Heart failure (HF) is a major part of the cardiovascular disease spectrum. The American College of Cardiology/American Heart Association guidelines define HF as a “complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or eject blood.” HF is a set of complex and heterogeneous conditions with underlying variability in etiology, pathophysiology, metabolic, and other individual factors that constitutes an end stage of several cardiovascular disorders, coronary heart disease (CHD) and hypertension being the most common in the Western world. The classification of HF is based on different etiologies and their associated mechanistic disturbances of cardiac function. The prevalence of HF is high and is increasing over time due to an increasing older adult population and an improved survival as well as to the increase in the prevalence of relevant to HF risk factors such as obesity and diabetes. A range of interventions can help improve quality of life (QOL) as well as reduce hospital admissions and mortality in chronic heart failure (CHF), including pharmacological, medical, and lifestyle. Nutrition is a critical factor in the incidence and progression of HF. Related features to HF are obesity, sarcopenia, sarcopenia in combination with obesity or weight loss (even tissue loss of both lean and fat mass, e.g., cachexia), dietary approaches such as restricting sodium and fluids as well as dietary plans such as the Mediterranean diet (MD) and Dietary Approaches to Stop Hypertension (DASH) diet. CHF is characterized by reduced functional ability, severe exercise intolerance, reduced QOL, increased dependence to complete daily activities, and an increased risk of adverse events. Physical activity (PA), generally, has a positive effect on many CHD and HF risk factors, such as hypertension. Exercise plays an important role in the development of HF, as it seems to have a protective role by positively affecting HF in secondary prevention and influencing the prognosis of HF in the future for HF patients. HF is a major part of the cardiovascular disease spectrum. American College of Cardiology/American Heart Association guidelines define HF as a “complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or eject blood” (Yancy et al., 2013). HF is a set of complex and heterogeneous conditions with underlying variability in etiology, pathophysiology, metabolic, and other individual factors that constitutes an end stage of several cardiovascular disorders, CHD and hypertension being the most common in the Western world (Lindgren & Börjesson, 2021). As a clinical syndrome, the diagnosis of HF is based on three cornerstones: typical symptoms (including shortness of breath, ankle swelling, orthopnea, lower limb swelling, and chronic fatigue), signs (jugular vein stasis, pulmonary crackles, and pitting edema), and results from relevant diagnostic tests (e.g., electrocardiogram, transthoracic echocardiography, serum natriuretic peptides) that can be linked to cardiac dysfunction (Ponikowski et al., 2016), often caused by a structural and/or functional cardiac abnormality that results in reduced cardiac output and/or elevated intracardiac pressures (Ponikowski et al., 2016). It is a complicated clinical syndrome regarding the implications in terms of mortality and morbidity of patients with HF as well as the plan for medical care. Many epidemiologic studies have relied on clinical diagnostic criteria for its identification. These criteria include the Framingham, Boston, Gothenburg, and cardiovascular health study criteria, all of which have relatively similar performance characteristics for the detecting HF with a high sensitivity compared with cardiologist evaluation (Dharmarajan & Rich, 2017). The classification of HF is based on different etiologies and their associated mechanistic disturbances of cardiac function. HF incidence is divided according to left ventricular ejection fraction (LVEF), an echocardiographic estimate of left ventricular systolic function. LVEF is a strong marker for underlying pathophysiology as well as a marker for sensitivity to pharmacotherapy (Lindgren & Börjesson, 2021). The classification also depends on the level of LVEF, therefore an LVEF < 40% is classified as HF‐reduced ejection fraction (HFrEF), whereas an LVEF of 50% is classified as HF‐preserved ejection fraction (HFpEF). Furthermore, HF could be characterized as a chronic state or an acute state. CHF is characterized by the reduced ability of the heart to pump and/or fill with blood, which results in fatigue, dyspnea, and exercise intolerance. Patients with CHF often have reduced functional capacity and a decreased QOL; the main causes for CHF are mentioned below (Table 12.1) (de Gregorio, 2018). Patients with acute heart failure (AHF) have a less well‐understood presentation and management of the disease. AHF is a clinical diagnosis based on symptoms and signs of fluid overload, with or without evidence of hypoperfusion, which may be supported by radiological evidence (pulmonary congestion on chest X‐ray) and biochemical markers (like B‐type natriuretic peptide, BNP, or N‐terminal pro‐BNP). AHF is characterized by a rapid onset, with new or worsening signs and symptoms that are potentially life‐threatening, and patients require immediate hospitalization. Although AHF may be the reason for hospitalization, usually a pre‐existing cardiomyopathy persists that foretells a poor prognosis with a high risk of readmission and death post‐discharge. For clinical and hemodynamic characteristics, older guidelines by the European Society of Cardiology classified patients with AHF into one of the below mentioned six groups (I–VI) (Table 12.2) (Kurmani & Squire, 2017). Table 12.1 Main causes of chronic left heart failure. Source: (de Gregorio, 2018). Table 12.2 Classification of patients with acute heart failure into one of six groups (I–VI), according to clinical conditions. Source: (Adapted from Kurmani & Squire, 2017). This classification system focuses on the treatment decision of the physician to manage the underlying cause of AHF. However, AHF patients may be also classified according to their initial clinical symptoms and signs for the attending physician to identify those most at risk and direct specific interventions. A usual marker is the level of systolic blood pressure (SBP) upon admission. Less than 10% of patients present with systolic hypotension (SBP < 90 mm Hg) which carries with it a poor prognosis and thereby leads the management of these patients to higher dependency areas with more aggressive therapy. Furthermore, there are also recent guidelines from the European Society of Cardiology. A more comprehensive method to classify patients presenting with AHF was developed by Stevenson and colleagues (Nohria et al., 2003), who used the severity of presentation rather than the underlying etiology. This method is based on the initial clinical assessment of the patient to consider signs and symptoms of congestion (orthopnea, dependent edema, elevated jugular venous pulsation) and peripheral perfusion (cold extremities, oliguria, and narrow pulse pressure). Moreover, patients are described as either ‘wet’ or ‘dry’ depending on their fluid status and either ‘cold’ or ‘warm’ depending on the assessment of their perfusion status. This combined clinical assessment identifies four groups of patients (warm and wet, warm and dry, cold and dry, and cold and wet) that not only allow for initial stratification as a guide to therapy (Figure 12.1) but also carries with it prognostic information. Warm and dry patients have a 6‐month mortality rate of 11% compared to 40% for the cold and wet profile (Nohria et al., 2003). As a practical measure, this method of classification and risk stratification is a prudent step in AHF management. However, compared to CHF, therapy that improves long‐term survival following admission with AHF, although characterized by a distinctive set of signs and symptoms, is a major challenge in classifying AHF as a single entity is that the patient population is not uniform. Most patients with AHF lie between these extremes and therefore also demonstrate a distribution of underlying pathology and precipitants, leading to the common endpoint of fluid overload. The prevalence of HF is high and increasing over time. It was estimated that 2% to 4% of the general adult population, corresponding to more than 60 million people worldwide, have HF, and it is characterized by a low 5‐year survival of 35–55% (Lindgren et al., 2017). However, there might be an underestimation of HF disease, since patients older than 65 years with asymptomatic left ventricular (LV) systolic dysfunction is 5.5% (Wickman et al., 2021). Generally, the increase in HF prevalence worldwide could be explained by an increase in older adult population and improved survival as well as an increase in the prevalence of HF‐related risk factors such as increased obesity and diabetes melitus (DM) (Dharmarajan & Rich, 2017). This could also explain the increase in the prevalence of HF in younger individuals who have a high body‐mass index (BMI) and characterize HF as an important component of non‐communicable diseases (Groenewegen et al., 2020). According to specific age ranges from NHANES data, in men over 18 years of age and specifically between 40 and 59 years present with a proportion of HF at 1.5%, with 6.6% in ages 