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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

sergio.caravita@unibg.it

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