aortic regurgitation
-What is the strongest indicator for surgery

A
  1. enlargement = aortic root > 55mm (>50mm in Marfans/bicuspid valve + RFs or coarctation, >45mm in Marfans +RFs)
  2. Follow up yearly, if worsening then 3-6months
  3. The presence of symptoms is the strongest indication for surgery, and LVEF <50% and/or ESD >50mm
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92
Q

Management of clinically significant mitral stenosis (MVA <1.5cm2)

A
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93
Q

Management of coarctation of the aorta

A
  • *1. Diuretics for CCF and Rx HTN
    2. Surgical repair**
  • acute reduction of pressure gradient to <20mmHg across lesion = successful treatment
  • *Indications for surgery**
  • Peak to peak coarctation gradient >20mmHg
  • Peak to peak coarctation gradient <20mmHg with radiographic evidence of significant coarctation
  • Non-invasive pressure difference >20mmHg between upper and lower limbs
  • Upper limb HTN with or without Sx
  • Significant LVH
  • Pathological BP response during exercise
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94
Q

Management of HTN

A
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95
Q

Management of left sided non-obstructive mechanical prosthetic thrombosis

A
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96
Q

Management of left-sided obstructive mechanical prosthetic thrombosis

A
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97
Q

Management of NSTEACS in non-valvular AF

A
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98
Q

Management of recent onset AF

A
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99
Q

Management of severe AS

A
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100
Q

Management of severe chronic primary mitral regurgitation

A
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101
Q

Management of tricuspid regurgitation

A

TA = triscuspid annulus. Dilated when ≥ 40 mm or > 21 mm/m2

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102
Q

Mechanism behind WPW

A
  • Normal - electricity goes atria –> ventricles via AV-His-Purkinje
  • WPW - accessory pathway which is faster = ventricles activated early (preexcitation)
  • =short PR interval and delta wave form
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103
Q

Medication therapy post STEMI

A
  1. Aspirin - indefinitely in all patients
  2. DAPT (Aspirin + ______)
    - if having PCI –> continue up to 12 months
    - Clopidogrel is favoured if patient had fibrinolysis prior to PCI
    - Otherwise Ticagrelor or Prasugrel should be used if not contraindicated
    - This can be shortened to 6 months if high bleeding risk (reduces bleeding Cx with nil trade-off in ischaemic events)
  3. Add PPI if PHx of GI bleed
  4. If LV thrombus –> anticoagulate with warfarin and bridging clexane
  5. Beta blockers if LVEF <40% if not contraindicated (acute heart failure, haemodynamic instability, higher degree AV block, obstructive airway disease)
  6. High dose statin - irrespective of lipid levels
    - aim LDL-C <1.8mmol/L or 50% reduction if LDL-C 1.8 - 3.5mmol/L
  7. ACEI in essentially all patients, especially if LVEF <40% OR CCF
    - also recommended in HTN, DM
    - ARB (Valsartan) is an alternative if unable to tolerate due to symptoms
  8. MRA if LVEF <40%, CCF or DM, already on ACEI and BB
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104
Q

Modified European Heart Rhythm Association (EHRA) Symptom Scale

A
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105
Q

Most common cause of dilated cardiomyopathy

A

Idiopathic

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106
Q

Most common ECG change in congenital myotonic dystrophy

A

PR prolongation

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107
Q

Most common genetic mutation associated with dilated cardiomyopathy

A

Lamin A/C gene

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108
Q

Most common underlying trigger of AF

A

Rapid firing from pulmonary veins

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109
Q

MS Grading of Severity

A
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110
Q

Mutation of this protein is associated with dilated cardiomyopathy

A

Titin

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111
Q

Name the what happens to pre-load, after-load, cardiac output in:
Cardiogenic Shock
Hypovolaemic Shock
Distributive Shock

A
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112
Q

Normal ECG changes with exertion (5)
Abnormal ECG changes with exertion (4)

A
  • *Normal**
    1. J point depression
    2. Up-sloping ST segments
    3. P wave amplitude increase
    4. R wave amplitude increase
    5. QT interval shortens
  • *Abnormal**
  • down sloping ST segment >1mm
  • ST elevation >1mm
  • U wave inversion
  • T wave changes
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113
Q

Old vs New Troponins

A
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114
Q

Old vs New Troponins

A

Route: PO
-Irreversibly (clopidogrel, prasugrel) or reversibly (ticagrelor, cangrelor) inactivates platelet P2Y12 receptors and inhibits ADP-induced platelet aggregration.
-Ticagrelor has the longest half life of 6 to 12 hours
-Cangrelor has the shorted half life of 5 to 10 min
Note Ticagrelor is a non-thienopyridine P2Y12 inhibitor
-is a nucleoside analogue, BD dosing

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115
Q

Pacemaker action potential (draw)

A
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116
Q

Pacemaker Nomenclature

A
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117
Q

Pathogenesis of CAD

A
118
Q

Patients potentially eligible for implantation of LV assist device

A
119
Q

Patterns of AF

A
120
Q

PCI Questions

  • Stenting or balloon angioplasty?
  • DES or BMS?
  • Radial or femoral access?
  • Thrombus aspiration? Yes or No
  • Do non-IRA lesions? Yes or No
A

IRA = infarct related artery

121
Q

PCI vs CABG

A

PCI

  • faster = faster revascularisation
  • lower risk of stroke
  • no need for cardio-pulmonary bypass
  • preferable in single vessel disease

CABG

  • more likely to offer complete revascularisation in advanced multivessel CAD
  • useful if PCI fails or anatomy unsuitable for PCI
122
Q

PCI vs CABG in stable CAD

A
123
Q

PFO vs ASD

A
  • PFO - failure of normally developed valve-like structures to fuse and close the interatrial septum in early infancy
  • ASD - true congenital defect in which abnormal development results in missing tissue of the interatrial septum that causes blood flow between the atria
124
Q

Preventative strategies for AF

A
125
Q

Principles of Reperfusion in STEMI

A
  • Reperfusion is indicated in ALL patients with symptoms of ischaemia of <12 hours duration and persistent ST elevation
  • PCI is preferred over fibrinolysis (if can be done in <120min)
  • Perform primary PCI if STEMI diagnosed within 12 hours of symptom onset if it can be done in <120min
  • If cannot have PCI within 120min –> FIBRINOLYSE (preferably pre-hospital if no CI) and transfer to cardiac centre
  • If patient presented >12 hours post symptoms, PCI is still indicated if any of:
      1. Ongoing ischaemia symptoms
      1. Haemodynamic instability
      1. Life-threatening arrythmia
  • IF not ST elevation, PCI is still indicated if any of:
      1. Haemodynamic instability or cardiogenic shock
      1. Recurrent or ongoing CP refractory to medical Rx
      1. Life-threatening arrhythmias or cardiac arrest
      1. Mechanical complications of MI
      1. Acute heart failure
      1. Recurrent, dynamic ST segement/T wave changes esp if tranisent ST- elevation
  • In asymptomatic patients, routine PCI of occluded IRA > 48 hours after onset is not indicated
126
Q

Prosthetic valves
-Mechanical vs Bioprosthetic

A

Similar

  • survival
  • rate of valve thrombosis and TE

Mechanical

  • higher rates of bleeding
  • avoid if CI to long term anticoagulation

Bioprosthetic

  • higher rates of reintervention
  • consider if life expectancy < durability of prosthesis or low risk for repeat interventions
  • preferred in pregnant people
  • preferred if high bleeding risk, unable/unwilling to have anticoagulants
127
Q

Protective Genetic Factors for CAD

A
128
Q

Rate vs Rhythm control in AF
-why might physician chose rhythm control?

