Heart failure definition classification

© 2017 Nigerian Journal of Cardiology | Published by Wolters Kluwer - Medknow 9
Heart failure: Definition, classification, and
pathophysiology – A mini‑review
Saheed O Adebayo, Taiwo O Olunuga, Amina Durodola, Okechukwu S Ogah1
Department of Internal Medicine, Cardiology Unit, Federal Medical Centre, Abeokuta, 1
Department of Medicine, Division of Cardiology,
University College Hospital, Ibadan, Nigeria
Review Article
INTRODUCTION
Heart failure (HF) is a clinical syndrome characterized by
dyspnea, fatigue, and clinical signs of congestion leading
to frequent hospitalizations, poor quality of life, and
shortened life expectancy.[1]
It is a final common pathway
to various heart diseases.[1]
HF is a growing problem
worldwide with serious consequences in Sub‑Saharan
Africa (SSA) where there is limited resources.[2‑4]
The incidence and prevalence of congestive HF vary
worldwide. In the United States of America, the incidence is
estimated as 500,000 new cases annually and prevalence of
5.1 million people.[5,6]
There is paucity of population‑based
data from developing countries including Nigeria.
Various studies from different regions of the country
have documented etiology of HF with hypertension,
cardiomyopathy, and rheumatic heart diseases (RHDs) as
the leading causes.[4,7‑17]
A recent report from the SSA Survey of HF revealed that
acute HF in SSA appears to affect younger patients in the
prime of their lives and is mainly caused by preventable
and treatable causes such as hypertension (43.9%), dilated
cardiomyopathy (DCM) (19.5%), and RHD (15%) among
other causes.[2,10]
Despite advancements in medical, device‑based, and surgical
management of HF, outcome is still not encouraging even
in Western countries. These could be attributed to aging
population, delay in instituting evidence‑based therapy
as a result of misdiagnosis, poor application of therapy,
nonavailability of therapy, comorbidities, complications,
noncompliance with medications, lack of funds, and
Heart failure is a clinical syndrome characterized by dyspnea, fatigue, and clinical signs of congestion
leading to frequent hospitalizations, poor quality of life, and shortened life expectancy. It is a final common
pathway to various cardiac conditions. It is a growing problem worldwide with serious consequences in
Sub‑Saharan Africa where it occurs at a younger age with limited resources to manage the condition. The
incidence and prevalence vary worldwide. In this mini‑review, we looked at the definition, classification,
and pathophysiology of the condition.
Keywords: Cardiac failure, classification, definition, heart failure, pathophysiology
Abstract
Access this article online
Quick Response Code:
Website:
www.nigjcardiol.org
DOI:
10.4103/0189-7969.201913
Address for correspondence: Dr. Okechukwu S Ogah, Department of Medicine, Division of Cardiology, University College Hospital, PMB 5116, Ibadan,
Nigeria. E‑mail: osogah56156@yahoo.com
How to cite this article: Adebayo SO, Olunuga TO, Durodola A, Ogah OS.
Heart failure: Definition, classification, and pathophysiology – A mini-review.
Nig J Cardiol 2017;14:9-14.
This is an open access article distributed under the terms of the Creative Commons
Attribution‑NonCommercial‑ShareAlike 3.0 License, which allows others to remix, tweak,
and build upon the work non‑commercially, as long as the author is credited and the
new creations are licensed under the identical terms.
For reprints contact: reprints@medknow.com
[Downloaded free from http://www.nigjcardiol.org on Sunday, December 2, 2018, IP: 117.248.142.125]

