Heart failure
Sergio Caravita, MD, PhD
Department of Management, Information and Production Engineering, University of Bergamo
Cardiology Unit, IRCCS Istituto Auxologico Italiano San Luca Hospital, Milano
11/05/2020
Definition
Clinical syndrome caused by a structural or functional cardiac abnormality, resulting in
failure
to pump blood commensurate with end-organ needs or
to do so at the expense of elevated filling pressures
Pathophysiology
Failure
to pump blood commensurate with end-organ needs
Low cardiacoutput
Fatigue, dyspnea
Dizziness, lethargy
Shock
Pathophysiology
Failure
to pump blood commensurate with end-organ needs or
to do so at the expense of elevated filling pressures
Low cardiacoutput
Left heart Right heart
↑ pulmonary pressure ↑central venous pressure
Pulmonary edema Visceral edemaLeg edema
Fatigue, dyspnea
Dizziness, lethargy
Shock
Dyspnea
Pulmonary edema
↑ filling pressure in the
LEFT side of the heart
↑ pulmonary capillary
pressure
Lung congestion /
edema
Peripheral edema
↑ filling pressure in the
RIGHT side of the heart
↑ peripheral vein
pressure
visceral
congestion / leg
edema
Etiology
Myocardial diseases
Ischemic heart disease
Toxic damage
Immune-mediated and inflammatory damage
Genetic abnormalities
…
Abnormal loading conditions
Hypertension
Valvular heart disease
Congenital heart defects
Pericardial diseases
Volume overload
…
Arrhythmias
Bradyarrhythmias
Tachyarrhythmias
Pathophysiology
↑ cardiacfilling pressure
↓cardiac output
Primary insult
CV risk factorsIschemia CardiomyopathyValvular diseaseVascular disease…
Pathophysiology
↑ cardiacfilling pressure
↓cardiac outputExtravascular fluid
accumulation
Arterial underfilling
Pathophysiology
↑ cardiacfilling pressure
↓cardiac output
Reflex mechanismsSympathetic nervous system activation
Renin-angiotensin-aldosterone system (RAAS) activation…
Renal sodium and water retention
Adverse cardiacremodeling
(fibrosis)
Pathophysiology
↑ cardiacfilling pressure
↓cardiac outputExtravascular fluid
accumulation
Reflex mechanismsSympathetic nervous system activation
Renin-angiotensin-aldosterone system (RAAS) activation…
Renal sodium and water retention
Adverse cardiacremodeling
(fibrosis)
Pathophysiology
↑ cardiacfilling pressure
↓ cardiac output
Upstream organcongestion
Downstream organhypoperfusion
↑ Venous pressure ↓ Arterial pressure
Organ* damage and dysfunctionSystemic inflammation
*Organs:LungKidneyLiverBrain Intestine…
Chronic vs acutely decompensated HF
Chronic HF Acutely decompensated HF
Acute worsening of symptomsOvert fluid overload
Overt cardiac low output
Chronic, slowlyprogressing symptoms
Chronic vs acutely decompensated HF
Chronic HF Acutely decompensated HFTrigger event ±(ischemia, infection, dysrhythmias, drugdiscontinuation, excess salt or water…)
Acute worsening of symptomsOvert fluid overload
Overt cardiac low output
Chronic, slowlyprogressing symptoms
Disease progression
Progression of heart failure
Epidemiology
The prevalence of HF depends on the definition applied, but is approximately 1–2% of the adult population in developed countries, rising to ≥10% among people > 70 years of age.
The lifetime risk of HF at age 55 years is 33% for men and 28% for women
Ponikowski P et al Eur Heart J 2015
Prognosis: HF paradox
Survival after a diagnosis of HF has improved during the past 30 years; the age-adjusted death rate has declined, and the mean age at death from HF has risen.
However, despite these modest improvements, the 5-year mortality is still approximately 50%—worse than that of many cancers
DOI: 10.1016/j.jchf.2012.10.002
HF paradox
Improvements in the prognosis of individual cardiac conditions, such as coronary syndromes, hypertension, valvular and congenital heart diseases growing prevalence of HF. Why?
1) the risk for mortality in each of these disorders has been reduced, the patients are not “cured”. For example, while early mortality in patients with acute myocardial infarction may have declined by 75% during the past half-century, survivors still have coronary artery disease (CAD) and remain at risk for subsequent episodes of ischemic myocardial damage with further loss of myocardium and possibly HF.
