Heart Failure. Dr. Voltaire Nadurata Clinical Director Cardiology Department

Heart Failure Dr. Voltaire Nadurata Clinical Director Cardiology Department

Introduction and diagnosis Treatment What s new in HF treatment? Atrial fibrillation

Heart failure definition - NHF and CSANZ Heart Failure Guideline 2018 complex clinical syndrome with typical symptoms and signs that generally occur on exertion, but can also occur at rest secondary to an abnormality of cardiac structure or function impaired ability of the heart to fill with blood at normal pressure or eject blood sufficient to fulfil the needs of the metabolising organs

Management of CHF in general practice in Australia NYHA FC for 216 patients (periods 1 and 3 2010 and 2014) - Taylor CJ, Valenti L, et al. AFP 45 (11), Nov 2016 50 45 NYHA FC II, 43.5% (n-94) 40 35 30 25 20 15 NYHA FC I, 25% (n-54) NYHA FC III, 23.1% (n-50) 10 5 0 NYHA FC IV, 6.9% (n-15) NYHA FC I NYHA FC II NYHA FC III NYHA FC IV

In-hospital mortality 4% (same as international benchmark) 30-day unadjusted mortality- 5.2% (lower than international benchmark) HFrEF 8.2% HFpEF 4.7% Readmission at 30 days 26.2% (higher than international benchmark 25%) VCOR-HF Snapshot 2017 Annual report

Precipitant for admission % Ischaemia 10.1 Medication non-adherence 9.6 Medication precipitating drugs 1.5 Rhythm disturbance 13.2 Infection 20.8

Definition of heart failure with reduced, mid-range and preserved ejection fraction - 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure Type of HF HFrEF (reduced) HFmrEF (mid-range) HFpEF (preserved) Criteria 1 Symptoms + Signs Symptoms + Signs Symptoms + Signs 2 LVEF < 40% LVEF 40-49% LVEF >50% 3-1. Elevated levels of natriuretic peptides 2. At least one additional criterion: a. relevant structural heart disease (LVH and/or LAE) b. diastolic dysfunction 1. Elevated levels of natriuretic peptides 2. At least one additional criterion: a. relevant structural heart disease (LVH and/or LAE) b. diastolic dysfunction

Heart failure diagnostic criteria - NHF and CSANZ Heart Failure Guideline 2018 HFrEF Symptoms +/- signs of heart failure HFpEF Symptoms +/- signs of heart failure LVEF < 50% LVEF > 50% Objective evidence of: - Structural heart disease (LVH, LAE) and/or - Diastolic dysfunction, with high filling pressure demonstrated by any of the following: cardiac cath, echo, BNP/NT probnp, exercise test

Vicious Cycle of heart failure pathophysiology - NHF and CSANZ HF guidelines 2011

Typical trajectory of illness in CHF compared to terminal malignancy - NHF and CSANZ HF guideline 2011

Severity of Heart FailureModes of Death - MERIT-HF Study Group. LANCET. 1999;353:2001-07 NYHA II (n-103) NYHA III (n-103) 12% CHF 26% CHF 24% Other 59% Other 64% Sudden Death 15% Sudden Death NYHA IV (n-27) 33% 56% CHF Other 11% Sudden Death

Drivers and potential targets for treatment in heart failure with reduced EF - NHF and CSANZ HF guidelines 2018

Signs and symptoms of heart failure - NHF and CSANZ HF guidelines 2018

Step by step assessment of NYHA FCs - National Heart Foundation. Congestive Heart Failure Guideline Any Yes 1. Can you walk down a flight of steps without stopping? Go to 2 Go to 4 2. Can you carry something up a flight of 8 steps with stopping? Or can you: a) Have sexual intercourse without stopping? b) Garden, rake, weed? c) Walk at 6km/hour on level ground? 3. Can carry at least 10 kgs up 8 steps? Or can you: a) Carry objects that are at least 36 kgs? b) Ski, play basketball, squash? 4. Can you shower without stopping? Or can you: a) Mop floors? b) Hang out wet clothes? c) Clean windows? d) Walk 4 km/hour? e) Play golf, walk and carry clubs? f) Push power lawn mower? Go to 3 Class I No Class III Class II Class III Go to 5 5. Can you dress without stopping? Class III Class IV

Diagnostic workup of a patient suspected of heart failure - NHF and CSANZ HF guidelines 2018