Adebayo, et al.: Heart failure: A mini‑review
10 Nigerian Journal of Cardiology | Volume 14 | Issue 1 | January-June 2017
negative sociocultural beliefs of patients, especially in the
developing world.[1]
The clinical manifestation of HF significantly impairs the
functional capability of the patients to varying degrees. This
is usually assessed with symptoms and noninvasively with
echocardiography. One of the widely employed methods
is New York Heart Association (NYHA) classification
which assesses the functional impairment and disease
severity. It is a simple, quick, and easily administered but
subjective assessment which has been widely used in routine
clinical and research activities. It has good correlation with
prognostic indices.[18]
Likewise, distance covered during
6 min walk test has also been employed to assess functional
status. It is an objective measure of submaximal exercise
capacity with good prognostic implications.[19‑23]
In addition,
left ventricular (LV) systolic function routinely determined
with LV ejection fraction (EF), though correlates poorly
with symptoms, has good prognostic and therapeutic
significance.
In this minireview, we explore the definition, classification,
and pathophysiology of HF.
Definitions of heart failure
HF is a complex clinical syndrome and as such many authors
have put forward different definitions in the past [Table 1].
European Society of Cardiology in 2008 defined HF as
“an abnormality of cardiac structure or function leading to
failure of the heart to deliver oxygen at a rate commensurate
with the requirements of the metabolizing tissues despite
normal filling pressures (or only at the expense of increased
filling pressures).”[26]
Table 2 shows the major and minor
criteria for the diagnosis of HF.
EPIDEMIOLOGY AND CLASSIFICATION
HF is a burgeoning problem worldwide with more than 26
million people affected.[28]
The overall prevalence of HF
in the adult population in developed countries is 1%–3%
with exponential rise with age. It affects 6%–10% of people
over the age of 65 years.[29]
Although the relative incidence of HF is lower in women
than men, women constitute at least half of the cases
because of their longer life expectancy.[29]
Population‑based studies on the incidence and prevalence
of HF in developing countries are evolving. It was
estimated that cardiovascular (CV) diseases accounted for
7%–10% of all medical admissions to African hospitals and
HF constitutes 3%–7% of these admissions.[10]
Several studies have demonstrated that hypertension
/hypertensive heart disease, DCM, chronic RHDs,
corpulmonale, and pericardial diseases constitute the major
etiological factors of HF in Nigeria.[3,14‑17,30‑32]
In the Abeokuta HF registry, (a local registry of HF
patients seen at Federal Medical Centre and Sacred
Heart Hospital, both in Abeokuta) the mean age of
56 ± 15 years was reported, with women being older than
Table 1: Some of the definitions of heart failure
Authors Year Definitions
Mann[24]
2012 HF is “the clinical syndrome characterized
by dyspnea, fatigue, and clinical signs
of congestion leading to frequent
hospitalizations, a poor quality of life, and
shortened life expectancy”
Mann DL et al.[25] 2012 HF may be viewed as a “progressive
disorder that is initiated after an index
event either damages the heart muscle,
with a resultant loss of functioning cardiac
myocytes or disrupts the ability of the
myocardium to generate force, thereby
preventing the heart from contracting
normally”
McMurray et al.[26] 2012 HF is “defined clinically as a syndrome
in which patients have typical symptoms
(e.g., breathlessness, ankle swelling, and
fatigue) and signs (e.g., elevated jugular
venous pressure, pulmonary crackles,
and displaced apex beat) resulting from
an abnormality of cardiac structure or
function”
Yancy et al.[27] 2013 HF has been defined by the ACC/AHA
(guidelines of HF) “as a complex syndrome
that results from any structural or
functional cardiac disorder that impairs the
ability of the ventricle to fill with or eject
blood”
ACC/AHA: American College of Cardiology/American Heart Association
Table 2: Major and minor criteria for the diagnosis of heart
failure
Major criteria
Paroxysmal nocturnal dyspnea or orthopnea
Neck‑vein distension
Rales
Cardiomegaly on chest X‑ray
Acute pulmonary edema
S3 gallop
Increased venous pressure >16 cm of water
Circulation time >25 s
Hepatojugular reflux
Minor criteria
Ankle edema
Night cough
Dyspnea on exertion
Hepatomegaly
Pleural effusion
Vital capacity decreased 1/3 from maximum
Tachycardia (rate of >120/min)
Major or minor criterion: Weight loss >4.5 kg in 5 days in response to
treatment. The clinical diagnosis of HF is based on 2 major criteria or 1
major with 2 minor criteria. HF: Heart failure