A
  • Main reason to pursue rhythm control is to improve symptoms
  • NO MORTALITY BENEFIT
129
Q

Recommendations for antithrombotic therapy in patients with mechanical prosthetic heart valves/valve repair

A
  1. Oral anticoagulation using VKA is recommended for all patients with bridging UFH or LMWH if VKA needs to be interrupted
  2. Consider adding aspirin post thromboembolism or if concomitant atherosclerosis
130
Q

Recommendations for inherited cardiomyopathies

A
131
Q

Recommendations for platelet inhibition in NSTEACS

A
  1. Aspirin (150-300mg loading, 75-100mg daily maintenance)- all patients (w/o CI) regardless of Rx strategy, long term
  2. P2Y12 inhibitor - all patients, for 12 months (unless CI)
  • Ticagrelor (180mg loading, 90mg BD maintenance) if mod-high risk of ischaemic events regardless of initial Rx strategry
  • Prasugrel (60mg loading, 10mg daily maintenance) who are proceding to PCI if no contraindication
  • Clopidogrel (300-600mg loading, 75mg daily) in patients who cannot have ticagrelor or prasugrel
  • Add PPI to DAPT if high risk of GI bleeding
132
Q

Recommendations for the management of HF post NSTEACS

A
  • *1. ACEI (or ARB) - if LVEF <40%**
  • reduces risk of death, recurrent MI, hospitalisation for HF
  • *2. Beta blocker - if LVEF <40%**
  • reduces risk of death, recurrent MI, and hospitalisation for HF
  • *3. ADD MRA - if despite ACEI/ARB + BB and LVEF <35%**
  • MRAs (preferably eplerenone) reduce risk of CV hospitalisation and death if LVEF <40%
  • all MRAs reduce risk of death, and hospitalisation for HF
  • *4. Device therapy (CRT-D or ICD) -** for symptomatic patients with severe LV dysfunction (<35%) despite optimal medical therapy >40 days after acute event and without options to revascularise.
  • Patients should be expected to survive >1year with good functional status
133
Q

RELATIVE contraindications for RHC

A
  • Coagulopathy, INR >1.5
  • Thrombocytopenia
  • Electrolyte disturbance
  • Severe acid-base disturbance
134
Q

RELATIVE contraindications to fibrinolytic therapy in STEMI (8)

A
  1. TIA in the preceding 6 months
  2. Oral anticoagulant therapy
  3. Pregnancy or being within 1 week post-partum
  4. Refractory HTN (SBP >180mmHg or DBP >110mmHg)
  5. Advanced liver disease
  6. Infective endocarditis
  7. Active peptic ulcer
  8. Prolonged or traumatic resuscitation
135
Q

Resistant HTN

A
  • Hypertension is defines as resistant to treatment when the recommended treatment strategy fails to lower office SBP and DBP values to <140mmHg and/or <90mmHg, respectively, and the inadequate control of BP is confirmed by ABPM and HBPM in patients who adherence to therapy has been confirmed.
  • The recommended treatment strategy should include appropriate lifestyle measures and treatment with optimal or best-tolerated doses of three or more drugs, which should include a diuretic, typically an ACE inhibitor or and ARB and a CCB.
  • Pseudo resistant hypertension and secondary causes of hypertension should also have been excluded.
136
Q

Risk of cardiac cath and angiography

  • What is the most common risk
  • What is the risk of death
A
137
Q

Risks and Benefits of Transradial access for PCI

A
  • Longer times - not real, reflects operator experience with newer technique
  • Also radial a. is a conduit for potential CABG surgery
138
Q

Role of medical therapy in aortic stenosis

A
  • NO medical therapy for aortic stenosis can imrove outcome compared to natural history
  • Treat co-existing disease
139
Q

Role of PCI in stable CAD
-does it improve angina

A

Conflicting studies. FAME 2 vs in contrast with COURAGE trial which did not show a difference

FAME 2

  • Among patients with stable CAD with FFR <0.80, PCI reduces the composite rate if death, non-fatal MI and urgent revascularisation - compared to OMT alone, driven primarily by a reduction in urgent revascularisation

COURAGE trial

  • In patients with stable angina despite medical therapy, PCI does not improve angina as measure by treadmill exercise time, validated questionaires. DID NOT improve overall quality of life
140
Q

Secondary causes of dyslipidaemia (9)

A
  1. Hypothyroidism - primarily LDL
  2. Nephrotic syndrome
  3. Diabetes
  4. Cholestatic liver disease
  5. Chronic kidney injury
  6. Obesity
  7. Cigarette smoking
  8. Alcohol excess
  9. Drugs - BB, thiazide, PO oestrogen, protease inhibitors, anti-psychotics (olanzapine, clozapine)
141
Q

Sick Sinus Syndrome (AKA sinus node dysfunction)

A
142
Q

Side effects of Class I anti-arrhythmic drugs/Na channel blockers

A
143
Q

Skeletal muscle AP vs Cardiac Muscle AP

A
144
Q

STEMI - approach

A

If Primary PCI capable centre - aim PCI <60min

145
Q

Stressors used in Myocardial Perfusion imaging

A
146
Q

Strongest predictors of familial hypercholesterolaemia

(Dutch criteria)

A
  1. LDL >8.5 + positive gene mutation
  2. Tendon Xanthomata
147
Q

Sudden cardiac death in WPW

A

VF develops during an episode of AF. There may be a higher likelihoof of SCD in:

  • Younger patients
  • Males
  • Inducible AVRT or AF during EP study
  • Multiple accessory pathways
  • Short refractory period of accessory pathway
  • Short pre-excited RR interval during AF
148
Q

The role and goal of lipid lowering therapy in ACS

A

Give to ALL patients regardless of lipid profile long term

  • Ezetimibe can be replacement/added if cannot have statin or not achieving goal despite maximal statin therapy
  • Aim LDL-C <1.8mmol/L or 50% reduction if baseline LDL is 1.8 to 3.5mmol/L
149
Q

Thrombus aspiration - should it be done in STEMI?

A
  • NO
  • No benefit + possible increased risk of stroke (TOTAL trial)
150
Q

TIMI flow grading

A

AKA thrombolysis in myocardial infarction (TIMI) flow grading

  • Grade 0 - no flow, no perfusion i.e. complete occlusion of IRA
  • Grade 1 - some flow distal to obstruction but nil perfusion of distal coronary bed
  • Grade 2 - perfusion of entire infarct vessel into distal bed, but flow is delayed
  • Grade 3 - normal flow and full perfusion
151
Q

Timing of Invasive Strategy in NSTEMI

A
152
Q

Treatment of HFpEF

A
  • NO treatment has convincingly shown to improve morb/mortality in HFpEF
  • However Spironolactone reduces hospitalisations
153
Q

Treatment of ischaemia in NSTEACS

A
  • Nitrates - sublingual or IV to relieve angina
  • Beta blockers - reduce myocardial O2 demand by reducing HR, BP and myocardial contractility. Check contraindications
154
Q

Treatment of Pericarditis

A
155
Q

Treatment of PFO

A
  • Asymptomatic - nil treatment
  • TIA/cryptogenic stroke - aspirin, consider closure
156
Q

Treatment of Stable Angina in symptomatic HFrEF

A
  • Step 1. Betablocker
  • Step 2 (or if Beta-blocker contraindicated): Ivabradine (SR + if HR >70)
  • Step 3: for additional Sx relief
    • Short >long acting nitrates
    • Trimetazidine
    • Amlodipine, Nicorandil, Ranolazine (if unable to tolerate BB)
  • Step 4: Myocardial revascularisation
157
Q

Treatment targets for HTN

A
  • Uncomplicated disease - 140/90
  • Associated condition or end organ damage - 130/80
  • Associated conditions include - CAD, DM, albuminuria, stroke, TIA
158
Q

Tuboeruptive xanthomas

A

Type III hyperlipoproteinaemia

159
Q

Types of myocardial infarction

A
160
Q

Types of Troponin

A

Troponin I is the most specific to cardiac muscle

161
Q

Valvular vs non-valvular AF

A
  • Valvular AF - AF patients with either rheumatic heart disease or mechanical heart valves
  • Non-valvular AF - all other AF patients
  • This terminology is going out of use
162
Q

Valvular heart disease lesions in which pregnancy is discouraged

A
  1. Severe mitral stenosis
  2. Severe symptomatic aortic stenosis and with aortic diameter >45mm in Marfan syndrome or >27.5mm/m2 in Turner syndrome
163
Q

Wellen’s syndrome and its significance

A

Patient has

  • Hx of CP with a normal looking ECG
  • minimally elevated cardiac enzymes
  • No pathological precordial Q waves or loss of R wave progression
  • Pain free ST elevation in V2 and V3 (minimal)
  • Pain free biphasic (up then down, type A - 25%) or symmetrical deep T wave inversion (type B - 75%) in V2-3 (may extend V1 - 6)
  • High risk of extensive anterior MI in the next few days - weeks
  • HIGHLY specific for critical stenosis of LAD
  • Often require invasive Rx, do poorly with medical Mx, and have high risk of arrest/MI with inappropriate stress testing
164
Q

What constitutes significant ST elevation?

