Cardiology Flashcards
Pathophysiology of heart failure
Catecholamines, angiotensin, aldosterone, endothelin, cytokines –> neurohormonal activation –> peripheral vasoconstriction –> fluid retention –> decreased contractility
Neurohormonal activation –> myocyte injury –> decreased contractility
Classes of heart failure
NYHA I - no symptoms, even during exercise
NYHA II - reduced physical capacity during medium exercise
NYHA III - severely reduced physical capacity during slight exercise but OK at rest
NYHA IV - symptomatic at rest
TTE for heart failure
LV size, shape, global and regional function
Complications - MR, pulmonary HTN, thrombus
Assessment of diastolic function
MRI for heart failure
Function
Structure
Viability
Composition
Right heart catherisation transportation
R atrium > R ventricle > Main pulmonary artery > PA branch > Pulmonary artery wedge pressure
Definition of HFrEF
Symptoms of HF with LVEF < 50%
Definition of HFpEF
Symptoms of HF, LVEF > 50% and diastolic dysfunction (evidence of high filling pressure and/or object evidence of relevant structural heart disease)
Role of natriuretic peptides
ANP - originated from cardiac atria, released by atrial distension
BNP - originated from ventricular myocardium, released by ventricular overload
CNP - originated from endothelium, released by endothelial stress
BNP physiologically increases with
Age
Females
Post menopause
Treatment for HFpEF
SGLT inhibitors
Diuretics
Angiotensin receptor blockers
Salt restriction, exercise training
Manage comorbidities (AF, HTN, CAD, OSA)
MOA of SGLT2 inhibitors
Blocks reabsorption in PCT –> increases glucose excretion
Outcomes of EMPEROR study
Reduced HF hospitalisations (and CV death to lesser degree) in patients who received empagliflozin and dapagliflozin
Goals of treatment in HF
Prevent diseases causing LV dysfunction
Prevent progression to symptomatic HF
Reduce symptoms
Reverse remodelling
Improve survival
Management of HFrEF
Stage A - high risk, no symptoms
- Risk factor reduction
- Education
- ACE inhibitor
- Treat HTN, DM, hyperlipidaemia
Stage B - structural heart disease, no symptoms
- ACE inhibitor
- B blockers
Stage C - structural disease, previous or current symptoms
- AICD if EF < 35%
- Diuretics
- Aldosterone blockers
- HF rehab
- Ivabradine if HR > 77
- SGLT2 inhibitor
- CRT if LBBB
- Specialised cardiac surgery
Stage D - Refractory symptoms requiring special intervention
- Inotropes
- Transplantation
- Palliation
Four pillars of heart failure
ACEI/ARNi/ARB
Beta blockers
Mineralocorticoid receptor antagonists
SGLT2 inhibitors
ARBS vs ACEI for heart failure
Far less data for ARBS
Strongest data for candesartan, but can use valsartan
Benefits greatest in ACE-I naive patients
Beta blockers proven benefit in CCF
Carvedilol
Bisoprolol
Nebivolol
Long acting metoprolol (succinate)
Evidence for beta blockers in CCF
Demonstrated improvement in mortality and morbidity in class II-IV
Must be stabilised and euvolaemic prior to initiation
Reduction in SCD
Spironolactone in CCF
Higher doses not shown to have greater benefit but have greater adverse effects
Caution in renal impairment
Indications for ivabradine
HR > 70/min (DESPITE adequate beta blocker dose)
If lung disease precludes beta blockers
Beta blockers truly not tolerated - unacceptable symptomatic hypotension, intolerable beta blockers side effects
How does Entresto cause rise in BNP?
Entresto - Valsartan + neprolysin inhibitor (sacubitril)
Causes rise in BNP (as BNP is neprolysin substrate), however causes fall in NT pro BNP
Current indications for Entresto in HRrEF
Add on therapy if NYHA II-IV (symptomatic HF) and LVEF < 40% after 3-6 months of optimal treatment
Practice point if ACEI already commenced and wanting to start Entresto
Need to wait 36 hours after cessation of ACE inhibitor before started Entresto
Role of digoxin and diuretics in HF
Nil effect on mortality
Reduces symptoms
Chemo agents associated with cardiotoxic effects
Anthracyclines - multiple mechanisms, dose related
Platinum-based agents - vascular disease
Antimetabolites (5-FU) - worsening of CAD
Taxanes - arrhythmia
Cyclosphosphamide - idiopathic HF
HER-2 targeted agents - myocardial dysfunction
Tyrosine kinase inhibitors - HTN
Features of hypertrophic cardiomyopathy
Autosomal dominant
Most common inherited cardiomyopathy
Very variable and dependent on LVH +/- obstruction
Palpitations and syncope
Sudden death in young (commonest cause)
Endocarditis
Dyspnoea
Angina
Pathophysiology of HCM
Abnormal hypertrophy
- asymmetric septal IVS:PW > 1.5
- mid ventricular
- giant negative T waves
Diastolic dysfunction
TTE findings in HCM
Wall thickness
- Asymmetrically thickened left ventricular wall, (≥ 15 mm), typically involving the septum
- LV wall thickness ≥ 30 mm is associated with a high risk of sudden death.