Nigerian Journal of Cardiology | Volume 14 | Issue 1 | January-June 2017 11
men and an overall prevalence of 9% among all medical
admissions.[33‑36]
The most common etiology is hypertensive HF (66%),
followed by DCM (12%), corpulmonale (8%),
RHDs (3%), and pericardial diseases.[36]
Hypertension
and cardiomyopathy are also the leading causes in Sagamu,
Kano, and other parts of the country.[3,16,17,30,31]
With widespread availability of the echocardiography,
HF is now routinely classified based on EF as HF with
preserved EF (HFpEF: EF ≥50%), HF with reduced
EF (HFrEF: EF ≤40%), and HF with mid‑range EF
(EF = 41%–49%).[37]
There are no symptoms or signs that specifically distinguish
between the three categories.[38]
However, the classification
has good therapeutic importance as HFrEF has clear line of
management with evidence‑based disease modifying agents
such as angiotensin‑converting enzyme inhibitor (ACEI),
angiotensin receptor blockers (ARB), beta blockers (BBs),
and aldosterone receptor blockers while the management
of the HFpEF currently focuses on comorbidities,
precipitants, and etiology as there is no treatment that
convincingly improves the morbidity and mortality.[28,39,40]
Patients with HFpEF are usually older, female, hypertensive
with nondilated chambers while the counterpart with
HFrEF is usually younger with progressive chamber
dilatation and reduced stroke volume, majorly due to
ischemic heart disease in Caucassians while hypertension
accounts chiefly for the cases in Africans.[28,41]
Use of the disease modifying agents in our environment
has been noted to be similar to what is obtainable in the
Western world as depicted by various studies.[10,36]
However,
digoxin use is significantly higher in our cohort. This may
be attributed to its relative availability and affordability as
compared to other inotropes and the prevalence of reduced
systolic function.[36]
The use of hydralazine/nitrates combination has also
been documented to be low.[10]
This is largely due to lack
of familiarity with the medications as well as lack of local
studies to corroborate beneficial outcomes from the
African‑American HF study.[42,43]
The result of bitreatment
with hydralazine/isosorbide dinitrate versus placebo on
top of standard care in African patients admitted with
acute HF (BAHEF trial) has just been released.[44]
The
authors found that hydralazine/isosorbide combination
showed nonstatistically significant benefit over placebo on
secondary end points (change in dyspnea severity at day 7
or discharge, systolic blood pressure, weight, 6‑min walk
test distance at week 24, and echocardiographic cardiac size
and function). There was no benefit on primary end point
of death or readmission within 6 months.[44]
As regards prognosis, Ogah et al. recently looked at the
short‑term outcomes after discharge in Abeokuta HF
registry and found that the mortality was 4.2% at 30 days
which increased to 7.5% at 6 months with patients with
pericardial diseases having initial highest mortality.[45]
Factors associated with poor outcomes as noted by various
authors in our environment include low EF, anemia, low
blood pressure, low body mass index, impaired renal
function, and rhythm disorders.[30,31]
Surprisingly, hyponatremia and hypokalemia were
predictors of favorable outcomes from the report by Ogah
et al. as opposed to what is known in Caucasians.[45‑49]
This
was attributed to better diuretic response in our cohort and
possibly due to the fact that the pathophysiology of HF in
blacks is less dependent on sodium.[32]
Likewise, obesity had
been associated with favorable outcome in HF patients.[50,51]
On the other hand, higher rates of readmission within
6 months were noted in those with older age, lower body
mass index, low literacy, presence of atrial fibrillation, renal
dysfunction, and valvular dysfunction.[52]
PATHOPHYSIOLOGY
HF is a complex pathophysiologic condition in which
complex compensatory mechanisms and adaptive changes
come into play.[1]
No single model has been able to fully
explain these pathophysiologic mechanisms. The clinical
models described so far include cardiorenal, hemodynamic,
and neurohumoral mechanisms.[53]
These mechanisms
initially are able to restore CV function to a normal
homeostatic range and the patient remains asymptomatic.
However, the sustained activation of these systems can
lead to end organ damage with worsening LV remodeling
and subsequent cardiac decompensation.[53]
T hese compensator y mechanisms include
adrenergic nervous system activation, activation of
renin‑angiotensin‑aldosterone system, cytokine system
activation, increased myocardial contractility, and increased
activation of vasodilatory molecules including atrial and
brain natriuretic peptides, prostaglandins (PGE2 and
PGI2), and nitric oxide that offsets the excessive peripheral
vascular constriction.[1,53]
It is also established that genetic background, sex, age,
and environment may influence these compensatory