2) increased frequency of myocyte death with aging and with the adverse cardiac consequences of comorbid conditions, the prevalences of which rise with age (hypertension; type 2 diabetes mellitus; chronic renal disease; chronic obstructive pulmonary disease; and dysrhythmias)
3) the slow but progressive improvement in HF prognosis mentioned previously simply increases the prevalence of this condition. Whatever the explanation(s), one might conclude that with the continued aging of the population, HF will remain a major health problem, not only in industrialized nations but also in the developing world.
DOI: 10.1016/j.jchf.2012.10.002
Clinical classification according to LV EF
HFrEFHeart Failure with reduced
Ejection Fraction
HFpEFHeart Failure with preserved
Ejection Fraction
Two distinct forms of HF that almost never cross each other
Clinical classification according to LV EF
HFrEFHeart Failure with reduced
Ejection Fraction
HFpEFHeart Failure with preserved
Ejection Fraction
Myocardial diseasesAgeing
EF and modes of death
Diagnosis
Signs and symptoms (dyspnea, fatigue, edema…)
Blood tests (natriuretic peptides: BNP and NTproBNP)
Electrocardiogram (conduction abnormalities, arrhythmias)
Echocardiography
Cardiac magnetic resonance imaging
Cardiopulmonary exercise test
Coronary angiography / coronary computed tomography
Cardiac catheterization
Symptoms assessmentNYHA class and INTERMACS profile
Natriuretic peptides
Natriuretic peptides (NPs) are released from the heart in response to pressure and volume overload.
B-type natriuretic peptide (BNP) and N-terminal-proBNP have become important diagnostic tools for assessing patients who present acutely with dyspnea.
The NP level reflects a compilation of systolic and diastolic function as well as right ventricular and valvular function.
Diagnostic value:
- In the emergency room (triage of dyspnea: cardiac vs non-cardiac)
- In office (severity of HF, prognosis)
Electrocardiogram
Some electrical features can suggest the presence of a specific myocardial disease(some cardiomyopathies) or an ischemic scar
Vicious circle between arrhythmias and HF:
1) Arrhythmias (brady- and tachy- arrhythmias) can predispose to HF or worsen HF
2) HF predisposes to arrhythmias
- atrial arrhythmias: atrial fibrillation
- Ventricular dysrhythmias: ventricular fibrillation and ventricular tachycardia
A subset of patients can present with interventricular conduction disorders
Left bundle branch block (electrical interventricular dyssynchrony) predisposes to mechanical dyssynchrony
EchocardiographyLV systolic function
HFrEFHeart Failure with reduced
Ejection Fraction
HFpEFHeart Failure with preserved
Ejection Fraction
LV systolic functionEchocardiography
Left ventricular ejection fraction
(stroke volume / end-diastolic volume)
Left ventricular global longitudinal strain
(systolic deformation of the left ventricle)
EchocardiographyLV diastolic function (LV filling pressure)
Surrogate for LV stiffness
Non invasive estimation of LV diastolic function and LV filling pressure
From LV diastolic dysfunction to left atrial (LA) failure
https://doi.org/10.1002/ejhf.645
Left atrial failure
EchocardiographyValvular function
Primary valve disease as a cause of HF
vs
HF as a cause of secondary (mitral or tricuspid) valve disease
Papillary muscle displacement occurs as a result of global LV enlargement or focal myocardial scarring, and can affect 1 or both papillary muscles, causing posteriorly directed or central MR
Echocardiographypulmonary circulation
Non-invasive estimation of pulmonary artery pressure
Echocardiographythe right heart
RV complex shape
2D assessment(oversimplification)
3D assessment(volumes, EF…)
Cardiac magnetic resonance imaging
1) Ventricular systolic function
2) Myocardial tissue characterization (scars, fibrosis, infiltration)
CMR is the preferred imaging method to assess myocardial fibrosis using late gadolinium enhancement (LGE) along with T1 mapping and can be useful for establishing HF aetiology.
For example, CMR with LGE allows differentiation between ischaemic and non-ischaemic origins of HF and myocardial fibrosis/scars can be visualized. In addition, CMR allows the characterization of myocardial tissue of myocarditis, amyloidosis, sarcoidosis, Chagas disease, Fabry disease non-compaction cardiomyopathy and haemochromatosis
3) assessment of myocardial ischaemia and viability in patients with HF and CAD (considered suitable for coronary revascularization).