Imaging in Heart Failure Transthoracic Echocardiography Transoesophageal Echocardiography Stress Echocardiography Contrast echo and strain imaging echocardiography Cardiac MRI Cardiac CT Nuclear imaging

LV dimension Ejection fraction Valvular abnormalities

Stress Echocardiography Used for assessment of flow limiting coronary artery disease Functional capacity testing Cardiac arrhythmia Invasive coronary angiography will be required if wall motion abnormality or exercise induced LV systolic dysfunction

Transeosphageal Echocardiography Useful in patient with poor transthoracic echo image quality Assessment for other abnormalities constrictive pericarditis intracardiac shunt intracardiac thrombus mitral regurgitation severity and mechanism

Coronary angiogram and cardiac catheterisation

Other imaging modalities CT coronary angiography non-invasive assessment of coronary arteries issue with radiation and image quality Cardiac MRI Highly specialized test LV function and structural heart disease No radiation Nuclear imaging myocardial perfusion scan gated heart pool scan to assess LV systolic function

Other diagnostic tests BNP and NTproBNP prognostic value most powerful predictors of mortality and adverse CV outcome clinical impact and change in management is uncertain Genetic testing cardiomyopathy associated with conduction disease

Introduction and diagnosis Treatment What s new in HF treatment? Atrial fibrillation

Beta-blockers ACE-inhibitors or Angiotensin receptor blocker Mineralocorticoid antagonist ARNI Hydralazine and nitrates Digoxin Diuretics Cardiac implantable electrical devices

Basis for beta-blocker usage in heart failure Upregulation of Beta receptors Direct myocardial protective action against cathecolamine toxicity Antiarrhythmic effects Increase coronary blood flow by reducing heart rate and improving diastolic perfusion time Vasodilation Prevention of ventricular muscle hypertrophy and vascular remodelling

Beta-blockers for HFrEF - ACC/AHA Heart failure guidelines 2014 Drug Initial Daily Dose(s) Maximum Doses(s) Mean Doses Achieved in Clinical Trials Beta Blockers Bisoprolol 1.25 mg once 10 mg once 8.6 mg/d Carvedilol 3.125 mg twice 50 mg twice 37 mg/d Nebivolol 1.25mg once 10 mg once --------- Metoprolol succinate extended release (metoprolol CR/XL) 23.75 mg once 190 mg once 159 mg/d

Properties of beta blockers with evidence on treatment of heart failure Bisoprolol Carvedilol Metoprolol Nebivolol Β1-selectivity Yes No Yes Yes Peripheral vasodilation No Yes No Yes Antioxidant effect No Yes No No Nitric Oxide release No No No Yes Drugs Aging 2007; 24 (12): 991-1006

Beta-blockers practice advise - NHF and CSANZ HF guidelines 2018 Ensure that the patient is clinically stable and euvolaemic before commencing beta blockers. Commenced after starting ACE inhibitors (or ARBs); however, if the patient is euvolaemic, they may be commenced before starting ACE inhibitors (or ARBs) Started at low doses and gradually uptitrated by doubling the dose every 2 4 weeks, aiming for target doses or maximum tolerated doses Patients should be reviewed following initiation and each dose escalation with monitoring of heart rate, blood pressure, and clinical evaluation of volume status at 1 2 weeks and 6- monthly long term Uptitration of beta blockers should not be to the detriment of starting other drugs that have been shown to decrease mortality in patients with HFrEF If the patient develops symptomatic bradycardia (<50 bpm), arrange an ECG to document the rhythm and review the need for other drugs lower heart rate If the patient develops symptomatic hypotension, assess volume status and review the need for other drugs not shown to improve outcomes in heart failure that lower blood pressure If the patient develops increasing congestion, this can usually be managed by increasing the diuretic dose, but occasionally may require a reduction in the beta blocker dose

ACE Inhibition and Angiotensin receptor blockade Reduce angiotensin II vasoconstriction Normalize peripheral vascular structure Improve endothelial dysfunction Reduce levels of circulating endothelin Reduce smooth muscle mass