A
  1. >2 contiguous leads with ST elevation >2.5mm in men <40years
  2. >2 contiguous leads with ST elevation >2mm in men >40years
  3. ST elevation >1.5mm in women in leads V2 to V3
  4. >2 contiguous leads with ST elevation >1mm in women in other leads (in the absence of LVH or LBBB)
165
Q

What is the benefit of spironolactone in HFpEF?

A
  • Reduced hospitalisations
  • but NO mortality benefit
  • Source: TOPCAT trial
166
Q

What is the best access for PCI and why?

A

TRANS-RADIAL
Benefits of transradial

  • Less short term adverse clinical events
  • Less cardiac death
  • Lower all cause mortality
  • Less bleeding
  • Less access site complications

Similar

  • Short term myocardial infarction

Negatives of transradial

  • Lower procedural success rate
167
Q

What is the GRACE score?

A

Global Registry of Acute Coronary Events score predicts cardiac mortality at 6 months following acute coronary syndrome

Takes into account pts age, HR, systolic BP, creatinine, cardiac arrest, ST changes, troponins and Killip class of sx

168
Q

What is the role of CK-MB in NSTEMI?

A

While troponin is more sensitive and specific c/f CK, CK-MB, myoglobin…
CK-MB, given it’s rapid decline after MI c/f troponin - should be useful in detecting early reinfarction

169
Q

What needs to be checked in inferior MI? eg STEMI of II, III and AVF

A

Check RIGHT precordial leads V3R and V4R to identify concomitant RV infarction
-These leads will have ST elevation in RV infarction

170
Q

When to Initiate BP medication in HTN

A
171
Q

When to start OAC post acute TIA/Stroke

A
172
Q

Which protein is the major component of active cardiac relaxation?

A

Tropomyosin

173
Q

Who does better with CRT? (cardiac resynchronisation therapy aka biventricular pacing)

A
174
Q

Xanthoma tendinosum

A

Type II hyperlipoproteinaemia

175
Q

STEMI

  • sequence of ECG changes AND
  • sites of infarction based on leads affected
A
176
Q

What are the factors affecting myocardial demand? Is there a calculation that can give a proxy?

A
  • HR
  • SBP
  • Myocardial wall stress
  • Myocardial contractility

Double Product: HR x SBP

177
Q

What are the factors affecting myocardial supply?

A

Coronary artery resistance (diameter and tone)
Collateral flow

HR
Perfusion pressure: Aorta -> coronary artery; coronary artery -> endocardial capillaries

178
Q

What is ‘optimal medical therapy’ of stable IHD?

A

Management of risk factors with a combination of medications and lifestyle:

  • Aspirin
  • Statin
  • Antianginals

Diabetes management
Hypertension management
Smoking cessation
Weight management/exercise

179
Q

What is the first line medication for acute angina?

A

Sublingual GTN

180
Q

What is the first line medication for the chronic management of angina? Is there a difference between agents?

Is there a survival benefit? In which patients?

A

Beta Blockers

No evidence supporting survival benefit in stable angina.
No difference between agents in stable angina.

  • Agents can be chosen based on their specific pharmacokinetic/dynamic properties

Evidence of a survival benefit in patients who’ve had a recent MI
OR
In CCF with LVEF <40% with metoprolol XR (succinate), bisprolol, carvedilol, nebivolol

181
Q

What is the second line therapy for stable angina? What about other options?

A

Calcium channel blockers in addition to, or replacing, beta blockers (if they’re not tolerated or contraindicated)

  • Diltiazem/verapamil SR or 2nd generation dihydropyridine (amlod/felod) preferred as they have similar outcomes
  • Short acting dihydropyridines, especially nifedipine has been shown to have increased CV mortality

Long acting nitrates

    • Improve exercise tolerance, time to angina, and STD during exercise testing
    • BB/CCBs show better antianginal/ischaemic effects with chronic nitrates than without

Ranolazine

    • Late Na channel blocker, decreases intra-myocyte Ca
    • Multiple trials showing benefit over placebo: MARISA, CARISA, TERISA, ERICA
    • Lengthens QTc so contraindicated with pre-existing long QT or other QT drugs

Ivabradine

    • Not recommended in stable angina without CCF
  • Patient must have a documented left ventricular ejection fraction (LVEF) of less than or equal to 35%
182
Q

What are the options for anti-platelet therapy with GI bleed?

A

Restarting aspirin with a PPI significantly reduces risk of re-bleed at 1yr compared to replacing with clopidogrel
- 0.7-1.6% compared to 8.6%

183
Q

What is the SBP goal in patients with CVD? Does the agent matter? In which populations?

A

SBP goal should be 120-130mmHg in patients with CVD

    • SPRINT and ACCORD pooled data show RR 0.81 favouring intensive treatment

A 2011 meta-analysis looking at all classes of antihypertensives showed no difference between mortality/MI using all agents vs solely ACEI/ARB.

ACEI/ARB show specific benefit in CCF, prior MI, and proteinuria in CRF/CKD, where they should be first line

184
Q

Is smoking cessation of benefit in reducing risk of CVD? Does risk ever return to baseline? When? So the benefits persist across age groups?

A

Yes

  • reduction in events 7-47% with cessation

RR of CV events returns to baseline ~3yrs after cessation

The benefits of cessation are equivalent regardless of age

185
Q

Does lipid management alter outcome in stable CVD? Does intensity matter? In which populations?

A
  • *Yes**
  • Multiple studies showing benefit vs placebo
    • Heart Protection Study (HPS) 13% reduction all cause
    • Scandinavian Simvastatin Survival Study (4S) RR 0.70 all cause
    • Long-Term Intervention with Pravastatin in Ischaemic Disease Study (LIPID) RR 0.78
    • The Cholesterol and Recurrent Events trial (CARE) reduction in MI, PCI, CABG but not mortality

Trend toward significance favouring intensity in patients with ACS

    • PROVE IT-TIMI 22
    • Phase Z of A to Z trial
  • *No benefit for intensive therapy in patients with stable CVD**
  • Treating to New Targets (TNT)
  • Incremental Decrease in END Points Through Aggressive Lipid Lowering (IDEAL)
  • Study of Effectiveness of Additional Reduction in Cholesterol and Homocysteine (SEARCH)
186
Q

Is BMI an important risk factor for CVD in the elderly?

A

No, it does not appear to be in patients >75yrs

187
Q

What waist circumference should trigger recommendation of lifestyle changes?

A

>89cm in women
>102cm in men

188
Q

In what ways is weight loss beneficial to risk factors for CVD?

A
  • Decrease BP
  • Decrease incidence of diabetes and insulin resistance
  • Improve lipids
  • Reduce CRP
  • Improve endothelial function
189
Q

Does intensive glycaemic control improve CVD outcomes? Does it differ depending on chronicity of diabetes or type?

A

Intensive glycaemic control improves CVD outcomes in T1DM as demonstrated in DCCT/EDIC

Benefit not clear in T2DM

    • UKPDS in newly Dx T2DM showed lasting benefit with tight glycaemic control despite difference in HbA1c lost at 1yr
    • Action in Diabetes and Vascular Disease: Preterax and Diamicron MR Controlled Evaluation (ADVANCE) in long standing T2DM showed
    • No difference in CVdeath, nonfatal MI, nonfatal stroke, nor all-cause mortality
    • Increased severe hypoglycaemia in the intensive arm
    • Action to Control Cardiovascular Risk in Diabetes (ACCORD) showed increased mortality with tight control
190
Q

Is exercise of benefit in patients with cardiovascular disease (CVD)? Are there recommendations?