mechanisms. The resultant adaptive changes within the
myocardium are collectively referred to as LV remodeling.
The LV remodeling stems from alteration in myocyte
biology, myocardial changes (myocardial loss, necrosis,
apoptosis, and autophagy), alteration in extracellular
matrix (matrix degradation and myocardial fibrosis), and
alteration in LV chamber geometry (LV dilation, increase
in LV sphericity, LV wall thinning and mitral valve
incompetence).[1,53]
CLINICAL PRESENTATION
The clinical features of HF have been classified into
major and minor criteria according to the Framingham
study [Table 3].[54]
STAGING OF HEART FAILURE
There are different ways of staging severity of HF based
on symptoms, functional capacity, and degree of structural
cardiac damage.
NYHA is a widely used classification. It emphasizes the
functional capacity of the patients. It is classified based on
severity of symptoms and limitation of activities [Table 4].
In the Abeokuta HF registry, majority of patients were in
NYHA Class III (65.3%) followed by 20% of patients in
Class IV and 14.7% in Class II.[36]
Karaye and Sani reported
that 22.8% of their HF patients were in NYHA III and
77.2% were in NYHA IV.[55]
The American College of Cardiology/American Heart
Association has staged HF based on the presence of
risk factors, degree of structural damage, and severity of
symptoms into Stages A to D with specific interventions
at each stage.[5,27]
• Stage A: At high risk for HF but without structural
heart disease or symptoms of HF. For example,
hypertensive patient without symptoms and cardiac
structural damage. Therefore, intervention at this stage
focuses on life style, health education, and optimal
control of blood pressure and other comorbidities
• Stage B: Presence of structural heart disease but
without symptoms or signs of HF, for example,
asymptomatichypertensivepatientwithLVhypertrophy
or asymptomatic mitral valve prolapse. Therefore,
intervention would be to reverse the damage, retard
the progression, and prevent the development of HF
in addition to the interventions for Stage A
• Stage C: Presence of structural heart disease with
previous or current symptoms of HF, for example,
hypertensive HF patient or symptomatic mitral valve
prolapse. Interventions at this stage entail all measures
under stage A and B, diuretics for fluid retention, use
of ACEI or ARB, BB, aldosterone antagonist, digitalis,
and in selected cases devices (biventricular pacing or
implantable defibrillators)
• Stage D: Presence of refractory symptoms that require
special interventions, for example, device‑based
treatment or cardiac transplantation.
CONCLUSION
HF is prevalent worldwide with variable etiology in the
Western world compared to SSA. Use of the disease
modifying agents in our environment has been noted to
be similar to what is obtainable in the Western world but
Table 3: New York Heart Association functional classification
of heart failure
NYHA class
Class I: No limitation of physical activity. Ordinary physical activity does
not cause undue breathlessness, fatigue, or palpitations
Class II: Slight limitation of physical activity. Comfortable at rest but
ordinary physical activity results in undue breathlessness, fatigue, or
palpitations
Class III: Marked limitation of physical activity. Comfortable at rest but
less than ordinary physical activity results in undue breathlessness,
fatigue, or palpitations
Class IV: Unable to carry on any physical activity without discomfort.
Symptoms at rest can be present. If any physical activity is undertaken,
discomfort is increased
NYHA: New York Heart Association
Table 4: Comparison of American College of Cardiology/
American Heart Association and New York Heart Association
classification of heart failure
ACC/AHA stages of
HF
NYHA classification of HF
A At high risk for HF but
without structural heart
disease or symptoms
None
B Structural heart
disease but without
signs and symptoms
of HF
Class I: No limitation of physical activity.
Ordinary physical activity does not cause
symptoms of HF
C Structural heart
disease with current or
prior symptoms of HF
Class I: No limitation of physical activity.
Ordinary physical activity does not cause
symptoms of HF
Class II: Slight limitation of physical
activity. Comfortable at rest but ordinary
physical activity results in symptoms of
HF
Class III: Marked limitation of activity.
Comfortable at rest but less than ordinary
activity causes symptoms of HF
D Refractory HF
requiring specialized
interventions
Class IV: Unable to carry on any physical
activity without symptoms of HF or
symptoms of HF at rest
Adapted from Yancy et al.[27]
HF: Heart failure; ACC/AHA: American
College of Cardiology/American Heart Association; NYHA: New York
Heart Association