ACE inhibitors and ARBs for HFrEF - ACC/AHA Heart failure guidelines 2014 Drug Initial Daily Dose(s) Maximum Doses(s) Mean Doses Achieved in Clinical Trials ACE Inhibitors Captopril 6.25 mg 3 times 50 mg 3 times 122.7 mg/d Enalapril 2.5 mg twice 10 to 20 mg twice 16.6 mg/d Fosinopril 5 to 10 mg once 40 mg once --------- Lisinopril 2.5 to 5 mg once 20 to 40 mg once 32.5 to 35.0 mg/d Perindopril 2 mg once 8 to 16 mg once --------- Quinapril 5 mg twice 20 mg twice --------- Ramipril 1.25 to 2.5 mg once 10 mg once --------- Trandolapril 1 mg once 4 mg once --------- ARBs Candesartan 4 to 8 mg once 32 mg once 24 mg/d Losartan 25 to 50 mg once 50 to 150 mg once 129 mg/d Valsartan 20 to 40 mg twice 160 mg twice 254 mg/d

ACE inhibitors and ARB practice advise - NHF and CSANZ HF guidelines 2018 ACE inhibitors are started at low doses and uptitrated by doubling the dose every two weeks, aiming for target or maximum tolerated doses. Patients should be reviewed following initiation and each dose increase with monitoring of BP and biochemistry (renal function, potassium) at 1 2 weeks and 6-monthly long term. Uptitration of ACE inhibitors should not be to the detriment of starting other drugs that have been shown to decrease mortality in patients with HFrEF. Small rises in serum creatinine and asymptomatic falls in blood pressure are common following the of ACE inhibitors. doses commencement If the patient develops symptomatic hypotension, the egfr decreases by more than 30%, or the K rises above 5.5 mmol/l, the volume status should be assessed and the need for other drugs not shown to improve outcomes in heart failure that lower blood pressure or impact on renal function and potassium should be reviewed. If the patient develops angioedema, ACE inhibitor ceased, and specialist advice sought. If the patient develops a cough, one should consider whether this is due to pulmonary congestion or lung disease. If it is felt likely that the cough is related to the ACE inhibitor is interfering with the patient s quality of life, the ACE inhibitor may be changed to an ARB.

Diuretics First line usually frusemide and up titrate dependent on the blood pressure and renal function. Hyponatraemia is independent predictor of poor outcome Mineralocortoid receptor antagonists (MRA) Spironolactone Eplerenone

Mineralocorticoid antagonists Drug Initial Daily Dose(s) Maximum Doses(s) Mean Doses Achieved in Clinical Trials Aldosterone Antagonists Spironolactone 12.5 to 25 mg once 25 mg once or twice 26 mg/d Eplerenone 25 mg once 50 mg once 42.6 mg/d ACC/AHA Heart failure guidelines 2014

Spironolactone RALES - Randomized Aldactone Evaluation Study 30% reduction in all-cause death 31% decrease in death from cardiac causes 30% reduction in hospitalizations for cardiac causes significant improvement in NYHA functional class. * very few patients were taking beta blockers Szady AD, Hill JA. Drugs 2009; 69 (17): 2451-2461

Eplerenone EPHESUS - Eplerenone Post-AMI Heart Failure Efficacy Survival Study * AMI within 3 14 days of randomization statistically significant decreases death from any cause death from cardiovascular causes 21% reduction in the rate of sudden death hospitalizations for cardiovascular events 23%reduction in the number of hospitalizations for heart failure Szady AD, Hill JA. Drugs 2009; 69 (17): 2451-2461

Diuretic resistance - Szady AD, Hill JA. Drugs 2009; 69 (17): 2451-2461 braking phenomenon in acute setting, kidney maintains a neutral sodium balance once the diuretic is no longer at therapeutic concentration, sodium reabsorption is stimulated and a new steady state is achieved where the same amount of diuretic induces less natriuresis and diuresis increased sodium delivery over time to the distal tubule stimulates hypertrophy of these cells and their increased reabsorption of sodium activation of the RAAS

Diuretic Resistance clinical strategy for diuretic use - Szady AD, Hill JA. Drugs 2009; 69 (17): 2451-2461 acute decompensated heart failure low sodium diet may lessen braking phenomenon continuous infusion chronic heart failure intermittent dosing higher doses to overcome the decreased secretion into the proximal tubule due to decreased renal blood flow switching to bumetanide due to its higher bioavailability combining the use of loop and thiazide diuretics blockade of RAAS with ACE inh and aldosterone antagonists