A

Yes - RR 0.72 for all cause mortality with exercise rehabilitation in CVD

ACC/AHA recommends 30-60mins of moderate intensity exercise 5-7 days/week

191
Q

What are the indications for angiography in patients with stable CVD?

A

Angina that significantly interferes with lifestyle despite maximum tolerable medical therapy

Patients with high risk criteria or selected patients with intermediate risk criteria on non-invasive testing, regardless of angina severity

192
Q

What types of cardiac stress tests are available? What are the broad risk stratifications?

A
  • Stress ECG
  • Radionucleotide Myocardial Perfusion Scan
    • exercise and pharmacologic tests have similar risk stratification ability
  • Stress Echocardiography

Broad risk stratification:

  • Low, Intermediate, and High
193
Q

In which patient populations does CABG confer a survival benefit?

A

Left main CAD

Three vessel CAD, particularly with LVEF <40%

Two vessel CAD with >75% stenosis in proximal LAD

194
Q

Does revascularisation improve angina compared to optimal medical therapy?

A

Yes

The Medicine, Angioplasty, or Surgery study (MASS-2) showed:
- 88% CABG, 79% PCI, 46% medical therapy free of angina at 1yr

195
Q

Does PCI affect survival compared to medical therapy in stable CVD?

A

No

Clinical Outcomes Utilising Revascularisation and Aggressive Drug Evaluation trial (COURAGE) is the landmark study

  • optimal medical therapy vs optimal medical therapy with BMS
  • *- no reduction in death, MI, or other major CV event**

There may be benefit in a more severe subset of CVD or with the newer generation of DES, but this is not yet clear

196
Q

In which patients with stable CVD is PCI indicated?

A

Those in whom CABG offers a survival advantage but cannot have it

Those dissatisfied with QOL due to symptoms or medication side effects

197
Q

By which enzyme system are the majority of statins metabolised?

A

CYP450

198
Q

Which statin carries the lowest risk of statin myopathy? Why?

A

Pravastatin

Hydrophilic and not metabolised via the CYP450 pathway

Hydrophilic statins less likely to cause
- pravastatin, rosuvastatin, fluvastatin

199
Q

When does statin myopathy usually present? Can it present late?

A

Usually within the first month.

Can present up to a few years after commencent.

200
Q

Does statin induced myopathy resolve? Over how long? Is it ever safe to restart statins?

A

Yes. Usually over weeks to months.

Modifiable risk factors must first be addressed: vit D, drug interactions, or hypothyroidism.

It is safe to restart on the lowest risk statin (pravastatin), with careful monitoring, once the myopathy has completely resolved.

It’s not recommended to restart in those who’ve suffered statin induced rhabdomyolysis due to the risk of recurrence.

201
Q

Describe the exogenous pathway of lipid metabolism

A

Ingestion: 95% as TGs, remainder as mixture

Digestion: TGs digested by the stomach and duodenum into MGs and FFAs by gastric lipase; then emulsified by peristalsis and pancreatic lipase.

Absorption: MGs, FFAs, free chol solubilised by bile acid micelles and moved to villa for absorption

Store: FFAs assembled into chylomicrons and transported to adipose/muscle where ApoC-II activates endothelial LPL to convert TGs into FFAs and glycerol for storage.

Remaining chol rich chylomicrons proceed to liver to be cleared.

202
Q

Describe the endogenous lipoprotein metabolism pathway

A

VLDL: Contains ApoB, formed to transport excess TGs and FFAs. Surface ApoC-II activates endothelial LPL to break down into FFAs and glycerol for storage in tissue

IDL: Remnant of processing of VLDL and chylomicrons. Cleared by liver or metabolised by hepatic lipase into LDL

LDL: Cholesterol rich. Cleared by process mediated by ApoB and hepatic LDL receptors. Remainder cleared by non-hepatic scavengers, mostly monocytes, leading to macrophage intrusion into arterial endothelium.
Small, dense LDL is rich in cholesters, stays circulating longer due to decreased affinity for hepatic receptors, enhanced oxidisability, and greater penetrance of endothelium

HDL: Free chol in cells combines with ApoA-I, mediates by ATP-binding cassette transporter to produce HDL. Esterified by lecithin-cholesterol acyl transferase (LCAT) to mature HDL

Obtain chol from tissues and lipoproteins for transport to cells, lipoproteins (using CETP), the liver (clearance).

203
Q

What lipid abnormalities typically accompany ETOH abuse?

A

Moderate drinking protective

Heavy drinking associated with increased TGs and HDL, reduction in LDL

204
Q

Draw a picture of the typical cardiac action potential and describe the ion influx/efflux associated.

A
205
Q

What is Beck’s Triad? What is it suggestive of?

A
  • Muffled heart sounds
  • Elevated JVP
  • Hypotension

Cardiac tamponade

206
Q

What aspect of NSAID action confers GI risk? What can be done to ameliorate this?

A

COX-1 inhibition decreases production of mucosal protective prostaglandins.

Choose a COX-2 selective NSAID

Use a PPI

207
Q

Which NSAID confers the least risk of cardiovascular disease? Why?

A

Naproxen

Completely non-selective COX-1/2 inhibitor
Near completely inhibits production of thromboxane A2, a potent vasoconstrictor and platelet aggregator

208
Q

How is atrial flutter categorised?

A
  • *Type 1**
  • Typical involves the cavotricuspid isthmus and is counterclockwise (up in V1; down in II, III, aVF); reverse typical is clockwise
  • 250-350bpm
  • *Type 2**
  • Classic undulating ECG pattern without typical pattern not localisable to high right atrium
  • >350bpm
209
Q

What are the management goals in atrial flutter?

Briefly expand on each of them

A

Control ventricular rate

  • Block AV with non DH CCB
  • Decrease sympathetic BB
  • Increase parasympathetic with Digoxin
  • Amiodarone

Reversion to sinus rhythm

  • DC cardioversion preferred
  • Urgent if HR >150bpm and unstable or with pre-excitation pathway
  • Drugs an option if DC can’t be done
  • Ibutilide best, dofetilide, amiodarone, Class 1A, Class 1C

Maintenance of sinus rhythm

  • Radiofrequency ablation best (92% successful, 80% sinus at 1yr)
  • Fibrillation ablation superior in those with both flutter and fib
  • Drugs an option if not possible
  • Amiodarone, flecainide with AV blocker, sotalol, dofetilide

Prevention of embolisation

    • Cardiovert ok if <48hrs
    • Anticoagulate for >3 weeks or TOE prior to cardiovert if >48hrs then anticoagulate for at least 4 weeks
    • Follow CHADS-VASc recommendations as if AF
    • 0 don’t, 1 consider, >=2 do
    • NOAC better than warfarin unless specific issue (ESRF, morbid obesity, valvular disease)
210
Q

What is the CHADS-VASc score? What are the rough rates of thromboembolism book-ends?

A

Stroke and age are significantly stronger predictors than hypertension or diabetes
- vascular disease also at lower end of risk range

Stroke risk without anticoagulation:

Anticoagulation reduces the risk of ischemic stroke (and other embolic events) by about two-thirds irrespective of baseline risk

211
Q

What is the HAS-BLED score? What are the rough book-ends for risk?

A
212
Q

What is pulsus alternans? What is it indicative of?

A

Alternating strong and weak beats.

Indicative of severe LVfailure.

  • EF reduced such that every second beat has greater filling and more advantageous location in frank-starling curve, resulting in higher EF%
213
Q

List the common JVP waveform abnormalities, their vague appearance, and their differentials

A
  • *A wave:**
    • Absent: AF,* sinus tachy
  • Prominent: 1st degree AV block
  • Large (increased atrial contraction pressure): TS, RA myxoma, pulm htn, pulm stenosis
  • Decreased complaince of RV
  • Occur on every beat
  • Cannon (atria contracting against closed tricuspid valve): AV dissociation, VT
  • Don’t occur every beat
  • *X descent: (RA relaxation)**
  • Absent: TR
  • Prominent: Conditions causing large A wave
  • *Y descent: (ventricular filling)**
  • Absent: Tamponade
  • Slow: TS, RA myxoma
  • Rapid: Constrictive pericarditis, severe RHF, TR, ASD
  • *CV wave:**
  • Increased atrial filling during systole
  • TR, contrictive pericarditis
214
Q

What are the 5 major and 4 minor manifestations of Rheumatic Fever? What constitutes an episode, acute or recurrent?