Nigerian Journal of Cardiology | Volume 14 | Issue 1 | January-June 2017 13
predictors of favorable outcomes were found not to be
necessarily the same. There is therefore need for further
studies on the similarities and differences in HF in different
geographic locations including genomics.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
REFERENCES
1. Gary SF, Tang WH, Walsh RA. Pathophysiology of Heart Failure. In:
Valentin Fuster RA, Harrington RA, editors. Hurst's The Heart. 13th
ed. 2011. p. 719-38.
2. Sliwa K, Mayosi BM. Recent advances in the epidemiology,
pathogenesis and prognosis of acute heart failure and cardiomyopathy
in Africa. Heart 2013;99:1317‑22.
3. Ojji D, Stewart S, Ajayi S, Manmak M, Sliwa K. A predominance of
hypertensive heart failure in the Abuja Heart Study cohort of urban
Nigerians: A prospective clinical registry of 1515 de novo cases. Eur J
Heart Fail 2013;15:835‑42.
4. Ntusi NB, Mayosi BM. Epidemiology of heart failure in Sub‑Saharan
Africa. Expert Rev Cardiovasc Ther 2009;7:169‑80.
5. Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS,
Ganiats TG, et al. ACC/AHA 2005 Guideline Update for the Diagnosis
and Management of Chronic Heart Failure in the Adult: A report of
the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines (Writing Committee to Update
the 2001 Guidelines for the Evaluation and Management of Heart
Failure): Developed in collaboration with the American College of
Chest Physicians and the International Society for Heart and Lung
Transplantation: Endorsed by the Heart Rhythm Society. Circulation
2005;112:e154‑235.
6. Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS,
Ganiats TG, et al. 2009 Focused update incorporated into the
ACC/AHA 2005 Guidelines for the Diagnosis and Management
of Heart Failure in Adults A Report of the American College of
Cardiology Foundation/American Heart Association Task Force on
Practice Guidelines Developed in Collaboration With the International
Society for Heart and Lung Transplantation. J Am Coll Cardiol
2009;53:e1‑90.
7. Amoah AG, Kallen C. Aetiology of heart failure as seen from a
National Cardiac Referral Centre in Africa. Cardiology 2000;93:11‑8.
8. Owusu I. Causes of heart failure as seen in Kumasi, Ghana. Internet
J Third World Med 2007;5:1538‑4646.
9. Ogah OS, Okpechi I, Chukwuonye II, Akinyemi JO, Onwubere BJ,
Falase AO, et al. Blood pressure, prevalence of hypertension and
hypertension related complications in Nigerian Africans: A review.
World J Cardiol 2012;4:327‑40.
10. Damasceno A, Mayosi BM, Sani M, Ogah OS, Mondo C, Ojji D, et al.
The causes, treatment, and outcome of acute heart failure in 1006
Africans from 9 countries. Arch Intern Med 2012;172:1386‑94.
11. Mayosi BM. Contemporary trends in the epidemiology and
management of cardiomyopathy and pericarditis in Sub‑Saharan Africa.
Heart 2007;93:1176‑83.
12. McMurray JJ, Stewart S. Epidemiology, aetiology, and prognosis of
heart failure. Heart 2000;83:596‑602.
13. Tantchou Tchoumi JC, Ambassa JC, Kingue S, Giamberti A,
Cirri S, Frigiola A, et al. Occurrence, aetiology and challenges in
the management of congestive heart failure in Sub‑Saharan Africa:
Experience of the Cardiac Centre in Shisong, Cameroon. Pan Afr
Med J 2011;8:11.
14. Antony KK. Pattern of cardiac failure in Northern Savanna Nigeria.
Trop Geogr Med 1980;32:118‑25.
15. Ladipo GO, Froude JR, Parry EH. Pattern of heart disease in adults
of the Nigerian Savanna: A prospective clinical study. Afr J Med Med
Sci 1977;6:185‑92.
