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HFmrEF = heart failure with mid-range ejection fraction LAE LVEF = left atrial enlargement
HFpEF = heart failure with preserved ejection fraction LVH = left ventricular ejection fraction
HFrEF = heart failure with reduced ejection fraction = left ventricular hypertrophy
* Signs may not be present in the early stages of HF (especially in HFpEF) and in patients treated with diuretics
**B-type natriuretic peptide (BNP) >35 pg/ml and/or N-terminal pro-B type natriuretic peptide (NT-proBNP) >125 pg/mL
1. Ponikowski P, Voors AA, Anker SD, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2016;37:2129-200
Common Causes and Risk Factors for HF
“Many cases of heart failure can be regarded as the end stage of other
“Many people have existing illnesses that
underlying illnesses and could be prevented if patients with these
place them at risk of heart failure.”1
illnesses were identified and treated appropriately at an earlier stage.”1
1. Ponikowski P, Anker SD, AlHabib KF, et al. Heart failure: preventing disease and death worldwide. ESC Heart Failure 2014;1:4-25
Models Explaining The Pathogenesis of Heart
Hailure1-4
1940s through the 1960s 1970s and 1980s
Cardiorenal model Cardiocirculatory model • Symptom relief
• Diuretics • Inotropes
• Digitalis • Vasodilators
Cardiorenal model1-4
• HF viewed as a problem of excessive salt and water retention caused by abnormalities of renal blood flow
• ® provided rational basis for use of digitalis and diuretics aimed at improving renal function
• HF as a result of abnormalities of the pumping capacity of the heart (® reduced cardiac output) and excessive peripheral vasoconstriction
• ® provided rational basis for use of inotropes, vasodilators to augment cardiac output
Neurohormonal model1-4
• activation of several neurohormonal systems explaining the progression of the disease and exerting direct toxic effects on the myocardium
• ® provided rational basis for use of neurohormonal antagonists (ACEIs, BBs, MRAs)
1. Packer M. How Should Physicians View Heart Failure? The Philosophical and Physiological Evolution of Three Conceptual Models of the Disease. Am J Cardiol 1993;71;3C-11C
2. Mann DL. Mechanisms and Models in Heart Failure. A Combinatorial Approach. Circulation 1999;100:999-1008
3. Mann DL, Bristow MR. Mechanisms and Models in Heart Failure. The Biomechanical Model and Beyond. Circulation 2005;111:2837-49
4. Pepper GS, Ree RW. Sympathetic Activation in Heart Failure and Its Treatment With β-Blockade. Arch Intern Med 1999;159:225-34
Neurohormonal and Compensatory Mechanisms
in the Pathophysiology of Heart Failure1
Poor ventricular function / myocardial damage
(e.g. post myocardial infarction, dilated cardiomyopathy)
Heart failure
Neurohormonal response
• Vasoconstriction: increased sympathetic tone, angiotensin II, endothelins, impaired nitric oxide release
• Sodium and fluid retention: increased vasopressin and aldosterone
1. Jackson G, Gibbs CR, Davies MK, Lip GYH. ABC of heart failure. Pathophysiology. BMJ 2000;320:167-70
ACCF/AHA Stages of Heart Failure Classification3
Comparison of ACCF/AHA stages of HF classification and NYHA functional classification3
I
No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF.
C Structural heart disease with prior or current
symptoms of HF
II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in
symptoms of HF.
III Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes
symptoms of HF.
IV
Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest.
D IV
Refractory HF requiring specialized interventions Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest.
3. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure. Circulation 2013;128:e240-e327
Symptoms and signs of HF
Symptoms Signs
Ankle swelling
ECG normal and BNP <35 pg/mL, or NT- ECG abnormal, BNP ≥35 pg/mL, or NT-proBNP
proBNP <125 pg/mL ≥125 pg/mL
Echocardiograpy
1. Symptoms typical of HF
2. Signs typical of HF
3. Reduced LVEF
Normal or mildly reduced LV systolic function (LVEF >50% and LVEDVI <97 mL/m2)
TD
Biomarkers
Invasive hemodynamic EIEʹ >15 15 >EIE′ >8 NT-proBNP >220 pg/mL or BNP >200
measurements pg/mL
mPCW >12 mmHg
or LVEDP >16 mmHg
or t >48 ms
or b >0.27
TD
Biomarkers
EIE′ >8
NT-proBNP Echo – blood flow Doppler
>220 pg/mL or EIA>50 yr <0.5 and DT>50 yr >280 ms
BNP >200 pg/mL or Ard–Ad >30 ms
or LAVI >40 mL/m2
or LVMI >122 g/m2(♀); >149 g/m2 (♂) or atrial fibrillation
HFpEF
Paulus et al. Eur Heart J 2007;28:2539–50
Particular Relevance of BNP
• diagnosis
• staging
• risk stratification
• monitor/titrate therapy
• admission/discharge decisions:
> rule out symptomatic LV dysfunction
*A new compound (LCZ696; angiotensin receptor neprilysin inhibitor = ARNI) that combines the moieties of an ARB (valsartan) and a neprilysin (NEP) inhibitor (sacubitril) has recently been
shown to be superior to an ACEI (enalapril) in reducing the risk of death and of hospitalization for HF in a single trial with strict inclusion/exclusion criteria. Sacubitril/valsartan is therefore
recommended to replace ACEIs in ambulatory HFrEF patients who remain symptomatic despite optimal therapy and who fit these trial criteria.2,3
1. McMurray JJV, Adamopoulos S, Anker SD, et al. for the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the ESC. Developed in
collaboration with the HFA of the ESC. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012. Eur Heart J 2012;33:1787-1847
2. Ponikowski P, Voors AA, Anker SD, et al. for the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC).
Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart
failure. Eur Heart J 2016;37:2129-2200
3. Metra M, Teerlink JR. Heart failure. Seminar. Lancet 2017;390:1981-95
Treatment options for HFpEF
Improving prognosis
‘No treatment has yet been shown, convincingly, to reduce morbidity and mortality in
patients with HFpEF.’ (ESC Guidelines 2012)
#
STUDY Study drug Endpoint Outcome Publication
Patients
Yusuf S et al
CHARM- CV death or HF
Candesartan 3023 Lancet 2003
Preserved hospitalization
Primary
Cleland JG et al
Death or HF end-point
PEP-CHF Perindopril 850 Eur Heart J 2006
hospitalization not met
Components
• Optimized medical and device management
• Adequate patient education, with special emphasis on adherence and self-care
• Patient involvement in symptom monitoring and flexible diuretic use
• Follow-up after discharge
• Increased access to healthcare
• Facilitated access to care during episodes of decompensation
• Assessment of (and appropriate intervention in response to) an unexplained increase in weight,
nutritional status, functional status, quality of life, and laboratory findings
• Access to advanced treatment options
• Provision of psychosocial support to patients and family and/or caregivers McMurray et al. Eur Heart J 2012;33:1787–847
Summary: HF Guidelines
• ACE-inhibitors, beta-blockers and mineralocorticoid receptor antagonists
form the cornerstone of HF therapy, given their mortality benefit. Incremental
addition of treatments is recommended as HF progresses: Adding therapies
is adding life.
• The ESC guidelines also recommend regular aerobic exercise and enrolment
in care-management programmes.
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