La IC es un síndrome clínico complejo con síntomas y signos que resultan de cualquier

deterioro estructural o funcional del llenado ventricular o la eyección de sangre. El comité

de redacción reconoce que las etapas asintomáticas con cardiopatía estructural o
miocardiopatías no están cubiertas por la definición anterior de IC. Dichos estadios
asintomáticos se consideran de riesgo para IC (estadio A) o pre-IC (estadio B), como se
explica en la Sección 2.1, “Estadios de IC”.

2.1. Stages of HF
The ACC/AHA stages of HF (Figure 1, Table 3) emphasize the development and
progression of disease (1,2), and advanced stages and progression are associated with
reduced survival (3). Therapeutic interventions in each stage aim to modify risk factors
(stage A), treat risk and structural heart disease to prevent HF (stage B), and reduce
symptoms, morbidity, and mortality (stages C and D). To address the evolving role of
biomarkers and structural changes for recognition of patients who are at risk of developing
HF, who are potential candidates for
targeted treatment strategies for the prevention of HF, and to enhance the understanding
and adoption of these classifications, the writing committee proposed the terminologies
listed in Table 3 for the stages of HF. For thresholds of cardiac structural, functional
changes, elevated filling pressures, and biomarker elevations, refer to Appendix 3.

Stage A: At Risk for HF At risk for HF but without symptoms, structural heart disease, or
cardiac biomarkers of stretch or injury (e.g., patients with hypertension, atherosclerotic
CVD, diabetes, metabolic syndrome and obesity, exposure to cardiotoxic agents, genetic
variant for cardiomyopathy, or positive family history of cardiomyopathy).

Stage B: Pre-HF No symptoms or signs of HF and evidence of 1 of the following:

Structural heart disease*

 Reduced left or right ventricular systolic function
 Reduced ejection fraction, reduced strain
 Ventricular hypertrophy
 Chamber enlargement
 Wall motion abnormalities
 Valvular heart disease
Evidence for increased filling pressures*

 By invasive hemodynamic measurements

 By noninvasive imaging suggesting elevated filling pressures (e.g., Doppler
echocardiography)
Patients with risk factors and
 Increased levels of BNPs* or
 Persistently elevated cardiac troponin
in the absence of competing diagnoses resulting in such biomarker elevations such as acute
coronary syndrome, CKD, pulmonary embolus, or myopericarditis.
Stage C: Symptomatic HF Structural heart disease with current or previous symptoms of
HF.

Stage D: Advanced HF Marked HF symptoms that interfere with daily life and with
recurrent hospitalizations despite attempts to optimize GDMT.

For thresholds of cardiac structural, functional changes, elevated filling pressures, and
biomarker elevations, refer to Appendix 3.
BNP indicates B-type natriuretic peptide; CKD, chronic kidney disease; CVD,
cardiovascular disease; GDMT, guideline-directed medical therapy; and HF, heart failure.

New York Heart Association (NYHA) Classification The NYHA classification is used to
characterize symptoms and functional capacity of patients with symptomatic (stage C) HF
or advanced HF (stage D). It is a subjective assessment by a clinician and can change over
time. Although reproducibility and validity can be limited (4,5), the NYHA functional
classification is an independent predictor of mortality (6,7), and it is widely used in clinical
practice to determine the eligibility of patients for treatment strategies. Clinicians specify
NYHA classification at baseline after the initial diagnosis and after treatment through the
continuum of care of a patient with HF. Although a patient with symptomatic HF (stage C)
may become asymptomatic with treatment (NYHA class I), that patient will still be
categorized as stage C HF. Patients with stage C HF can be classified according to the
trajectory of their symptoms (Figure 2).

Type of HF According to LVEF Criteria

HFrEF (HF with reduced EF)
LVEF menor o igual 40%

HFimpEF (HF with improved EF)

Previous LVEF #40% and a follow-up measurement of LVEF >40%

HFmrEF (HF with mildly reduced EF) n LVEF 41%–49%

Evidence of spontaneous or provokable increased LV filling pressures (e.g., elevated

natriuretic peptide, noninvasive and invasive hemodynamic measurement)

HFpEF (HF with preserved EF)

-LVEF $50%
-Evidence of spontaneous or provokable increased LV filling pressures (e.g., elevated
natriuretic peptide, noninvasive and invasive hemodynamic measurement)
EPIDEMIOLOGY AND CAUSES OF HF

3.1. Epidemiology of HF

Trends in Mortality and Hospitalization for HF

HF is a growing health and economic burden for the United States, in large part because of
the aging population (1,2). Beginning in 2012, the age-adjusted death rate per capita for HF
increased for the first time in the United States (3). A recent U.S. evaluation found total
deaths caused by HF have increased from 275,000 in 2009 to 310,000 in 2014 (3). U.S.
hospitalizations for HF decreased up until 2012 (4); however, from 2013 to 2017, an
increase in HF hospitalizations was observed. In 2017, there were 1.2 million HF
hospitalizations
in the United States among 924,000 patients with HF (4). This represents a 26% increase in
HF hospitalizations and number of patients hospitalized with HF. Although the absolute
number of patients with HF has partly grown as a result of the increasing number of older
adults, the incidence of HF has decreased (5). Among U.S. Medicare beneficiaries, HF
incidence declined from 36 cases per 1000 beneficiaries in 2011 to 27 cases per 1000
beneficiaries in 2014 and remained stable through 2016 (5). Divergent trends in the
incidence of HF have been observed for those with HFrEF (decreasing incidence) and
HFpEF (increasing incidence) (6,7). Deaths attributable to cardiomyopathies have been
increasing globally because of, in part, increased recognition, diagnosis, and documentation
of specific cardiomyopathies and cardiotoxicity (2).