A
  • *Mitral involvement** in nearly all with valvular disease, aortic 20-30%
  • Early MR/AR, late MS/AS
215
Q

Diastolic heart murmur - Mitral Stenosis

A

Auscultation

  • Loud S1
  • Loud P2 if associated with pulm htn
  • Opening snap following S2 (before S3)
  • Low pitched, rumbling diastolic murmur best heard in left lateral position (late in mild; early in severe)

Signs

  • Tachypnoea, peripheral cyanosis
  • Palpable S1, RV heave
  • Large A wave on JVP

Symptoms

  • Dyspnoea, orthopnoea, PND, ascites, oedema

Causes

  • Rheumatic heart disease, congenital parachute valve (rare)
216
Q

Diastolic heart murmur - AR

A

Aortic Regurgitation
Auscultation

  • Soft A2
  • Decrescendo, high pitched diastolic murmur immediately following S2, extending into diastole
  • Loudest at 3rd/4th left parasternal
  • systolic AS murmur usually accompanies

Signs

  • Collapsing pulse (waterhammer)
  • Wide pulse pressure
  • Prominent carotid pulsations
  • Displaced, hyperkinetic apex

Symptoms

  • Exertional dyspnoea, fatigue, angina, palpitations

Causes

  • Congenital
  • Rheumatic heart disease
  • IE
  • Seronegative arthropathy
  • Ankylosing spondylitis most common
  • Marfans
  • Aortic dissection/root dilatation

Tricuspid Stenosis

  • Auscultation
  • Low pitched, rumbling diastolic murmur at left sternal edge, accentuated by inspiration
  • Signs
  • Giant A waves and slow y descent on JVP
  • Presystolic pulsation of liver (forceful atrial contraction)
  • Causes
  • Rheumatic heart disease

Pulmonary Regurgitation

  • Auscultation
  • Decrescendo, high pitched diastolic hurmur loudest at left sternal edge, accentuated with inspiration
  • Causes
  • Pulmonary htn
  • IE
  • Following repair of pulmonary stenosis/atresia
217
Q

Less common diastolic heart murmus - TS and PR

A

Tricuspid Stenosis
Auscultation

  • Low pitched, rumbling diastolic murmur at left sternal edge, accentuated by inspiration

Signs

  • Giant A waves and slow y descent on JVP
  • Presystolic pulsation of liver (forceful atrial contraction)

Causes

  • Rheumatic heart disease

Pulmonary Regurgitation
Auscultation

  • Decrescendo, high pitched diastolic hurmur loudest at left sternal edge, accentuated with inspiration

Causes

  • Pulmonary htn
  • IE
  • Following repair of pulmonary stenosis/atresia
218
Q

Mitral Regurgitation

A

Auscultation

  • Soft/absent S1
  • S3 (rapid filling in early diastole)
  • Pansystolic murmur loudest at apex, radiating to the axilla

Signs

  • Tachypnoea
  • AF common
  • Displaced apex
  • Pansystolic thrill at apex
  • When severe: big LV, loud S3, soft S1, pulm htn/LVF

Symptoms

  • Fatigue, dyspnoea

Causes

  • prolapse
  • rheumatic heart disease
  • IE
  • connective tissue disease
  • Marfans, RA, ankylosing spondylitis
  • LVF/ischaemia (ruptured chordae etc)
219
Q

Aortic Stenosis

A

Auscultation

  • Narrowly split/reverse S2 (delayed LV ejection)
  • Harsh, midsystolic ejection murmur in aortic area radiating to carotids
  • Loudest when sitting up in full expiration

Signs

  • plateau pulse, may be late peaking
  • hyperdynamic, displaced apex
  • Systolic thrill at base

Symptoms

  • Exertional: chest pain, dyspnoea, syncope

Causes

  • Degenerative aortic valve
  • Rheumatic heart disease
220
Q

Tricuspid Regurgitation

A

Auscultation

  • Pansystolic murmur loudest at lower edge of sternum, increasing with inspiration

Signs

  • Large V waves on JVP, elevated JVP if associated with RVF
  • RV heave
  • Pulsatile, large, tender liver
  • Ascites, oedema, pleural effusion

Causes

  • Functional: RVF
  • Rheumatic heart disease (rarely isolated)
  • IE
  • Prolapse
  • Congenital: Ebsteins anomaly
  • RV papillary muscle infarction
221
Q

What are the absolute contraindications for thrombolysis for STEMI? Relative?

A

Absolute:

  • Prior ICH
  • CVA within 12 months
  • Marked hypertension
  • Suspicion of aortic dissection
  • Active bleeding (excluding menses)

Relative:

  • INR >2
  • Invasive procedure <=2 weeks, CPR >=10mins
  • Pregnancy
  • Haemorrhagic opthalmopathy
  • Active PUD
  • Controlled severe hypertension
222
Q

When should a patient presenting with STEMI be thrombolysed?

A
  • Within 30 mins of FMC if time to PCI >120 mins and <12hrs symptoms.
  • May be considered at up to 24hrs if symptoms ongoing and PCI not available.
223
Q

When should a pt presenting with STEMI receive primary PCI?

A

If FMC to PCI time <90mins, or if requiring transfer to PCI centre and FMC to PCI time <120mins

224
Q

Is there evidence behind which fibrinolytic should be used in STEMI?

A

Fibrin specific preferred:

  • Alteplase better than streptokinase in GUSTO-1
  • Tenectoplase equivalent to alteplase in ASSENT-2, less non-cerebral bleeding
225
Q

When might emergency CABG be indicated in STEMI?

A
  • Failed PCI
  • Anatomy not amenable for PCI
  • If STEMI occurs during operative repair of a mechanical defect
226
Q

Are antiplatelets indicated in STEMI? Does the agent matter? For how long?

A

Aspirin always and continued indefinitely

P2Y12 agent depends:

  • In fibrinolysis addition of clopidogrel to aspirin superior
  • In PCI ticagrelor superior to clopidogrel
  • In PCI prasugrel superior to clopidogrel

DAPT:

  • For minimum 1yr after AMI

Glycoprotein IIb/IIIa receptor blockers

  • Only indicated in select patients
  • No flow or giant thrombus or pending PCI
  • Studies in P2Y12 era show no benefit in routine use
227
Q

When are beta-blockers contraindicated in STEMI?

A
  • Haemodynamic compromise
  • Decompensated heart failure
  • Active bronchospasm
    • Have been demonstrated safe in mild/moderate COPD
  • >1st deg AV block
228
Q

Do calcium channel blockers decrease mortality in STEMI?

A
  • Never been demonstrated.
  • Diltiazem/verapamil may be used to control hypertension in addition to beta-blockers and ACEI/ARB
229
Q

Do beta-blockers decrease mortality in STEMI? In which patients? When should they be commenced?

A

Improve long term mortality in both PCI and fibrinolysis, but bulk of evidence from prior to reperfusion therapy

Long term therapy seems to only be of benefit in high risk patients:

  • Failure, CKD, T2DM >3yrs
  • Remainder reconsider ~3yrs

Should be commenced within 24hrs unless contraindicated. If contraindicated should be revisisted soon after.

230
Q

Is there any clear best beta-blocker in AMI? Any worse? HR and BP goals?

A

Trend toward less benefit in those with intrinsic sympathomimetic activity

  • *Bisoprolol, carvedilol, metoprolol XR (succinate), nebivolol in LVE**F <40%
  • nebivolol was studied in >70yo

Aim for HR <70 and SBP <90 or whatever tolerated. Rapidly titrate up to maximum tolerated

231
Q

Do ACE Inhibitors decrease mortality in AMI? In which populations? Are they safe in renal failure? Does the agent matter? What about ARB?