60 to 79 years of age, and 10.6% in people 80 years and older, whereas women in the same age ranges are 1.2%, 4.8%, and 13.5%, respectively. Figure 12.2 shows that for women 80 years and older, HF is of higher prevalence compared to men of the same age (Dharmarajan & Rich, 2017). Regarding the epidemiology of AHF, the data derive from large‐scale registries in the USA and Europe, which demonstrate that patients are mostly men diagnosed at a mean age of more than 70 years, and thus, are related to ischemic heart disease and CHF. Additionally, 66% to 75% of these patients do not have de novo AHF, on the contrary, they already had a previous history of HF, which was identified during their hospitalization, and many also were diagnosed with a co‐morbid disease such as DM (≥ 40% in some registries) and chronic obstructive pulmonary disease (COPD) (almost 20% of patients). Most of these registries show a difference in hospital mortality rate depending on the age, from 4% to 7%, which rises to 12% for patients aged 75 years. Mortality after hospitalization was also high and appears not to have improved significantly over the past decade. Furthermore, in terms of cardiovascular death and hospitalizations, there is a difference between patients with HFpEF and HFrEF, probably due to the fact that no treatment convincingly reduces mortality or morbidity in HFpEF (Kurmani & Squire, 2017). FIGURE 12.1 Layering patients with AHF according to their initial clinical presentation, and perfusion status, i.e., COLD or WARM and degree of fluid congestion (WET or DRY). Adapted from 2016 ESC guidelines. FIGURE 12.2 Prevalence of HF in the United States by age and sex. Source: (Dharmarajan & Rich, 2017 / with permission of Elsevier). Patients diagnosed with HF have a poor prognosis and are characterized by a poor nutritional status that can influence the disease’s development and progression. Related features to HF are obesity, sarcopenia, sarcopenia in combination with obesity or weight loss (even tissues loss of both lean and fat mass, e.g., cachexia). Regarding the weight loss, which causes many nutritional deficiencies, it could be the result of different etiologies, including what was suggested two decades ago, that HF patients present a hypercatabolic state that results in a chronic negative energy balance and protein‐calorie malnutrition (Aggarwal et al., 2018). HFpEF is more prevalent with metabolic syndrome (MetS) and cardiac hypertrophy. Insulin resistance is involved in the development of HF and cardiac hypertrophy and is correlated with hypertension, coronary artery disease, LV hypertrophy, DM, and obesity (Aggarwal et al., 2018). HF is related to hypertension, type 2 diabetes mellitus (T2D), chronic inflammation, coronary artery disease, sarcopenia, and obesity, so it is important to study possible nutrition recommendations regarding prevention as well as HF therapy to improve clinical outcomes (Billingsley et al., 2019). Overweight, obesity, and abdominal obesity, in particular, are implicated as independent risk factors for the development of cardiovascular disease, including HF. Concerning the impact of obesity on the incidence of HF, a higher BMI in midlife enhances the risk of HF in later life, and a 30% hypothetical reduction in obesity/overweight would potentially prevent 8.5% of HF events. Moreover, the American Heart Association has recognized obesity as a qualifying risk factor for HF and released a specific scientific statement on HF prevention, thus recommending the maintenance of normal weight as one way to prevent HF. Despite the unfavorable impact that obesity has on risk factors for CHD, and other cardiovascular diseases (CVD) such as hypertension, HF and atrial fibrillation, several studies and metanalysis have demonstrated the so called “obesity paradox,” which indicates that once CVD (including HF) becomes established, patients with overweight and obesity have a better prognosis than do their lean counterparts with the same CVD. Oreopoulos et al., (Oreopoulos et al., 2008) reviewed 29,000 patients from nine major HF studies and demonstrated reductions in CVD and total mortality of 19% and 16% in those overweight, and 40% and 33% in those with obesity, compared with normal‐weight patients with HF, even after adjusting for well‐known risk factors. In patients with dilated cardiomyopathy at the first‐onset of decompensated HF, the group with patients suffering from obesity had an improved LVEF versus patients without obesity after treatment for one year, and a multivariate regression analysis revealed that independent predictors of LVEF improvement after 12 months were nuclear diameter and absence of myofilament lysis in