Outflow tract abnormalities
- Systolic anterior motion of the mitral valve
- Mitral regurgitation
- ↑ LVOT pressure gradient via Doppler echocardiography
Other findings
- Left atrial enlargement
- Systolic function typically normal
- Diastolic dysfunction
- Symmetrically thickened interventricular septum
- Dynamic LVOT obstruction due to contact between the septum and mitral valve during systole
Management of HCM
Treatment heart failure
Improve diastolic filling and reduced ischaemia
Reduce outflow obstruction
- avoid things that increase obstruction
- alcohol septal ablation
- surgery: severe LVOT obstruction and symptoms
Prevent sudden death
Screen first degree relatives
Risk factors for SCD in HCM
FHx of premature sudden death
Recurrent syndrome (in young)
NSVT
Severe LVH (septum >2.5-3cm)
Severe obstruction
Abnormal exercise BP pressure response
Level of myocardial fibrosis on MRI
Specific genotypes e.g. Arg719Trp mutations
Types of amyloidosis
AL amyloid (primary) - plasma cell dyscrasia
AA amyloid (secondary)
ATTR amyloid (wild type or inherited)
Other - dialysis related, age related, organ specific
Presentation of cardiac amyloidosis
HFpEF, low voltage ECG, AF
Heart failure
HTN (low output state)
AF common
Hepatomegaly
Periorbital purpura, if present with HF usually AL amyloidosis
ECG - low voltage, AF
High NT pro-BNP
Ventricular hypertrophy
TTE findings for amyloidosis
Increase LV wall thickness
Diastolic dysfunction
Dilated atria
Abnormal longitudinal strain (apical sparing)
Small pericardial effusion
Pulmonary HTN
Speckled myocardium
MRI findings for amyloidosis
Structural findings similar to TTE
Abnormal deposition of GAD contrast
Suspect restrictive cardiomyopathy if
Predominant right heart failure
LV systolic function relatively preserved
Ventricular wall thickness increased
Diastolic dysfunction
Atria dilated
AV regurgitation common
Features of advanced HF
Severe symptoms despite optimal medical therapy
Frequent hospitalisations
Secondary organ dysfunction
Ventricular arrhythmias
Progressive cardiac remodelling
Inotrope requirement
High mortality
Use of inotropes in heart failure
Critical support until definitive therapy
Support until resolution form other conditions
Acute decompensation form poor tissue perfusion
Bridging to definitive treatment
Devices for heart failure
Implantable defibrillators (AICD)
Biventricular pacing (CRT)
Left ventricular assist device (LVAD)
Indications for HF
NYHA II-III HF with LVEF <35% despite optimal medical treatment
Class I HF with IHD if more than 40 days post AMI + EF measured more than 3 months post revascularisation
Primary prevention
Selected patients with an expected survival of > 1 year and any of the following:
- Arrhythmogenic right ventricular cardiomyopathy
- Hypertrophic obstructive cardiomyopathy
- Cardiac channelopathies (e.g., congenital long QT syndrome, Brugada syndrome)
- Severe congestive heart failure
- Neuromuscular disorders (e.g., Duchenne muscular dystrophy, Becker muscular dystrophy)
- Cardiac sarcoidosis
Secondary prevention
All patients with an expected survival of > 1 year, an irreversible cause of ventricular tachyarrhythmias, and any of the following:
- Sudden cardiac arrest (e.g., due to Vfib)
- Unstable VT
- Stable sustained VT
- Inducible VT and/or Vfib on an EP study AND underlying:
- Unexplained syncope and ischemic heart disease
- NSVT due to previous MI or LVEF ≤ 40%
Reason for pacemaker in heart failure
LBBB common in heart failure
Leads to LV ‘dysynchrony’
Bi-V pacing aims to resynchronise LV and RV contraction
Effects of LBBB
Ventricular systole
- LV activates late
- Relaxed septum pushed into RV
- Aortic valve opens
- Lateral papillary muscle activated late –> MR
Ventricular diastole
- Passive filling late
- Atrial contraction during passive filling
Biventricular pacing indications for CCF
Wide QRS >/ 150ms
Low EF < 35%
NYHA II-IV
CRT indications for HF
LVEF </35%, NYHA II-IV, optimal medical therapy
Recommended if SR and QRS >/ 150ms
Consider CRT if AF
Consider CRT if QRS 131-140ms