A
  • Mortality benefit in all populations. Absolute benefit greater in higher risk populations as they have a higher baseline mortality
  • Safe in renal failure, demonstrated in a large retrospective cohort study in patients with LVEF <40%
  • Seems to be a class effect.
  • ARB/ACEI shown to be equivalent in:
  • Shouldn’t use both together
232
Q

When are ACEI contraindicated?

A

History of prior decrease in renal function with ACEI

  • Hypotension
  • Shock
  • Bilateral renal artery stenosis
233
Q

In which patients with heart failure are aldosterone antagonists recommended? What is their mechanism of action? What percentage of patients experience endocrine side effects?

A

Systolic function <40% and NHYA >=2, including post AMI

  • RALES study
    • spironolactone vs plac in NYHA III/IV and sys <40%, mort 30% reduced
  • EPHESUS
    • eplerenone vs plac post AMI with LVEF <40% and HF or T2DM, mort 15% reduced
  • EMPHASIS HF
    • epler vs plac NYHA II and LVEF <30% or 30-35% and QRS >130ms, mort 24% reduced

Raising serum potassium

Blocking effect of aldosterone on heart:

  • locally produced aldosterone promotes hypertrophy, fibrosis, arrhythmias, and the transition from hypertrophy to failure
  • mediated by collegen synthesis

~10% experience endocrine side effects

234
Q

When do most deaths due to VF in STEMI occur?

A

Most in first 24hrs, with >50% in first hour

235
Q

What are the range of ECG findings in hyperkalaemia? Why do they occur?

A

Changes occur due to modification of the resting membrane potential upward, with subsequent inactivation of Na channels

Peaked Ts

  • Altered repolarisation

Long, flat, or absent Ps

  • Atrial paralysis

Wide, bizarre QRS; high grade AV block; sinus bradycardia; sinusoidal appearance

  • Conduction abnormalities

PEA; Asystole; VF

236
Q

Which electrolyte abnormalities predispose to torsades de pointes? What is the first line treatment of torsades de pointes?

A

Hypo-calcaemia, magnesaemia, kalaemia

Management (avoid amiodarone)

  • address underlying cause
  • magnesium sulphate
  • consider: overdrive pacing or isoprenaline
  • consider cardioversion if unstable
237
Q

What is the first line medication for shock resistant VT? Are there other options?

A

Amiodarone is first line

  • While slower acting, increased reversion and decreases recurrence

Other options are IV lignocaine and procainamide

238
Q

What is the Pulmonary Artery Wedge Pressure (PAWP)? How is it obtained? What does it measure?

A
  • Pressure measured by a pulmonary artery catheter with the balloon inflated to occlude a subsegmental pulmonary artery.
  • Reflects left atrial end diastolic pressure, and in the absence of complicating disease processes, left ventricular end diastolic pressure.
  • <=12mmHg is normal
239
Q

What is the definition of pulmonary hypertension?

What are the WHO Classification Categories?

A

PAMP >25mmHg

  • PAH (group 1) defined as PAMP >25mmHg with PCMP <15mmHg

Group I - PAH

  • Idiopathic
  • Heritable (70-80% BMPR2)
  • Drug/toxin induced
  • Associated with
    • CTD
    • HIV
    • Portal HTN
    • Congenital heart disease
    • Schistosomiasis
    • Chronic haemolytic anaemia
  • Persistent PH of the newborn
  • Pulmonary veno-occlusive disease

Group II - PH owing to left heart

    • Systolic
    • Diastolic
    • Valvular

Group III - PH owning to lung disease/hypoxia

    • COPD
    • ILD
    • Pulmonary diseases with mixed restrictive/obstructive pattern
    • Sleep disordered breathing
    • Alveolar hypoventilation disorders
    • Chronic high altitude
    • Developmental abnormalities

Group IV

    • Chronic thromboembolic PH

Group V - PH with unclear multifactorial mechanisms

  • Haematologic
    • MPD, splenectomy
  • Systemic
    • Sarcoid, histiocytosis, vasculitis, neurofibromatosis
  • Metabolic
    • Thyroid, glycogen storage, Gaucher
  • Other
    • Tumour, CKD/dialysis
240
Q

How is cardiogenic pulmonary oedema defined? Name the broad aetiological categories

A
  • Dyspnoea associated with accumulation of fluid in alveoli/lung interstitiium resulting from elevated cardiac filling pressures
  • Largely result of acute decompensated heart failure.
    • Impaired LV contractility
    • Diastolic dysfunction
    • Aortic outflow obstruction
    • MS
    • Renovascular hypertension
    • Fluid overload
241
Q

Describe the NYHA functional classification and its associated 1yr mortality and hospitalisation rates

A
  • Class I: Hospitalisation rare. Yearly mortality <10%
  • Class II: 2 blocks/flights of stairs. <=1 hospitalisation per year. Yearly mortality 10-15%
  • Class III: 1 block/flight of stairs. 2-4 hospitalisations per year. Yearly mortality 20%
  • Class IV: >4 hospitlisations per year. Yearly mortality 50%
242
Q

Is baseline Troponin I predictive of mortality in AMI?

A

YES, TIMI 3B demonstrated

243
Q

Briefly describe the characteristics of a murmur that would indicate further investigations or referral

A
244
Q

What is the definition of low QRS voltage on ECG?

A

<= 5mm in limb leads +/- <=10mm in praecordial leads

245
Q

What is the definition of cardiotoxicity?

A

Symptomatic heart failure or

  • drop to LVEF <45% or
  • drop LVEF by 15%

Mainly used in monitoring of trastuzumab, which has reversible cardiotoxicity

246
Q

Is the majority of cardiac malignancy primary or metastatic?

In whom is primary malignancy most common?

A

Majority is metastatic.

  • melanoma, leukaemia, lymphoma highest relative risk
  • breast and lung higher overall due to much larger prevalence than melanoma

Primary benign lesions are most common in children and adolescents

  • 75% of atrial myxoma in left atrium
  • usually at the fossa ovalis border

Primary malignant tumours are extremely rare.

247
Q

What is a secundum type ASD?

A

ASD that occurs in the region of the fossa ovalis

248
Q

Describe Janeway Lesions and Osler’s nodes

A

Janeway:

  • Non-tender, slightly raised haemorrhages
  • Palm/Sole

Osler:

  • Tender (ow!) , raised nodules
  • Pads of fingers/toes
  • immunological phenomenon
249
Q

What additional clinical findings may suggest venous insufficiency rather than fluid overload in lower limb oedema?

A

Lack of elevated JVP
Varicosities
Haemosiderin deposition in skin

250
Q

Why is the internal carotid preferred to examine the JVP? What are some differentiators between JV and CA?

A

The EJV is valved and not directly in line with the IVC/RA, so the IJV is preferred.

  • *Differentiators:**
  • JVP is biphasic
  • JVP changes with posture and respiration
  • JVP can be obliterated with palpation
251
Q

What is Kussmaul’s sign? What is the classic cause? What about some others?

A
  • *Rise** or lack of fall in JVP with inspiration.
  • Expect >=3cm fall

Classically in constrictive pericarditis

Less commonly in:

  • Restrictive cardiomyopathy
  • Massive PE
  • RV infarction
  • Advanced LVSHF
252
Q

What is the abdominojugular reflex? When is it abnormal?

A

Rise of >3cm for >15 seconds after release of >= 10seconds of pressure on RUQ.

Reflects overload/venous distension of the IVC/RA

253
Q

What is the ankle-brachial index? How is it calculated? Does it predict anything?

A

Lower of dorsalis pedis or posterior tibial divided by higher of the brachial artery systolic pressures.

Strong predictor of cardiovascular mortality

254
Q

What is the definition of orthostatic hypotension?

A
  • Fall of >20mmHg systolic or >10mmHg diastolic within 3 mins of transitioning from lying to standing.
  • Sign of autonomic instability
255
Q

What is pulsus paradoxus? What is it classically associated with? Anything less common?