16. Onwuchekwa AC, Asekomeh GE. Pattern of heart failure in a Nigerian
teaching hospital. Vasc Health Risk Manag 2009;5:745‑50.
17. Ojji DB, Alfa J, Ajayi SO, Mamven MH, Falase AO. Pattern of heart
failure in Abuja, Nigeria: An echocardiographic study. Cardiovasc J
Afr 2009;20:349‑52.
18. Holland R, Rechel B, Stepien K, Harvey I, Brooksby I. Patients’
self‑assessed functional status in heart failure by New York Heart
Association class: A prognostic predictor of hospitalizations, quality
of life and death. J Card Fail 2010;16:150‑6.
19. Roul G, Germain P, Bareiss P. Does the 6‑minute walk test predict the
prognosis in patients with NYHA class II or III chronic heart failure?
Am Heart J 1998;136:449‑57.
20. Guimarães GV, Bellotti G, Bacal F, Mocelin A, Bocchi EA. Can the
cardiopulmonary 6‑minute walk test reproduce the usual activities of
patients with heart failure? Arq Bras Cardiol 2002;78:553‑60.
21. Adedoyin RA, Adeyanju SA, Balogun MO, Akintomide AO,
Adebayo RA, Akinwusi PO, et al. Assessment of exercise capacity in
African patients with chronic heart failure using six minutes walk test.
Int J Gen Med 2010;3:109‑13.
22. Adedoyin RA, Adeyanju SA, Balogun MO, Adebayo RA,
Akintomide AO, Akinwusi PO. Prediction of functional capacity
during six‑minute walk among patients with chronic heart failure.
Niger J Clin Pract 2010;13:379‑81.
23. Cahalin LP, Mathier MA, Semigran MJ, Dec GW, DiSalvo TG. The
six‑minute walk test predicts peak oxygen uptake and survival in
patients with advanced heart failure. Chest 1996;110:325‑32.
24. Mann DL, Chakinala M. Heart failure and Cor pulmonale. In:
Longo DL, Fauci AS, Kasper DL, et al., editors. Harrison's Principles
of Internal Medicine. 18th
ed. 2012. p 1901-15.
25. Mann DL. Pathophysiology of Heart Failure. In: Bonow RO, Mann
DL, Zipes DP, Libby P, editors. Brauward's Heart Disease: A Textbook
Of Cardiovascular Medicine. 9th
ed. Philadelphia PA: 2012. p. 487-503.
26. McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Böhm M,
Dickstein K, et al. ESC Guidelines for the diagnosis and treatment of
acute and chronic heart failure 2012 The Task Force for the Diagnosis
andTreatmentof AcuteandChronicHeartFailure2012of theEuropean
Societyof Cardiology.DevelopedinCollaborationwiththeHeartFailure
Association (HFA) of the ESC. Eur Heart J 2012;33:1787-847.
27. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE, Drazner MH,
et al. 2013 ACCF/AHA guideline for the management of heart
failure: A report of the American College of Cardiology Foundation/
American Heart Association Task Force on Practice Guidelines. J Am
Coll Cardiol 2013;62:e147‑239.
28. Steinberg BA, Zhao X, Heidenreich PA, Peterson ED, Bhatt DL,
Cannon CP, et al. Trends in patients hospitalized with heart failure and
preserved left ventricular ejection fraction: Prevalence, therapies, and
outcomes. Circulation 2012;126:65‑75.
29. Mosterd A, Hoes AW. Clinical epidemiology of heart failure. Heart
2007;93:1137‑46.
30. Familoni O, Olunuga T, Olufemi B. A clinical study of pattern and
factors affecting outcome in Nigerian patients with advanced heart
failure. Cardiovasc J Afr 2007;18:308‑11.
31. Karaye KM, Sani MU. Factors associated with poor prognosis among
patients admitted with heart failure in a Nigerian tertiary medical centre:
A cross‑sectional study. BMC Cardiovasc Dis 2008;8:16‑24.
32. Falase AO, Aje A, Ogah OS. Management of hypertension in Nigerians:
Ad hoc or rational basis? Niger J Cardiol 2015;12:158.
33. Ogah O, Akinyemi R, Ogbodo E, Ogah F. Cardiac emergencies in a