Consider if HFrEF and need for RV pacing
CRT contraindications
If QRS < 130ms
Surgical management options
Mitral valve repair/replacement
Coronary artery bypass
Aortic valve replacement (surgical, TAVI)
Ventricular assist devices) - bridge to more permanent management i.e. transplant, recovery
Indications for cardiac transplant
Refractory NYHA Class IV HF
VO2 max < 14ml/kg/min + anaerobic metabolism
Severe ischaemia not amenable to intervention
Recurrent refractory ventricular arrhythmias
AF epidemiology
Prevalence increases with age, gender, comorbidities and heart disease
M > F (30% greater risk)
Associated with 1.5-2 fold increase in all cause mortality
Comorbidities associated with AF
HTN
Valvular heart disease
Heart failure
Hypertrophic cardiomyopathy
Hyperthyrodiism
Cardiopulmonary disease
Obesity
Diabetes
AF pathogenesis
Left atrial stretch affecting haemodynamics (via HTN, heart failure, mitral disease)
Genetic
Inflammation
Metabolic syndrome
Classification of AF
Paroxysmal - terminates spontanously or with intervention within seven days of onset
Persistent - fails to self-terminate within seven days
Long standing persistent - > 12 months
Mechanisms of AF
1st stage - arrhythmic foci within muscular sleeves extending into pulmonary veins
2nd stage - arrhythmic burden +/- other cardiac factors lead to atrial remodelling
3rd stage - gross electrical and structural atrial remodelling
Purpose of beta blocker with flecainide
Flecainide organises AF into macro-circuits (often goes from AF to flutter) and simultaneously reduces the refractoriness of the AV node so it can conduct at fast rates can cause unstable rhythm and cause VF
Thus, AV node blocker needs to be used concurrently with flecainide
AF ablation indication
Symptomatic AF refractory to medications
Successful in 60-70%
Often requires multiple ablation procedures
Definition of atrial flutter
Macro re-entrant circuit in RA (between IVC and tricuspid valve)
CHA2DS2-Vasc score simplified
Risk stratify with
- Congestive heart failure
- Hypertension
- Age > 75 yrs
- Diabetes
- Ischaemic stroke, TIA< systemic emboli (2 points)
If one positive - ?anticoagulation
If two positive - anticoagulation
NOACs contraindications
Mechanical heart valves
Rheumatic heart disease
Different manifestations of WPW
Accessory pathway - Delta wave
Orthodromic tachy - narrow complex
Antidromic tachy - wide complex
Differentiating VT from aberrancy
Definite VT
- AV dissociation, fusion, capture beats
Probable VT
- No RS pattern, > 100ms from beginning of R-wave to nadir of S-wave
Probable not VT
- Typical RBBB or LBBB pattern
Hypertrophic cardiomyopathy features
Autosomal dominant
Commonest cause of SCD age < 35 yrs
Phenotypes of HOCM
Septal hypertrophy with or without outflow obstruction
Concentric hypertrophy
Apical hypertrophy
LV free wall hypertrophy
RV hypertrophy
Risk stratification of HOCM for consideration of ICD insertion
- FHx of SCD
- Unexplained syncope
- NSVT on Holter
- IVS > 30mm
- Abnormal BP response during exercise
ARVC diagnostic criteria
- Dysfunction and structural abnormalities of RV (can be revealed by echocardiography, MRI, or RV angiography)
- Histological characteristics (require myocardial biopsy)
- Abnormal repolarization (diagnosed with ECG)
- Depolarization/conduction abnormalities (diagnosed with ECG)
- Arrhythmias (diagnosed with ECG)
- Family history (confirmation of ARVC in a relative either by criteria, pathological examination in surgery or autopsy, or by genetic testing)
ARVC biopsy results
Fibrofatty replacement of myocardial tissue
Long QT syndrome genes
LQT1 - KCNQ1
LQT2 - KCNH2
LQT3 - SCN5A
Autosomal dominant
Long QT syndrome types
LQT1 - normal but long (associated with exercise)
LQT2 - biphasic (associated with loud noises, emotions)
LQT3 - late peaking (associated with sleeping)
Management of LQTS
Avoid QT prolonging drugs
Avoid competitive sports
Beta blockers
ICD if high risk VT or previous VT
Brugada features
Autosomal dominant
Peak prevalence of SCD in 4th decade
ECG - septal downslopign ST elevation