ACE inhibitors and ARB practice advise - NHF and CSANZ HF guidelines 2018 MRAs should be avoided or used cautiously in patients with stage 4 or 5 chronic kidney disease or serum potassium above 5 mmol/l. Patients should be instructed to avoid foods high in potassium and potassium supplements Low doses are prescribed, starting with 25 mg daily for spironolactone or eplerenone and uptitrating in 4 8 weeks, aiming for target doses of 50 mg daily spironolactone or eplerenone. Patients should be reviewed following initiation and each dose escalation with monitoring of blood pressure and blood biochemistry at 1 2 weeks, then every 4 weeks for 12 weeks, at 6 months and then 6-monthly If the egfr decreases by more than 30% or the serum potassium rises above 5.5 mmol/l, assess volume status and review the need for other drugs that affect renal function and potassium If the serum potassium rises above 6.0 mmol/l, the MRA should be ceased Patients who develop gynaecomastia on spironolactone may be switched to eplerenone.

ARNI angiotensin receptor neprilysin inhibitor New drug on the market at the moment Stopped early due to the finding of both significantly reduced risk of CV death vs. enalapril (HR: 0.80, p<0.001) and the primary endpoint being met Needs a washout period of 36 hours if from ACEi Based on the previous ACEi/ARB will dictate the dose that it is started on. Gradual increase in dose over a period of 2 weeks

The SNS and RAAS are over-activated in HF and are responsible for many of the pathophysiological responses that contribute to disease progression SNS HEART FAILURE SYMPTOMS & PROGRESSION Adrenaline Noradrenaline α 1, β 1, β 2 receptors Vasoconstriction RAAS activity Vasopressin Heart rate Contractility RAAS Ang II AT 1 R Vasoconstriction Blood pressure Sympathetic tone Aldosterone Hypertrophy Fibrosis

Secretion of natriuretic peptides results in a number of responses that act to reduce the symptoms and progression of HF NP system NPRs NPs Vasodilation Blood pressure Sympathetic tone Natriuresis/diuresis Vasopressin Aldosterone Fibrosis Hypertrophy INACTIVE FRAGMENTS HEART FAILURE SYMPTOMS & PROGRESSION

Imbalance in these key neurohormonal systems drives HF progression Pathologic activation ARB - valsartan RAAS SNS Natriuretic peptide system e.g. ANP, BNP, CNP Compensatory activation sodium/water retention and BP Vasoconstriction cardiac output Cardiac and vascular hypertrophy Blood vessel dilation (vasodilation) sodium/water excretion Fibrosis inhibition Inhibition of aldosterone release Sacubitril neprilysin inhibitor Persistent pathophysiological HF progression

ARNI angiotensin receptor neprilysin inhibitor - NHF and CSANZ HF guidelines 2018 Recommended as a replacement for an ACE inhibitor or an ARB in patients with HFrEF associated with an LVEF of less than or equal to 40% despite receiving maximally tolerated or target doses of an ACE inhibitor (or ARB) and a beta blocker (unless contraindicated), with or without an MRA, to decrease mortality and decrease hospitalisation.

ARNI practice advise - NHF and CSANZ HF guidelines 2018 Ensure that ACE inhibitors are stopped at least 36 hours before commencing Start at a low or moderate doses and uptitrated by doubling the dose every 2 4 weeks, aiming for target doses or maximum tolerated doses Reviewed following initiation and each dose escalation with monitoring of blood pressure and blood biochemistry (renal function and potassium) at 1 2 weeks and 6- monthly long term Uptitration of ARNIs should not be to the detriment of starting other drugs (beta blockers and MRAs) that have been shown to decrease mortality in patients with HFrEF Small rises in serum creatinine and asymptomatic falls in blood pressure are common following the commencement. If the patient develops symptomatic hypotension, the egfr decreases by more than 30% or the serum K rises above 5.5 mmol/l, assess volume status and review the need for other drugs that lower blood pressure or affect renal function and K If the patient develops angioedema, this should be managed, the ARNI should be ceased

Ivabradine Act specifically on the sinus node, by selective inhibition of the I f current Has no impact on atrioventricular conduction or QT interval, no negative inotropic properties, no effect on blood pressure or the electrophysiological properties of the heart and can be safely coadministered with other therapies including beta-blockers Potent anti-anginal agent Steg P G Eur Heart J Suppl 2010;12:C11-C15

Ivabradine practice advise - NHF and CSANZ HF guidelines 2018 Should be considered in patients with HFrEF associated with an LVEF of less than or equal to 35% and with a sinus rate of 70 bpm and above despite receiving maximally tolerated or target doses of an ACE I inhibitor (or ARB) and a beta blocker (unless contraindicated), with or without an MRA, to decrease the combined endpoint of cardiovascular mortality and hospitalisation for heart failure.