A
  • Reduction in BP of >10mmHg with inspiration
  • Result of exaggeration of interventricular dependence
  • Classically associated with tamponade
  • May also be seen in:
    • Massive PE
    • Severe COPD
    • Tension pneumothorax
256
Q

What should the A2-P2 interval normally do with respiration? When is it fixed? When is it reversed/paradoxical?

A

S2 - comprised of A2 and P2, A2 should nomrally be much louder

Interval should normally get longer with inspiration and shorter with expiration

Should widen in:

  • RBBB due to delayed PV closure
  • Severe MR due to premature AV closure

Fixed split in:

  • ASD

Reversed in (delayed AV closure):

  • LBBB
  • HOCM (HCM)
  • Severe AS
  • Ischaemia
  • Interval narrows with inspiration and prolongs with expiration
257
Q

What is a systolic ejection sound? What is it usually associated with? What about non-ejection sounds?

A
  • High pitched, early systolic sound corresponding with upstroke of carotid pulse.
  • Usually associated with congenital bicuspid AV/PV
    • PV ejection sound is the only right sided sound that gets quieter with inspiration
  • Non-ejection sounds are usually related to mitral valve prolapse
258
Q

Name some diastolic sounds and their causes

A

Opening snap

  • High pitch
  • MS
  • Right after S2

Pericardial knock (special form of S3)

  • Constrictive pericarditis
  • Related to abrupt cessation of filling
  • Occurs after opening snap

Tumour plop

  • Positional
  • Related to tumour movement across mitral valve

S3

  • Occurs during rapid filling phase of diastole
  • May be normal in children-> young adults (not in >40yrs)
  • Signifies heart failure or mitral regurgitation

S4

  • Occurs during atrial kick, overcoming stiff or hypertrophic LV
  • Reflects a stiff ventricle and is most common in patients who benefit from atrial kick
  • Ischaemia, LV hypertrophy (AS, HOCM (HCM), hypertension)
259
Q

What manoeuvres can help to differentiate the murmur of HOCM (HCM)?

A

People with HOCM are preload dependent.

Manoeuvres that decrease preload or increase contractility intensify

  • Valsalva or standing rapidly from squatting

Manoeuvres that increase preload decrease intensity

  • Leg raise or squatting
260
Q

Give examples of early, mid, late, and holosystolic murmurs

A
  • *Early**
  • Acute, severe MR and TR
  • *Mid**
  • Starting after S1, ending before S2
  • Crescendo-decrescendo
  • *- AS** most common
  • HOCM (HCM)
  • Increased pulmonary flow in ASD with L->R shunt
  • Accelerated flow murmur –> Fever, thyroid, pregnancy, anaemia, adolescence
  • *Late**
  • MV prolapse
  • *Holo**
  • Plateau, reflecting continuous, wide pressure gradient
  • Chronic MR and TR –> Chronic allows for atria enlargement and increased compliance that result in lower pressure differential
  • VSD
261
Q

What is the expected effect of respiration, valsalva, position, and exercise/vasopressors on murmurs?

A

Respiration

  • Right sided increase with inspiration except pulmonic ejection sound
  • Left sided increase with expiration

Valsalva

  • Most murmurs decrease in length and intensity
  • HOCM (HCM) and MVP increase
  • Right sided murmurs return to baseline quicker than left sided

Standing

  • Most get softer
  • HOCM and MVP increase

Squatting

  • Most get louder
  • HOCM and MVP decrease

Exercise/vasopressors

  • Most get louder
  • HOCM decreases
262
Q

What are the risks of cardiac catheterisation/angiography? Absolute/relative contraindications?

A

All risks increased in emergent cases

Main:

  • MI 0.05%
  • Stroke 0.07%
  • Death 0.08-0.14%

Additional

  • Arrhythmias
  • ARF (AKI)
    • 2-7% of patients, 20-30% of high risk patients
    • T2DM, CCF, elderly, CKD
  • Reduced incidence with pre and post hydration
  • Vascular complications
  • Significant bleeding

Absolute:

  • None

Relative:

  • Decompensated HF
  • ARF
  • Severe CRF unlessplanned for dialysis
  • Bacteraemia
  • Acute stroke
  • Active GI beed
  • Contrast allergy
  • Allergy to aspirin if PCI likely
263
Q

Run through the differentiators between tamponade, constrictive pericarditis and restrictive cardiomyopathy

A
264
Q

What are the cardiac catheter methods for measuring CO? Vascular resistance?

A

Fick

  • Uses oxygen consumption as a product of flow to calculate CO

Thermodilution

  • Uses temperature change to calculate CO

Ohm’s law
SVR
- (MAP-RAP)/CO
PVR
- (PAMP-PAWP)/CO

265
Q

What does coronary artery dominance refer to?

What are the possibilities and their prevalence?

A

Refers to the side from which the AV nodal, posterior descending, and posterior lateral arteries arise

  • Right
    • 85%
    • rise from right coronary
  • Left
    • 5%
    • Arise from left circumflex
  • Codominant
    • 10%
266
Q

What is considered a ‘significant’ coronary artery stenosis?

What is fractional flow reserve?

A
  • >50% reduction in diameter compared to proximal or distal ‘normal’
  • Intermediate stenoses may need to be further classified
  • Fractional flow reserve - FFR
    • Ratio of pressure at the aorta and post the stenosis
    • <0.80 signifies a significant reduction that would benefit from intervention
  • The FAME study in NEJM 2009
    • FFR guided vs angiogram guided PCI in those with multivessel disease being considered for revascularisation
267
Q

Where is the SA node? What s its arterial supply?

A

Sulcus terminalis at the junction of RA and SVC

  • RCA in 60% of cases
  • LCA in 40% of cases
268
Q

How is SA nodal disease classified? Give some examples of causes for each category

A

Extrinsic

    • Drugs
    • Increased parasympathetics
    • hypothyroid, hypothermia, increased ICP

Intrinsic

    • Degenerative
    • Characterised by fibrous replacement of SA node
    • Ischaemic
    • Inflammatory
    • Traumatic
    • Genetic
269
Q

Is tachycardia common in SA dysfunction (sick sinus syndrome)? What are the most common subtypes?

A

Yes, 1/3-1/2 develop tachcardia.

Atrial flutter/fibrillation

270
Q

Can the SA node be tested for dysfunction? How?

A

Intrinsic HR

  • 0.2mg/kg propranolol + 0.04mcg/kg atropine
  • Expected HR 117.2 - (0.53 x age)

Sinus Node Recovery Time

  • Overdrive pace then time pause on cessation
  • <1500ms normal

Sinoatrial Conduction Time

  • 1/2 difference between intrinsic sinus cycle and non-compensatory pause after stimulus
  • <125ms normal
271
Q

What is the treatment for SA dysfunction (sick sinus syndrome)? Does it carry a mortality benefit? What are the indications for treatment?

A

Rule out and correct extrinsic factors first

  • *PPM is the only proven therapy**
  • No mortality benefit, only symptomatic
  • Isoprenaline/atropine can temporise in the acute setting
  • *Class I**
  • Symptomatic bradycardia
  • SA dysfunction when you can’t stop the responsible medication
  • Symptomatic chronotropic incompetence
  • *Class II**
  • SA dysfunction suspected but not proven
  • Syncope of unexplained origin in presence of abnormal SA
  • *Not indicated**
  • Asymptomatic
  • If you can stop the responsible medication
272
Q

Outline optimal pharmacologic (medical) therapy (management, treatment) (omt) of heart failure with reduced ejection fraction

A
  • Note that it’s important to get to maximum tolerable dose of ACEi and beta blockers as it confers significant additional benefit
    • doesn’t matter which order as long as they’re both started and titrated up in a timely manner (CIBIS III trial)
    • if you have to choose between increasing dose of BB or ACEI push the BB dose first
  • ACEi decreases mortality but not SCD
  • BB decreases mortality and SCD
  • Eplerenone decreases mortality (NYHA 2 EF <=30%)
  • Spironolactone decreases mortality (NYHA 3-4 <=30%)
    • increased dose doesn’t increase effect but does increase AEs
    • dose at 25mg max, increased dose increases AEs but not efficacy
  • Should note that valsartan/sacubitril was shown to decrease mortality c/w enalapril in NYHA 2-4 with LVEF <=40%
  • Note that amlodipine has been shown to be safe in HFrEF
    • on the off chance you need better BP control after having maxed BB, ACEi, spiro
273
Q

When is the highest risk of death after hospitalisation for heart failure?