Racial and Ethnic Disparities in Mortality and Hospitalization for HF

Racial and ethnic disparities in death resulting from HF persist, with non-Hispanic Black
patients having the highest death rate per capita (4). A report examining the U.S. population
found age-adjusted mortality rate for HF to be 92 per 100,000 individuals for non-Hispanic
Black patients, 87 per 100,000 for non-Hispanic White patients, and 53 per 100,000 for
Hispanic patients (4). Among Medicare beneficiaries, non-Hispanic Black beneficiaries had
a slightly greater decrease in HF incidence (38 cases per 1000 to 26 cases per 1000,
P¼0.009) than non-Hispanic White beneficiaries (36 cases per 1000 to 28 cases per 1000,
P¼0.003) from 2011 to 2016 (4). Among patients with established HF, non-Hispanic Black
patients experienced a higher rate of HF hospitalization and a lower rate of death compared
with non-Hispanic White patients with HF (8-10). Hispanic patients with HF have been
found to have similar (8) or higher (10) HF hospitalization rates and similar (10) or lower
(8) mortality rates compared with non-Hispanic White patients. Asian/Pacific Islander
patients with HF have had a similar rate of hospitalization as non-Hispanic White patients
but a lower rate of death (8,10). These racial and ethnic disparities in outcome, for those
with HF, warrant studies and health policy changes to address health inequity.

3.2. Cause of HF
In the United States, approximately 115 million people have hypertension, 100 million have
obesity, 92 million have prediabetes, 26 million have diabetes, and 125 million have
atherosclerotic CVD (1). These are known risk factors with high relative risk and
population attributable risk for development of HF. Therefore, a large proportion of the
U.S. population can be categorized as being at-risk for HF or stage A HF. The common
causes of HF include
ischemic heart disease and myocardial infarction (MI), hypertension, and valvular heart
disease (VHD). Other causes can include familial or genetic cardiomyopathies;
amyloidosis; cardiotoxicity with cancer or other treatments or substance abuse such as
alcohol, cocaine, or methamphetamine; tachycardia, right ventricular (RV) pacing or stress-
induced cardiomyopathies; peripartum cardiomyopathy; myocarditis; autoimmune causes,
sarcoidosis; iron overload, including hemochromatosis; and thyroid disease and other
endocrine metabolic and nutritional causes (Table 5). Furthermore, with cardiac imaging
and biomarkers, myocardial injury or cardiac maladaptive structural changes can be
detected at earlier phases with a higher sensitivity, even in the absence of gross LV
dysfunction or symptoms. With the coronavirus disease 2019 (COVID-19) pandemic,
investigators are gaining better insights into infection and inflammationrelated myocardial
injury and myocarditis. With the increasing ability to detect myocardial injury and with an
increasing awareness of cardiotoxicity and injury patterns including inflammation, pre-HF
or stage B HF will likely continue to increase. Beyond classifications of EF and staging in
HF, clinicians should seek the cause of HF because appropriate treatment may be
determined by the cause (Table 5).

Other Potential Nonischemic Causes of HF

Cause Reference
 Chemotherapy and other cardiotoxic medications (23-25)
 Rheumatologic or autoimmune (26)
 Endocrine or metabolic (thyroid, acromegaly, pheochromocytoma, diabetes,
obesity) (27-31)
 Familial cardiomyopathy or inherited and genetic heart disease (32)
 Heart rhythm–related (e.g., tachycardia-mediated, PVCs, RV pacing) (33)
 Hypertension (34)
 Infiltrative cardiac disease (e.g., amyloid, sarcoid, hemochromatosis) (21,35,36)
 Myocarditis (infectious, toxin or medication, immunological, hypersensitivity)
(37,38)
 Peripartum cardiomyopathy (39)
 Stress cardiomyopathy (Takotsubo) (40,41)
 Substance abuse (e.g., alcohol, cocaine, methamphetamine)

Selected Potential Causes of Elevated Natriuretic Peptide Levels (50-53)

Cardiac
HF, including RV HF syndromes
ACS
Heart muscle disease, including LVH
VHD
Pericardial disease
AF
Myocarditis
Cardiac surgery
Cardioversion
Toxic-metabolic myocardial insults, including cancer chemotherapy
Noncardiac
Advancing age
Anemia
Renal failure
Pulmonary: Obstructive sleep apnea, severe pneumonia
Pulmonary embolism, pulmonary arterial hypertension
Critical illness
Bacterial sepsis
Severe burns

ACS indicates acute coronary syndromes; AF, atrial fibrillation; HF, heart failure; LVH,
left ventricular hypertrophy; RV, right ventricular; and VHD, valvular heart disease.

for suggested thresholds for laboratory findings. The classification for baseline and
subsequent LVEF is shown. Patients with HFrEF who improve their LVEF to >40% are
considered to have HFimpEF and should continue HFrEF treatment. HF indicates heart
failure; HFimpEF, heart failure with improved ejection fraction; HFmrEF, heart failure
with mildly reduced ejection fraction; HFpEF, heart failure with preserved ejection
fraction; HFrEF, heart failure with reduced ejection fraction; and LVEF, left ventricular
ejection fraction. *There is limited evidence to guide treatment for patients who improve
their LVEF from mildly reduced (41%-49%) to $50%. It is unclear whether to treat these
patients as HFpEF or HFmrEF.

New onset/de novo HF:

-newly diagnosed HF
-No previous history of hf
Resulution of symptoms:
- Stage c with previous simtomps of hf with persisten lv dysfunction
- HF in remission with resolution of previous structural and/or functional heart
desease
Persistent hf:
- Persistent hf with ongoing symptoms/ signs and/or limited functional capacity
Worsening hf:
Worsening symtomps/signs/functional capacity