Ivabradine practice advise - NHF and CSANZ HF guidelines 2018 Ensure patients are on maximally tolerated or target doses of beta blockers (unless contraindicated) If sinus rate is 70 bpm or above despite maximally tolerated or target doses of beta blockers (unless contraindicated), ivabradine should be considered Start at 2.5 5.0 mg twice daily and uptitrate by doubling the dose every 2 4 weeks, aiming for a target dose of 7.5 mg twice daily or the maximum tolerated dose. Patients should be reviewed following initiation and each dose escalation with monitoring of heart rate at 1 2 weeks and 6-monthly long term. Aim for a sinus rate between 50 and 60 bpm Prescribing and uptitration of ivabradine should not be to the detriment of starting other drugs that have been shown to decrease mortality in patients with HFrEF If the patient develops symptomatic bradycardia or asymptomatic bradycardia below 50 bpm, arrange an ECG to document the rhythm and review the need for other drugs that lower heart rate (e.g., digoxin and amiodarone). If the patient develops persistent or permanent AF, cease ivabradine and review the need for ivabradine if and when the patient reverts to sinus rhythm

Hydralazine plus Nitrates practice advise - NHF and CSANZ HF guidelines 2018 Hydralazine plus nitrates may be considered in patients in whom ACE inhibitors and ARBs are contraindicated or not tolerated, and in patients with refractory moderate or severe symptoms despite best practice therapy Low doses of hydralazine (25 mg three times daily) plus nitrates (isosorbide dinitrate 20 mg three times daily or isosorbide mononitrate 60 mg once daily) are usually started and uptitrated over two to four weeks, aiming for target doses of hydralazine (50 75 mg three times daily) plus nitrates (isosorbide dinitrate 60 mg three times daily or isosorbide mononitrate 120 mg once daily) or maximum tolerated doses Review following initiation and each dose escalation with monitoring of blood pressure at 1 2 weeks and 6-monthly long term Prescribing and uptitration of hydralazine plus nitrates should not be to the detriment of starting other drugs that have been shown to decrease mortality in patients with HFrEF If the patient develops symptomatic hypotension, assess volume status and review the need for other drugs that lower blood pressure (e.g., calcium channel blockers, diuretics).

Digoxin No effect on mortality in heart failure. May be useful for maintaining clinical stability and exercise capacity in patients with symptomatic heart failure. Second-line drug after diuretics, angiotensin-converting enzyme inhibitors and β-blockers in patients with congestive heart failure who are in sinus rhythm. First-line drug in patients with congestive heart failure who are in atrial fibrillation. Campbell TJ, MacDonald PS. MJA 2003; 179 (2): 98-102

Optimal dosing for digoxin Low serum digoxin concentrations reduces HF mortality HF hospitalizations < or = 0.125 mg/ day Ahmed A, Pitt B, Braunwald E, et al. Int J Cardiol. 2008 Jan; 123 (2), 138-146

HFrEF Management Algorithm - NHF and CSANZ HF guidelines 2018

Treatment of Heart Failure With Recovered Ejection Fraction - NHF and CSANZ HF guidelines 2018 Cardiac function may not be normal despite a normal LVEF, with in patients with a normal LVEF. Recovery is likely to represent remission rather than cure in most cases persistent abnormalities in biomarkers, abnormal functional capacity, and poor contractile reserve Three small clinical trials of beta blocker withdrawal iwere associated with decreases in EF, and recurrence of heart failure and deaths; a retrospective study identified cessation of heart failure medications as the only predictor of recurrence in heart failure with recovered EF Unless a reversible cause has been corrected, medications should be continued at target doses in patients with heart failure to decrease the risk of recurrence Loop diuretics and thiazides may be weaned and ceased as tolerated

Follow-up 7-14 days following discharge (OPTIMISE-HF: associated with significant reduction in readmission) frequency should be guided by clinical state Self-management patient and carer education patient centred revised as required and literacy guided taking right meds at right dose and time monitoring of signs and symptoms collaboration with health professionals - NHF and CSANZ HF guidelines 2018