AV blocks
1st degree - PR prolongation
Mobitz I - prolonging PR until QRS drop
Mobitz II - no variation in PR interval, non-conducted P waves
3rd degree - no association between P wave and QRS
Preferred pacing for heart failure and why
Biventricular pacing
RV pacing causes mechanical dysynchrony –> RV depolarises first causing discoordination contraction –> results in increased rate of heart failure and mortality
Valves of each heart and amount of cuspids
Left heart
- Aorta (3)
- Mitral (2)
Right heart
- Pulmonary (3)
- Triscuspid (3)
Bicuspid aortic valve features
Most common congenital abnormality
Aortopathy - dilation of aortic sinuses, ascending aorta, arch
Coarctation
Aortic stenosis symptoms
SOB on exertion/reduced exercise tolerance
Fatigue
Angina
Syncope
LV failure
Clinical signs of severe AS
Plateau pulse
Aortic thrill
Systolic murmur
S4
Parodoxical splitting of S2
LV failure
Grading aortic stenosis factors
Peak velocity
Mean gradient
AVA
Indexed AVA
Velocity ratio
Definition of low flow low gradient AS
AVA < 1
Mean gradient < 40mmHg
LVEF < 50%
SVi < 35ml/m2
Investigation to distinguish between true severe AS and pseudo severe AS
Dobutamine stress echo
No change in gradient with inotropes –> more likely pseudo severe AS
Definition of parodoxical low flow low gradient
AVA < 1
Mean gradient < 40
Peak velocity < 4m/s
Normal LVEF
SAVR vs TAVI
SAVR
- Survival benefit
- Valve durability
- Avoid permanent pacer
- Annular enlargement
- Aortic dilatation
- Concurrent valve disease
Recommended < 65yrs
TAVI
- Survival benefit
- Short hospitalisation
- Transfermoral only
- Less pain
- Good haemodynamics
- Durability less important
Recommended > 65s and high perioperative risk
Causes of aortic regurgitation
Valve disease
- congenital
- degenerative
- endocarditis
- rheumatic
Aortic root/ascending aorta abnormalities
- aortic root dilatation (Marfans/Loeys-Dietz, AS)
- Aortic dissection
Symptoms of AR
Usually asymptomatic for prolonged period
Dyspnoea
Orthopnoea/PND
Chest pain - noctural/exertional angina
Clinical signs of severe AR
Wide pulse pressure
Water-hammer/collapsing pulse
Long decrescendo diastolic murmur
S3
Soft A2
Austin flint murmur (mid diastolic rumble/murmur)
Echo features of AR
Jet width, regurgitant volume
Holodiastolic flow reversal in proximal abdominal aorta
Features of LV dilatation
Surgical management for AR
Significant enlargement of ascending aorta
Symptomatic
LVESD > 50mm or LVEF < 50%
Recommendations for aortic root aneurysm
Valve sparing aortic root replacement recommended in young patients with dilation
Ascending aortic surgery recommended in pts with Marfan syndrome with maximal ascending aortic diameter >/ 50mm
Should be consider in pts with aortic root disease with maximal ascending aortic diameter:
- >/55mm in all pts
- >/45mm in presence of Marfan syndrome and additional risk factors
- >/ 50mm in presence of bicuspid valve with additional risk factors or coarctation
Replacement of aortic root or tubular ascending aorta considered when >/ 45mm
Mitral regurgitation causes
Primary
- primary valve disease - due to abnormality of leaflets, chordae tendinae, papillary muscles, annulus
Secondary
- primary myocardial disease - functional regurgitation due to abnormalities of left ventricle or left atrium
Acute MR cause
Occurs with spontaneous chordae tendinae or papillary muscle rupture secondary to MI
Management of acute MR
Medical
- primary goal is to stabilise the pt in preparation for surgery
- temporary mechanical support device
Surgery
- repair/replacement
Signs of severe MR
LV dilatation
Soft S1, split S2 S3
Pansystolic murmur radiates to axilla
Pulmonary HTN
Small volume pulse
Signs of LV failure
Early diastolic rumble
Management of severe primary MR
Symptomatic = surgery
Asymptomatic
- TTE every 6-12 months
- Exercise testing with haemodynamics
- Goal directed medical therapy
Indications for surgery with MR
Symptomatic
If no symptoms, LVEF </ 60% or LVESD >/ 40mm OR new onset AF OR SPAP > 50mmHg OR high likelihood of durable repair, low surgical risk and LA dilatation