heart biopsies, in part from the effect of diuretics (Lavie et al., 2012). However, even in patients with obesity, body weight could be reduced by following a well‐balanced hypocaloric diet (Carbone et al., 2019). Normal weight is important in HF, as underweight patients or those with lean sarcopenia are associated with advanced HF and poor outcomes. These conditions may lead to a reduction of cardiac output and eventually predispose HF patients to complications, including higher rates of hospital (re)admissions and mortality. Malnutrition is a common sign in HF patients, especially in severe HF, reaching 30% to 70% of HF patients (Rahman et al., 2016). It results from a series of pathophysiological mechanisms based on an imbalance between anabolism and catabolism, neurohormonal factors, intestinal edema, sense of anorexia, and pathogenic effects of HF progression. A chronic state of malnutrition in HF patients increases the risk for developing cardiac cachexia, characterized as unintentional edema‐free weight loss through loss of muscle, fat, and bone mass, which is strongly associated with decreased health‐related QOL and increased mortality (Ishikawa & Sattler, 2021). Intestinal edema‐induced malabsorption and anorexia with inadequate food consumption cause a series of macronutrient and micronutrient deficiencies, e.g., in vitamins B, C, D as well as low levels of calcium, selenium, zinc, iron, and coenzyme Q10 (CoQ10) (Wickman et al., 2021). Sarcopenia that generally presents in 5% to 20% of the population greater than 60 years of age and even more (50%) in patients more than 80 years was also seen in individuals with high fat mass, a condition known as sarcopenic obesity. HF patients with sarcopenia may be in a worse situation than patients with cachexia and have a more pronounced decline in CRF and QOL. Increased protein intake, creatine, the amino acid leucine, vitamin D, and n‐3 PUFA were proposed for treatment but there are still no firm recommendations (Billingsley et al., 2019). A very low BMI (< 18 kg/m2), is linked to macro‐ and micronutrient deficiencies and it could be of benefit for these patients to follow a hypercaloric (35–40 kcal/kg/day), high‐protein diet (1.5 g/kg body weight), with a fat content of 1.0–1.5 g/kg/body weight and a high‐carbohydrate intake of almost 4–5 g/kg of body weight, in the context of a healthy diet pattern like MD or DASH diet (Bianchi, 2020). A number of cohort studies have evaluated the associations between DM and HF, with most of them showing a positive correlation and only a few no association. In the systematic review and meta‐analysis by Aune et al., (Aune et al., 2018) conducted in 2018, 77 prospective studies (e.g., population‐ and patient‐based studies) were included, aiming to investigate associations between diabetes and blood glucose and HF risk. According to the results, a diabetes diagnosis was associated with a twofold increase in HF risk in the general population, while in the patient‐based studies, a 69% increase in the relative risk (RR) of HF. Considering the type of diabetes, T1D was associated with a 3.6‐fold increase in HF risk. Moreover, the RR of HF was associated with an increase of 23% per 20mg/dl increase in blood glucose, in population‐based studies. In total, a nonlinear, J‐shaped association was revealed between blood glucose and HF risk. In another meta‐analysis by Ohkuma et al., (Ohkuma, Komorita, Peters, & Woodward, 2019) with data from 47 cohorts including 12,142,998 individuals and 253,260 heart failure events, T2D was associated with a 9% greater HF risk in women than men (Ohkuma et al., 2019). The mechanisms that could explain the increased risk of HF observed in patients with diabetes include risk factors that are common in diabetes and HF. In particular, diabetes increases the risk of hypertension, CHD, and atrial fibrillation, conditions that are strongly related to HF. Moreover, diabetes is linked to the development of diabetic cardiomyopathy, which is characterized by microangiopathy, myocardial fibrosis, and autonomic neuropathy and makes the heart unable function properly (Aune et al., 2018). HF is often observed in older adults, and this seems largely related to the high prevalence of traditional cardiovascular risk factors (e.g., CHD, diabetes, obesity) in this population (Dharmarajan & Rich, 2017). Epidemiological prospective data support an increased risk of HF in older adults that could be attributed by 13.1% to the CHD and 12.8% to the SBPs greater than 140 mm Hg found in this population. Both the atherosclerosis risk in communities study (Folsom, Yamagishi, Hozawa, & Chambless, 2009) and NHANES study (He et al., 2001) have confirmed