Nigerian hospital: Data from the Abeokuta heart disease registry. Niger
J Cardiol 2013;10:14.
34. Ogah OS, Adegbite GD, Akinyemi RO, Adesina JO, Alabi AA,
Udofia OI, et al. Spectrum of heart diseases in a new cardiac service
in Nigeria: An echocardiographic study of 1441 subjects in Abeokuta.
BMC Res Notes 2008;1:98.
35. Ogah OS, Falase AO, Carrington M, Stewart S, Sliwa K, editors.
Hypertensive heart failure in Nigerian Africans: Insights from the
Abeokuta heart failure registry. J Clin Hypertens 2015;17:263-72.
36. Ogah OS, Stewart S, Falase AO, Akinyemi JO, Adegbite GD, Alabi AA,
et al. Contemporary profile of acute heart failure in Southern Nigeria:
Data From the Abeokuta heart failure clinical registry. JACC Heart
Fail 2014;2:250‑9.
37. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JG, Coats AJ,
et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and
chronic heart failure. Eur Heart J 2015. doi:10.1093/eurheartj/ehw128.
38. OyatiA,DanbauchiS.DiastolicHeartFailure:AreThereSpecificBedside
Clinical Markers for its Diagnosis? Ann of Afr Med 2006;4:96-8.
39. Shah SJ, Gheorghiade M. Heart failure with preserved ejection fraction:
Treat now by treating comorbidities. JAMA 2008;300:431‑3.
40. Bhuiyan T, Maurer MS. Heart failure with preserved ejection fraction:
Persistent diagnosis, therapeutic enigma. Curr Cardiovasc Risk Rep
2011;5:440‑9.
41. Adebayo AK, Adebiyi AA, Oladapo OO, Ogah OS, Aje A, Ojji DB,
et al. Characterisation of heart failure with normal ejection fraction in
a tertiary hospital in Nigeria. BMC Cardiovasc Disord 2009;9:52.
42. Taylor AL, Ziesche S, Yancy C, Carson P, D’Agostino R Jr.,
Ferdinand K, et al. Combination of isosorbide dinitrate and hydralazine
in blacks with heart failure. N Engl J Med 2004;351:2049‑57.
43. Taylor AL, Ziesche S, Yancy CW, Carson P, Ferdinand K, Taylor M,
et al. Early and sustained benefit on event‑free survival and heart failure
hospitalization from fixed‑dose combination of isosorbide dinitrate/
hydralazine: Consistency across subgroups in the African‑American
Heart Failure Trial. Circulation 2007;115:1747‑53.
44. Sliwa K, Damasceno A, Davison BA, Mayosi BM, Sani MU, Ogah O,
et al. Bi treatment with hydralazine/nitrates vs. placebo in Africans
admitted with acute HEart Failure (BA‑HEF). Eur J Heart Fail
2016;18:1248‑58.
et al. Short‑term outcomes after hospital discharge in patients admitted
with heart failure in Abeokuta, Nigeria: Data from the Abeokuta heart
failure registry: Cardiovascular topic. Cardiovasc J Afr 2014;25:217‑23.
46. Kearney MT, Fox KA, Lee AJ, Prescott RJ, Shah AM, Batin PD,
et al. Predicting death due to progressive heart failure in patients
with mild‑to‑moderate chronic heart failure. J Am Coll Cardiol
2002;40:1801‑8.
47. Kearney MT, Nolan J, Lee AJ, Brooksby PW, Prescott R, Shah AM,
et al. A prognostic index to predict long-term mortality in patients
with mild to moderate chronic heart failure stabilised on angiotensin
converting enzyme inhibitors. Eur J Heart Fail 2003;5:489‑97.
48. Klein L, O’Connor CM, Leimberger JD, Gattis‑Stough W, Piña IL,
Felker GM, et al. Lower serum sodium is associated with increased
short‑term mortality in hospitalized patients with worsening
heart failure: Results from the Outcomes of a Prospective Trial
of Intravenous Milrinone for Exacerbations of Chronic Heart
Failure (OPTIME‑CHF) study. Circulation 2005;111:2454‑60.
49. Lee WH, Packer M. Prognostic importance of serum sodium
concentration and its modification by converting‑enzyme inhibition in
patients with severe chronic heart failure. Circulation 1986;73:257‑67.
50. Oyedeji AT, Balogun MO, Akintomide AO, Sunmonu TA, Adebayo RA,
Ajayi OE. The “obesity paradox” in Nigerians with heart failure. Ann
Afr Med 2012;11:212‑6.
51. Chase PJ, Davis PG, Bensimhon DR. The obesity paradox in chronic
heart failure: What does it mean? Curr Heart Fail Rep 2014;11:111‑7.
et al. Predictors of rehospitalization in patients admitted with heart
failure in Abeokuta, Nigeria: Data from the Abeokuta heart failure
registry. J Card Fail 2014;20:833‑40.
53. Mann DL. Mechanisms and models in heart failure: A combinatorial
approach. Circulation 1999;100:999‑1008.
54. Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart
failure: The Framingham Study. J Am Coll Cardiol 1993;22 4 Suppl
A: 6A‑13A.
55. Karaye K, Sani M. Demographic and clinical characteristics of heart
failure patients in a Nigerian Tertiary Health Centre. Nig J Basic Clin
Sciences 2008;1:26-36.

Heart failure definition classification

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Heart failure definition classification

Similar to Heart failure definition classification (20)

More from Ramachandra Barik

More from Ramachandra Barik (20)

Recently uploaded

Recently uploaded (20)

Heart failure definition classification