Cardiopulmonary exercise test
Characterization of functional
limitation
≈ severity of the disease
≈ cardiac output reserve
Risk stratification
Oxygen
consumption
(VO2)
Respiratory
reserve
Mechanisms of exercise intolerance
≈ etiology of symptoms
Exercise
hyperventilation
VE/VCO2 slope
Oscillatory
ventilation
(EOV)
Pathophysiological assessment
Multiparametric evaluation informing on the extent of exercise limitation, on the etiology of
symptoms (cardiac vs non-cardiac) and on disease severity
Oxygen uptake (VO2), i.e.:
how much my patient is limited
VO2 = CO x O2(A-V)diffCardiac
output
Guyton, Texbook of Medical Physiology
Guazzi M et al. Circulation 2012;126:2261-74
Guazzi M et al. J Am Coll Cardiol 2017
Caravita S et al. J Heart Lung Transpl 2017;36:754-62
CO
(L
/min
)VO2 (L/min)
VO2 is a quite good noninvasive surrogate
of CO response to exercise in HF.
O2 peripheral
extraction
RV systolic
dysfunction
LV systolic
dysfunction
Coronary angiography / computedtomography
Exclusion of coronary artery disease as a treatable cause of HF
Cardiac catheterization:
Swan-Ganz catheter
Direct measure of Filling pressurePulmonary pressureCardiac output
Prognostic assessment
Multiparametric (e.g. symptoms severity, frequency of hospitalizations, pulmonaryhemodynamics, oxygen consumption..…)
Several scores have been developed in order to help clinicians in stratifying diseaseseverity and allocation of resources (in particular: LVAD and heart transplant)
Treatment
Several clinical trials showing benefits No positive clinical trial
TreatmentHFpEF
Diuretics
Treatment of comorbidities or predisposing factors to HF (LV ischemia, sleepdisordered breathing, anemia, chronic obstructive pulmonary disease)
Treatment HFrEF
Drugs
- Diuretics (reduce/avoid fluid retention and volume overload)
- Drugs acting against the neurohumoral activation (ACE-inhibitors or angiotensin-receptor blockers; beta-blockers)
Cardiac resynchronization therapy (CRT)
Implanted cardioverter defibrillator (ICD)
Cardiovascular rehabilitation
Left ventricular assist device (LVAD)
Heart transplant
Pharmacological treatment of HF
4-5 classes of drugs, some of them subdivided in 2 doses
ACE-inhibitors or AT2-receptor blockers or ARNIs
Beta-blockers
Diuretics
Spironolactone
…
Drugs for CV and non-CV comorbidities
(multimorbid elderly people)
≥5-10 pills per day
potential for drug-drug interactions, non-adherence
Cardiovascular rehabilitation
VO2 = CO x O2(A-V)diffCardiac
output
Guyton, Texbook of Medical Physiology
Guazzi M et al. Circulation 2012;126:2261-74
Guazzi M et al. J Am Coll Cardiol 2017
Caravita S et al. J Heart Lung Transpl 2017;36:754-62
CO
(L
/min
)VO2 (L/min)
VO2 is a quite good noninvasive surrogate
of CO response to exercise in HF.
Cardiovascular rehabilitation:
- Well trained or «hyper O2 extractor»
subjects (can compensate cardiac output
deficit with superoptimal peripheral O2
extraction)
O2 peripheral
extraction
RV systolic
dysfunction
LV systolic
dysfunction
Implanted cardioverter defibrillator
Patients with heart failure and reduced ejection fraction (LVEF < 35%) are at an increased risk of sudden cardiac death due to ventricular arrhythmias.
This risk is highest in those who already suffered from previous ventricular arrhythmic events.
ICD (transvenous vs subcutaneous)
N Engl J Med 2003; 349:1836-1847 J Am Coll Cardiol 2013;61. DOI: 10.1016/j.jacc.2012.07.069
Conduction abnormalities in HFrEFLeft bundle branch block
Typical Left Ventricular Motion Pattern in a Patient With Left Bundle Branch Block and Mechanical Dyssynchrony
Septal regions of the left ventricle (LV) shorten very early during isovolumiccontraction (within QRS width) and cause the apex to move septally (white arrow, middle panel) while the septum moves leftward (septal flash, red arrow, middle panel).
A delayed onset of systolic shortening in the lateral and posterior LV region pulls the apex laterally during the ejection phase (white arrow, right panel) while stretching the septum. This typical sequence of the septal-to-lateral apex motion is described as apical rocking
Conduction abnormalities in HFrEFLeft bundle branch block
Cardiac resynchronization therapy(biventricular pacing)
Cardiac resynchronization therapy(biventricular pacing)
Left ventricular assist device
Heart transplant
Increase in pulmonary artery pressure precedes pulmonary edema and acute decompensation
↑ filling pressure in the
LEFT side of the heart
↑ pulmonary pressure Lung congestion /
edema
Remote pulmonary pressure monitoring
Remote pulmonary pressure monitoring