Nigerian Journal of Cardiology

: 2017  |  Volume : 14  |  Issue : 1  |  Page : 9--14

Heart failure: Definition, classification, and pathophysiology – A mini-review

Saheed O Adebayo1, Taiwo O Olunuga1, Amina Durodola1, Okechukwu S Ogah2,  
1 Department of Internal Medicine, Cardiology Unit, Federal Medical Centre, Abeokuta, Nigeria
2 Department of Medicine, Division of Cardiology, University College Hospital, Ibadan, Nigeria

Correspondence Address:
Okechukwu S Ogah
Department of Medicine, Division of Cardiology, University College Hospital, PMB 5116, Ibadan


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.

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

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Adebayo SO, Olunuga TO, Durodola A, Ogah OS. Heart failure: Definition, classification, and pathophysiology – A mini-review. Nig J Cardiol [serial online] 2017 [cited 2021 Dec 4 ];14:9-14
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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],[3],[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],[8],[9],[10],[11],[12],[13],[14],[15],[16],[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 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],[20],[21],[22],[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].{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.{Table 2}

 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 men and an overall prevalence of 9% among all medical admissions.[33],[34],[35],[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],[46],[47],[48],[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]


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]

These compensatory 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]{Table 3}

 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].{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 comorbiditiesStage B: Presence of structural heart disease but without symptoms or signs of HF, for example, asymptomatic hypertensive patient with LV hypertrophy 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 AStage 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.


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 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


Conflicts of interest

There are no conflicts of interest.


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