Features of rheumatic heart disease
Result of valvular damage caused by abnormal immune response to group A strep infection
Mitral valve is most common valve involved
Female predominance 2:1
Echo gold standar
Characteristic features of rheumatic heart disease on TTE
Mitral valve features
- prolapse of anterior leaflet
- Thickened leaflet tips
- Restricted posterior leaflets
- Chordal thickening
- Leafleft calcification
- Diastolic doming of anterior leaflet
Aortic valve features
- Cusp prolapse
- Cusp thickening
- Rolled cusp edges
- Cusp restriction
- Cusp fibrosis, retraction, calcification
- Dilated aortic root
Manifestations of acute rheumatic fever
Major
- Carditis
- Polyarthritis or aspetic monoarthritis or polyarthralgia
- Sydenham chorea
- Erythema marginatum
- Subcutaneous nodules
Minor
- Fever
- Monoarthralgia
- ESR > 30 or CRP > 30
- Prolonged PR interval
Causes of mitral stenosis
- Rheumatic heart disease
- Nonrheumatic calcific mitral stenosis
- Congenital
- Post radiation
- Endocarditis
- Endomyocardial fibroelastosis
Clinical signs of mitral stenosis
Pulse - AF
Malar flush
Prominent A wave
Apex beat - tapping, palpable S1
Associated valve lesions
Severe MS
- Small pulse pressure, opening snap close to S2
- Rumbling diastolic murmur
- Pulmonary HTN
- Apical diastolic thrill
Medical management of rheumatic mitral stenosis
Warfarin (NOACs contraindicated)
Percutaneous balloon mitral valvuloplasty
Contraindications for percutaneous mitral commisurotomy in rheumatic MS
- MVA > 1.5
- LA thrombus
- More than mild MR
- Severe or bi-commissural calcification
- Absence of commissural fusion
- Severe concomitant aortic valve disease or severe combined TS and regurg requriing surgery
- Concomitant CAD requiring bypass
Causes of tricuspid regurgitation
Primary
- IE
- RHD
- Carcinoid
- Congenital i.e. Ebstein’s anolamy
- Thoracic trauma
- Iatrogenic valve damage
Secondary
- Due to pressure and/or volume overload
- Mediated RV dilatation or enlarged R atrium and triscupid annulus due to chronic AF
Causes of cardiac manifestations in carcinoid disease
Caused by paraneoplastic effects of vasoactive substances such as 5-hydroxytrypptamine (5-HT or serotonin), histamine, tachykinins and prostaglandins released by malignant cells
Findings on carcinoid heart disease
Characteristic pathological findings - endocardial plaques of fibrous tissue involving tricuspid valve, pulmonary valve, cardiac chambers, venae cavae, pulmonary artery and coronary sinus
Results in distortion of valves
Ebstein’s anomaly
Congenital malformation in which there is apical displacement of insertion of septal and posterior tricuspid valve leaflets
Clinical signs of tricuspid regurgitation
Pansystolic murmur, left LSE, loud on inspiration
JVP with prominent V wave
Pulsatile liver
Signs of pulmonary HTN - loud and palpable P2, RV heave
Management of TR
If left sided valve disease –> severe primary or secondary TR or TA dilatation (>40mm) is indicated for TV repair or replacement
If severe primary TR and symptomatic + RV dilatation –> should have TV repair or replacement
If no RV dilatation –> medical therapy
If severe secondary TR + severe RV/LV dysfunction or pulmonary HTN –> medical therapy
If severe secondary TR + RV dilatation with NO severe RV/LV dysfunction or pulmonary HTN –> indicated for TV repair or replacement
Pulmonary regurgitation features
Sequelae of treatment of congenital disorder involving pulmonary valve and/or RV outflow tract - Tetralogy of Fallot, pulmonary stenosis
Severe PS pulmonary artery catherisation findings
Peak gradient 64mmHg
Mean gradient > 35mmHg
How much do PCKS9 inhibitors reduce LDL in addition to statin therapy?
60% further reduction
Have PCSK9 inhibitors been proven to reduce risk of AMI and death?
ODYSSEY OUTCOMES - 15% reduction in mortality (alirocumab)
FOURIER trial - reduction in myocardial infarction but not death (evolocumab)
Inhibition of which proteins lowers LDL cholesterol
PCSK9
HMG-CoA reductase
ANGPLT3
ATP Citrate lyase
