Definitions
The term ‘heart failure’ (HF) is generally used to describe the physiological state in which cardiac function is insufficient to meet the metabolic needs of the tissues. There are detailed criteria for the diagnosis of HF (Framingham criteria and European Society of Cardiology [ESC] guidelines; see Table 5.4, page 72). A complete description of the HF syndrome in every patient should also recognize the following entities:
• diastolic versus systolic HF
• acute versus chronic HF
• right versus left (and biventricular) HF
• high versus low output HF.
Each of these has implications for investigation, management and outcome.
Diastolic versus systolic heart failure. The outcome of these entities is similar, although their treatment is different. The definition of ejection fraction (EF) (the percentage of blood pumped from the ventricles with each heart beat) is fundamental to defining diastolic and systolic HF (Figure 1.1).
Figure 1.1 Description of diastolic versus systolic heart failure (HF), according to left ventricular ejection fraction (LVEF): (a) normal heart function; (b) systolic HF, or HF with reduced ejection fraction (HFrEF); and (c) diastolic HF, or HF with preserved (or normal) ejection fraction (HFpEF/HFnEF). A gray area exists between (b) HFrEF and (c) HFpEF. Patients with an LVEF of 40–49% have been classified by the European Society of Cardiology as having heart failure with mid-range ejection fraction (HFmrEF). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
An EF over 50% is generally regarded as normal, although there remains some debate regarding the specific cut-off point. The latest (2016) ESC guidelines divide patients into three groups according to their left ventricular ejection fraction (LVEF):
• heart failure with reduced EF (HFrEF) when EF is less than 40%
• heart failure with mid-range EF (HFmrEF) when EF is 40–49%
• heart failure with preserved (or normal) EF (HFpEF/HFnEF) when EF is 50% or more.
Systolic heart failure or heart failure with reduced ejection fraction results from myocardial injury, which leads to impaired pumping function of the left ventricle (LV) and significantly reduced LVEF (< 40%). This is the typical manifestation of patients with ischemic heart disease and multiple infarcts.
HFpEF is common in the elderly (affecting more women than men) in whom combined ischemia, hypertrophy and age-related fibrosis may act together to produce increased myocardial stiffness and delayed relaxation. Prevalence increases with age.
Heart failure with normal systolic and diastolic function describes a group of patients with symptomatic HF but no evidence of systolic or diastolic dysfunction on resting echocardiography. In one study, 15% of patients with clinical HF had normal LVEF and normal tests of diastolic function at rest. Historically, these patients would have been diagnosed with HFpEF, but dobutamine stress echocardiography has helped to reclassify about 60% of these patients with various diagnoses, including left ventricular outflow tract obstruction, development of restrictive filling pattern at stress, chronotropic incompetence or underlying ischemic heart disease.
In addition, some symptomatic patients do not have HF. Their symptoms may be caused by fluid overload (due to renal disease) or obesity and physical deconditioning.
Acute versus chronic heart failure. The terminology ‘acute’ and ‘chronic’ in this context relates to time rather than severity. An episode of acute HF can be defined as the sudden onset or gradual worsening of signs and symptoms of HF resulting in hospital admission. The typical presentation of acute HF is pulmonary edema. Acute LV failure elevates LV diastolic pressure, which causes a significant rise in pulmonary venous pressure, resulting in pulmonary congestion (edema) as well as subendocardial ischemia, further LV remodeling and worsening of mitral valve regurgitation. The patient presents with severe dyspnea at rest, pink frothy sputum, sweating and clamminess, and sometimes shock. Raised right-sided filling pressure in response to LV dysfunction contributes to the development of systemic congestion with elevated jugular venous pressure and peripheral edema. The combination of poor cardiac output (in 50% of patients with acute HF) and renal venous hypertension may precipitate a worsening of renal function and could cause cardiorenal syndrome (see Chapter 4). In acute HF, the degree of pulmonary congestion (wet vs dry) and state of tissue perfusion (warm vs cold) varies (see Chapter 5).
HF may often be provoked by an acute illness (e.g. myocardial infarction [MI]) and may not be preceded by chronic symptoms. Conversely, chronic HF has a background of gradually worsening exertional dyspnea, edema, orthopnea and paroxysmal nocturnal dyspnea.
Recognizing the acuity of HF symptoms is an important aspect of managing HF as a chronic disease. Recognizing an exacerbation in a patient with chronic HF should lead to a search for the etiology of this change (see Chapter 3).
Right, left and biventricular failure. Left ventricular HF is the most common type of HF. It is associated with exertional dyspnea, orthopnea and paroxysmal nocturnal dyspnea. Right ventricular HF, most commonly caused by left ventricular HF, is characterized by peripheral edema, abdominal distension (due to ascites), right upper quadrant discomfort (due to liver congestion) and elevated jugular venous pressure, often with prominent v waves due to tricuspid regurgitation (see Chapter 5). Either left- or right-sided HF may occur in the context of low output (fatigue, syncope and hypotension).
High versus low output. The distinction between high and low (cardiac) output has etiologic and therapeutic implications. Low-output HF is associated with pale cool extremities, which reflects vasoconstriction and reduced cardiac output. High-output HF is associated with warm extremities and bounding pulses. In its most extreme state, high-output HF may be due to arteriovenous shunts or diseases associated with severe vasodilation (e.g. vitamin B1 deficiency – beri-beri). The most common cause of high-output HF is marked obesity.
Epidemiology
HF affects an estimated 26 million people worldwide. Although advances in the treatment of acute coronary syndromes have reduced deaths from coronary artery disease (CAD), in the USA in 2014 non-cardiovascular disease was the underlying cause of death for more than one-third of HF-related deaths of adults aged 45 or over. This shift toward less ischemic heart disease is important for HF management approaches.
The enormous impact of HF on individuals and their families is compounded by the huge costs to healthcare budgets around the world. The burden associated with HF is expected to keep rising over the next 20 years due to a number of factors:
• aging populations in developed countries
• an increase in the number of elderly people with CAD and hypertension
• a decrease in case–fatality rates associated with acute coronary syndromes
• improved diagnosis using sensitive techniques such as echocardiography.
The rising prevalence of obesity, metabolic syndrome and diabetes mellitus with associated cardiovascular complications is likely to result in further increases. Some of the factors listed above cannot be modified (e.g. aging of the population), but prevention of those that precede the development of HF (CAD, diabetes mellitus, arterial hypertension, obesity) should be a priority.
Prevalence of HF in developed countries has increased over time; current estimates are shown in Table 1.1. In those with CAD, a 28% decrease in 5-year mortality after MI was associated with a 25% increase in the 5-year rate of HF. About 70% of patients developed HF within 5 years, with two-thirds of clinical cases in the first year.
TABLE 1.1 Prevalence of heart failure – current estimates | |
• ∼ 26 million people have heart failure (HF) worldwide: 6.5 million in Europe; > 5 million in the USA; ∼ 900 000 in the UK; > 350 000 in Australia • 8 per 1000 people aged 50–59 years are affected by HF* • 66 per 1000 men aged 80–89 years are affected by HF* • 79 per 1000 women aged 80–89 years are affected by HF* | |
*The known prevalence in African-Americans is around 25% higher. | |
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