A

Peaks at 1 month and gradually declines from then

274
Q

What’s the most common precipitant of readmission for patients with heart failure? What % of admissions are preventable?

A
  • Poor compliance
  • >=50%
275
Q

What are the indications for a VAD?

A

Bridge to cardiac transplantation

Bridge to a decision regarding transplantation in those who could improve with time

Destination therapy in those not candidates for transplantation

276
Q

When is an intra-aortic baloon pump used? How does it work?

A
  • Cardiogenic shock not responsive to pharmacologic therapy
  • Acute mitral regurgitation
    • papillary/septal rupture
  • Inflates during diastole, increasing diastolic pressure. Deflates during systole, with a vacuum effect decreasing systolic afterload
277
Q

When is ivabradine of benefit in heart failure?

A

As per SHIFT trial, Lancet 2010

  • NYHA II-III
  • LVEF <35%
  • Sinus rhythm
  • HR >=77 (PBS criteria, trial showed benefit >70bpm)
  • Maximum tolerable dose of beta blockers and OMT

Reduces cardiovascular death and hospitalisation for heart failure (in addition to beta blocker)

  • benefit seen in those with HR >75 rather than <75

Adverse effects

  • transient luminous phenomenon in 15%

Can be useful in those where lung disease precludes beta blockers or where they’re truly not tolerated

  • as increased HR carries significant increased morbidity and mortality in HFrEF
278
Q

In which patient population does hydralazine + ISDN confer a survival benefit in heart failure?

A

Black with NYHA >=3

May be used in non-blacks if ACEI/ARB can’t be used

279
Q

What are the indications for insertion of AICD?

A

Primary prevention of SCD

  • Must have stabilised the function, i.e. >40 days post AMI and >3 months post revascularisation
  • Must have reasonable expectation of survival with good functional status >1yr
  • Antiarrhythmic medications not of benefit (don’t ‘save lives’), can be used to decreased symptomatic shocks

Note that DANISH trial in NEJM 2016 will likely bring into question use of AICD in non-ischaemic cardiomyopathy

Secondary prevention of SCD

  • Patients who have experienced symptomatic life threatening sustained VT/VF or those successfully resuscitated from sudden cardiac arrest.
  • Patients with heart failure or cardiomyopathy with syncope and induced or spontaneous VT.
280
Q

What types of VT don’t generally require insertion of an ICD?

A
  • Preceded by ischaemia
  • In setting of prolonged QT
  • In setting of WPW with a structurally normal heart
  • Idiopathic in setting of structurally normal heart
    • Medical therapy or catheter ablation
  • In setting of overdose
281
Q

Why might antiarrhythmics be prescribed with ICD in situ?

A
  • Improve quality of life via reducing shocks
    • Amiodarone
    • Sotalol
    • Mexiletine
  • Suppress both VT and SVT, both of which can initiate shocks
282
Q

What are the indications for insertion of a cardiac resynchronisation device (CRT)?

A
  • Those with LBBB at increased risk of all cause mortality and SCD
    • LBBB results in dyssynchrony such that the left ventricle contracts against a flaccid rather than rigid septum, with loss of mechanical efficiency and resultant mitral regurgitation
  • Pacing improves the synchrony and the mitral regurgitation -> improved function
  • NYHA II-IV on OMT with LBBB and QRS >=130ms
    • Highest benefit in those with LBBB
  • NYHA II-IV on OMT without LBBB and QRS >150ms
  • No benefit in HF with QRS <130ms
    • some have worse outcomes

Benefits

  • improvement in 6MWT
  • improve QoL
  • Improvement in VO2 max
  • Improvement in hospitalization for HF
  • reduction in NYHA class score
  • decreased mortality
283
Q

When is cardiac rehabilitation indicated? What are its components?

A

NYHA II-III without advanced arrhythmia or limitation to exercise.

Not recommended in NYHA IV.

General

  • Evaluation and baseline assessment
  • Education: Na/fluid restriction, importance of compliance
  • Risk factor reduction: stop smoking, stop ETOH, lose weight
  • Psychosocial support

Training

  • Aerobic
    • Reduce admissions, no change in mortality
  • Resistive

Direct benefits along with benefits from monitoring, allowing for early detection of decompensation

284
Q

What are the indications for cardiac transplantation?

A
  • Refractory NYHA 3-4
  • VO2 max <14mL/kg/min + anaerobic metabolism
  • Severe ischaemia not amenable to intervention
  • Recurrent refractory ventricular arrhythmias
  • Above is despite optimal medical therapy
285
Q

What are the most significant stress ECG predictors of poor outcome?

A
  • Poor exercise capacity
    • One of the strongest predictors
  • Angina
  • Abnormally low BP or decrease in BP during exercise
  • Chronotropic incompetence
286
Q

What are the indications for stress ECG testing?

A
  • Intermediate likelihood of CHD and symptoms of angina
  • Acute chest pain, to diagnose CHD
  • Within 3 months of ACS for risk assessment
  • Known CHD with worsening symptoms
  • Valvular heart disease
  • Newly diagnosed failure/cardiomyopathy
    • Assess viable myocardium
  • Arrhythmias
    • Looking for exercise induced arrhythmias and chronotropic incompetence
  • Prior to elective non-cardiac surgery
    • Surgical prognostication
    • No benefit to prophylactic revascularisation
287
Q

What are the options for acute management of symptomatic AV nodal dysfunction? Chronic? Indications?

A

Acute:

  • Medications
    • Atropine
    • Isoprenaline
  • Pacing
    • Transcutaneous
    • Transvenous

Chronic

  • PPM
    • All patients with symptomatic 2nd/3rd degree
    • Selected asymptomatic patients
288
Q

Where is the AV node located? Describe its sections

A

Apex of triangle of Koch

  • posteriorly by coronary sinus
  • anteriorly by septal leaflet of tricuspid
  • superiorly by tendon of Todaro

Superior, medial, posterior transitional atrionodal bundles converge into compact AV node.
Continuous as penetrating bundle through fibrous body
Right bundle arises from distal AV node

289
Q

Do AMI locations have particular AV block patterns? What type?

A
  • ~7% cases of AMI develop AV block
  • >=2nd degree more common in inferior
    • Usually at the nodal level and therefor narrow with stable escape rhythm
  • Anterior often lower AV node and associated with unstable and wide escape rhythms
290
Q

What factors can help differentiate physiologic sinus tachycardia from atrial tachycardia?

A
  • Focus away from the SA node points to atrial
  • Gradual onset/offset or causative factor point toward physiological
  • Sudden onset and offset point toward atrial
291
Q

What are the types of non-physiologic sinus tachycardia? Their treatment?

A

Inappropriate sinus tachycardia

  • Out of keeping with the stimulus
  • Young/middle aged women
  • Careful titration of CCBs/BBs, but difficult to treat

Postural Orthostatic Tachycardia Syndrome

  • Sinus tachycardia with postural hypotension
  • Salt supplementation, mineralocorticoid, midodrine
292
Q

What is focal atrial tachycardia? From where does it arise? How might it be distinguished from flutter? How from AV nodal SVTs? How is it treated?

A
  • Paroxysmal, non-sustained, sustained, or incessant tachycardia mediated by abnormal automacity, triggered automacity or a small re-entry circuit confined to the atrium.
  • Usually arises from complex atrial anatomy
    • Crista terminalis, annuli, the veins
  • Often discrete p waves differentiate it from flutter
  • Lack of termination with AV block differentiates it from AVN dependent SVTs
  • Can be difficult to treat:
    • Triggered activity may revent with adenosine
    • Cardioversion won’t work in increased automacity
    • BB/CCBs can help tolerate by lowering rate
    • I/III antiarrhythmics can work
    • Ablation is usually very successful in the recurrent or those developing tachycardia mediated cardiomyopathy

Cardiology (3 decks)

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