these results, showing also that diabetes and obesity are responsible for a significant proportion of HF incidence. The higher prevalence of HF in the elderly is also associated with age‐associated changes in cardiovascular structure and function including diminishing chronotropic and inotropic responses, raising intracardiac pressures with ventricular filling, and increasing afterload. These conditions result in reducing the ability of the heart to respond to stress, whether that stress is physiologic (e.g., exercise) or pathologic (e.g., myocardial ischemia or sepsis) (Dharmarajan & Rich, 2017). Cognitive impairment is common in HF and is approximately found in 40% of patients, in contrast to the general population where prevalence ranges from 16% to 20%. Apart from the age‐related cognitive decline that older adults are at risk of, namely Alzheimer’s disease and other etiologies of dementia, they are also at risk for HF‐related cognitive impairment (recently termed “cardio‐cerebral syndrome”). This syndrome refers to cardiac dysfunction due to varying brain injuries, e.g., stroke. Cognitive impairment may be severe or mild severity evolving into dementia (representing a significant decline from prior level of function), and to more severe dementia (marked by significant impairment that interferes with activities of daily living) (Gorodeski et al., 2018). Cognitive impairment in patients with HF is associated with poor outcomes namely worse QOL, family member/caregiver distress, increased disability, high hospital readmission risk and mortality risk. The mechanisms for cognitive impairment in older adults with HF are complex and involve several parameters. Some of them include reduced cardiac output; a high burden of cardiovascular risk factors; other neurohormonal, nutritional, and inflammatory mechanisms; and sleep apnea (more in Chapter 19) (Gorodeski et al., 2018). Frailty (more in Unit 3) is extremely common in older adults with HF, and it is not related to age or functional classification. In a recent metanalysis (Denfeld et al., 2017) of 26 studies involving 6896 patients with HF, the overall estimated prevalence of frailty in HF was 44.5%, while it was not associated with age or functional class. In fact, frailty was high among studies with younger HF patients. The mechanisms through which frailty could be explained in patients with HF include interrelationships between neurohormonal dysregulation, inflammation, and skeletal muscle dysfunction, which have been noted to also parallel the pathogenesis of HF (Denfeld et al., 2017). A range of interventions can help improve QOL, reduce hospital admissions, and mortality in CHF, such as pharmacological (e.g., angiotensin II receptor blockers, diuretics, beta‐blockers, cardiac glycosides, and anticoagulants), medical (cardiac resynchronization therapy), and lifestyle (smoking cessation, dietary changes, and exercise) (Billingsley et al., 2019). According to the type, for HFrEF there is a standardized approach for treatment despite the heterogeneity of etiologies, whereas, for HFpEF there is not a specific treatment due to the difficulty in identifying phenotyping subgroups with differential responses to therapy and cohorts for personalized interventions (Wickman et al., 2021). A range of exercise frequencies, intensities, modalities, and durations are reported for the management of CHF. Regarding AHF, to date, there is little information as to the therapy guidelines that may improve long‐term outcomes since patients remain heterogeneity and present at different stages of decompensation of cardiac function. For AHF, the pharmacological treatment (loop diuretics, vasodilators, and inotropes) has remained largely unchanged since the 1970s and is predominantly aimed at correcting hemodynamic compromise and fluid overload with no standard therapy. Patients with AHF are treated according to their clinical condition and is largely based on factors such as SBP and renal function. In this case, structured exercise training is also recommended and should be an integral part of the treatment pathway (Billingsley et al., 2019). HF patients should remain functional before and after hospitalizations and succeed at QOL. There are various factors involved to reinforce this (Table 12.3) (de Gregorio, 2018). Unhealthy dietary models, body weight and consumption of low nutritional quality foods, low PA, and mental stress, may influence the rapidly changing epidemiology of HF, as shown in Figure 12.3 (Aggarwal et al., 2018) and Figure 12.4 (de Gregorio, 2018). Table 12.3 Essential factors for Cardiac Rehabilitation (CR) programs. Source: (de Gregorio, 2018). A high BMI results in metabolic and