Fluid restriction for patients with overt congestion, restrict to 1.5L/day if weight increases by 2kg in 2 days, see doctor and consider increase in diuretic sliding scale of diuretics for competent patients Sodium intake no clear evidence consensus recommendation is to follow NHF guideline of <2g/day Exercise training continuous endurance training resistance training may be more beneficial for advance HF - NHF and CSANZ HF guidelines 2018

Introduction and diagnosis Treatment Acute heart failure What s new in HF treatment? Atrial fibrillation

Cause of acute decompensation of chronic heart failure - NHF and CSANZ HF guidelines 2018 Acute MI or ischemia Arrhythmia (AF, VT) Infection (respiratory, endocarditis) Anaemia Thyroid disorder Increased sympathetic drive (acute hypertension, pheochromocytoma, takotsubo cardiomyopathy) Acute renal failure Hypoxia (pneumonia, PE) Noncompliance with medications, fluid, salt restriction Pericardial tamponade Drugs that may worsen heart failure Adrenal insufficiency or steroid excess Mechanical issue (myocardial rupture, acute valve regurgitation

CRT (with or without an ICD) - NHF and CSANZ HF guidelines 2018 Should be considered for patients with heart failure associated with an LVEF of less than or equal to 35% and a QRS duration of 130 ms or more despite optimal medical therapy The benefit of CRT is greater in patients with a broader QRS duration (especially QRS duration 150 ms) Other factors that may influence decision-making If CRT is performed in patients in AF, measures are required to ensure at least 92% biventricular capture

Implantable Cardiac Defibrillator - NHF and CSANZ HF guidelines 2018 Generally single-chamber ICDs are recommended with an atrial lead included only if there is a separate bradycardia indication CRT should also be considered in patients with HFrEF associated with a QRS duration of 130 ms or more and an LVEF of less than or equal to 35% Multicenter Automatic Defibrillator Implantation Trial Reduce Inappropriate Therapy (MADIT-RIT) study demonstrated the importance of programming with a reduction in inappropriate ICD therapy and total mortality with device therapies delivered at ventricular rates of more than 200 bpm or with a 60-second delay for rates of more than 170 bpm Device programming for bradycardia parameters should be at a lower rate of 40 bpm, to minimise ventricular pacing Subcutaneous ICDs may be considered in younger people for primary prevention, however, do not provide antita- chycardia pacing or bradyarrhythmia pacing support

Remote monitor network within 3-5 metre distance area where patient spend at least 3 minutes at home

SCRAM - Smartphone Cardiac Rehabilitation Assisted self-management intervention

AF and Heart Failure - NHF and CSANZ HF guidelines 2018 Under-recognised reversible cause of HFrEF, particularly in patients who present with both conditions in the absence of other identifiable causes Common in patients with heart failure prevalence ranges from 5% in FC I up to 50% in FC IV, with annual incidence of 2 5% Common precipitant of heart failure, and conversely, heart failure is the strongest predictor for AF, and AF can result in myocardial dysfunction and heart failure [399]. Combination of loss of the atrial kick and irregular fast heart rhythm can reduce the cardiac output by up to 30% Although a randomised comparison of rate compared with rhythm control using pharmacological strategies in AF in HFrEF did not demonstrate superiority, this has been challenged by catheter ablation studies.

Anticoagulation is recommended AF and Heart Failure - NHF and CSANZ HF guidelines 2018 Pharmacological therapy for rate control aiming for a resting ventricular rate of 60 100 bpm Reversion to normal sinus rhythm for rhythm control Catheter ablation for AF (either paroxysmal orpersistent) should be considered who present with recurrent symptomatic AF

Treatment options Anticoagulation imperative Electrical cardioversion Anti-arrhythmic therapy Beta-blockers Amiodarone Digoxin

Pulmonary vein Isolation procedure Ablate & pace

Acute rate control of AF with rapid ventricular response - NHF and CSANZ AF guideline 2018

Chronic rate control of AF with rapid ventricular response - NHF and CSANZ AF guideline 2018

Long-term rhythm control strategy - NHF and CSANZ AF guideline 2018

Bendigo Health Comprehensive cardiac care Community health care HARP Cardiac rehabilitation Palliative Care Cardiologist Cardiac Liaison nurse

Clinical pathways Murray PHN