neurohormonal pathways that increase the risk for HF (Figure 12.5) (Bianchi, 2020) as well as the symptomatology, so weight loss in overweight and patients with obesity and HF may prevent further progression of the disease, improve cardiac function, improve symptoms, and decrease the possibility of hospitalization (Billingsley et al., 2019). Obesity increases specifically the risk of HFpEF, due to HF signs in the presence of a normal LVEF (Carbone et al., 2019). A review by Bianchi (Bianchi, 2020), indicates that although following a controlled diet is still inconclusive regarding heart function and clinical outcomes in patients with CHF, it is important to succeed in reducing body weight, thus insulin activity and glucose regulation on the basis of a dietary plan. Thus, HF patients with an increased BMI could attempt a reduction in body weight by an average reduction in energy intake of 20% to 30% of their usual daily caloric intake, with a macromolecule composition of 1.5 g/kg bodyweight for protein, 3–4 g/kg/body weight for carbohydrates, and 0.8–1.0 g/kg body weight for fat, because this will also improve insulin activity and glucose control. Such a diet should include lifestyle interventions and there must be great caution so as not to lose fat‐free mass. There is strong scientific evidence from clinical trials and meta‐analyses that salt restriction may prevent hypertension, stroke, and CVD, but not for the role of sodium restriction in reducing the incidence of HF. The current primary dietary approaches for HF management include sodium and fluid restriction, but individualization to patient needs is essential as multiple variables need to be considered in advanced HF. Strict low‐sodium recommendations may cause adverse nutritional and physiologic situations, whereas strict to low‐sodium recommendations or modest sodium intake may contribute to cardiac performance in compensated HF, and the exact level recommended should be adjusted based on the patient’s clinical evaluation. On the other hand, excessive sodium and fluid intake that could reflect non‐compliance may cause HF exacerbation and hospitalizations, and excessive sodium and fluid restrictions increase the perception of thirst (Wickman et al., 2021).
CHAPTER 12
Heart Failure
INTRODUCTION
DEFINITION
CLASSIFICATION
With left ventricular ventilation
Ischemic heart disease and previous myocardial infarction
Primary or secondary dilated cardiomyopathy
Previous myocarditis
End‐stage hypertensive heart disease
End‐stage hypertrophic cardiomyopathy
Aortic regurgitation
Without left ventricular dilatation
Hypertensive heart disease
Ischemic heart disease
Hypertrophic cardiomyopathy
Left ventricular (pseudo)hypertrophy from storage/infiltrative/systemic disease
Restrictive cardiomyopathy
Category
Signs
Acute decompensated HF (ADHF) (I)
With signs and symptoms of acute heart failure (AHF), which are mild and do not complete criteria for cardiogenic shock, pulmonary oedema or hypertensive crisis.
Hypertensive AHF (II)
Of HF together with high blood pressure and relatively preserved left ventricular function with a chest radiograph compatible with acute pulmonary oedema.
AHF with pulmonary oedema (III)
Of severe respiratory distress, with crackles over the lung and orthopnoea.
Cardiogenic shock (IV)
Of reduced blood pressure (systolic BP <90 mmHg or a drop of mean arterial pressure >30 mmHg) and/or low urine output (0.5 ml/kg/h). The pulse rate is over 60 beats per minute, with or without evidence of organ congestion.
High output failure (V)
Of high cardiac output, commonly with high heart rate as a result of arrhythmias, thyrotoxicosis, anaemia, Paget’s disease, iatrogenic or by other mechanisms.
Right‐sided HF (VI)
Of low output syndrome with increased jugular venous pressure, liver size and hypotension.
PREVALENCE
CLINICAL CONDITIONS ASSOCIATED WITH HEART FAILURE
OBESITY
OBESITY PARADOX
MALNUTRITION AND SARCOPENIA HEART FAILURE PATIENTS
DIABETES AND HEART FAILURE
HEART FAILURE IN OLDER ADULTS
COGNITIVE IMPAIRMENT IN PATIENTS WITH HEART FAILURE
THERAPEUTIC MANAGEMENT OF HEART FAILURE
LIFESTYLE FACTORS AND HEART FAILURE
People’s need centered
Refining patient’s ability and skills for daily routines
Encouraging social activities and return to work
Enabling patient’s psychological course
Improving people’s relationship with relatives
Responding to changes in people’s needs
Taking patients part of their therapy
Helping patients to change lifestyle
Providing interdisciplinary team counseling
Reducing re‐hospitalization and clinical outcomes
BODY WEIGHT AND CALORIC RESTRICTION
NUTRITION AND DIETARY APPROACHES
SODIUM RESTRICTION
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